Sympathetic discharge and vascular resistance after bed rest

Shoemaker, J. Kevin, Cynthia S. Hogeman, Urs A. Leuenberger,Michael D. Herr, Kristen Gray, David H. Silber, and Lawrence I. Sinoway. Sympathetic discharge and vascular resistance after bedrest. J. Appl. Physiol. 84(2):612-617, 1998.The effect of 6° head-down-tilt bedrest (HDBR) for 14 days on supine sympathetic discharge andcardiovascular hemodynamics at rest was assessed. Mean arterialpressure, heart rate (n = 25), musclesympathetic nerve activity (MSNA; n = 16) burst frequency, and forearm blood flow(n = 14) were measured, and forearmvascular resistance (FVR) was calculated. Stroke distance,our index of stroke volume, was derived from measurements of aorticmean blood velocity (Doppler) and R-R interval(n = 7). With these data, an index oftotal peripheral resistance was determined. Heart rate at rest wasgreater in the post (71 ± 2 beats/min)- compared with the pre-HDBRtest (66 ± 2 beats/min; P < 0.003), but mean arterial pressure was unchanged. Aortic strokedistance during post-HDBR (15.5 ± 1.1 cm/beat) was reduced frompre-HDBR levels (20.0 ± 1.5 cm/beat)(P < 0.03). Also, MSNA burstfrequency was reduced in the post (16.7 ± 2.8 beats/min)- comparedwith the pre (25.2 ± 2.6 beats/min)-HDBR condition(P < 0.01). Bed rest did not alterforearm blood flow, FVR, or total peripheral resistance. Thusreductions in MSNA with HDBR were not associated with a decrease inFVR.

     

Instantaneous force-velocity-length relationship in diaphragmatic sarcomere

Coirault, Catherine, Denis Chemla, Jean-Claude Pourny,Francine Lambert, and Yves Lecarpentier. Instantaneousforce-velocity-length relationship in diaphragmatic sarcomere.J. Appl. Physiol. 82(2): 404-412, 1997.The simultaneous analysis of muscle force, length, velocity, andtime has been shown to precisely characterize the mechanicalperformance of isolated striated muscle. We tested the hypothesis thatthe three-dimensional force-velocity-length relationship reflectsmechanical properties of sarcomeres. In hamster diaphragm strips,instantaneous sarcomere length (SL) and muscle length were simultaneously measured during afterloaded twitches. SL was measured by means of laser diffraction. Wealso studied the influence of initialSL, abrupt changes in total load, and2 × 10⁷ M dantrolene.Baseline resting SL at the apex of thelength-active tension curve was 2.2 ± 0.1 µm, whereasSL at peak shortening was 1.6 ± 0.1 µm in the preloaded twitch and 2.1 ± 0.1 µm in the "isometric" twitch. Over the whole load continuum and at anygiven level of isotonic load, there was a unique relationship between instantaneous sarcomere velocity and instantaneousSL. Part of this relationship was timeindependent and initial SL independent and was markedly downshifted after dantrolene. When five different muscle regions were considered, there were no significant variations ofSL and sarcomere kinetics along themuscle. These results indicate that the time- and initiallength-independent part of the instantaneous force-velocity-lengthrelationship previously described in muscle strips reflects intrinsicsarcomere mechanical properties.

     

Myocardial blood flow heterogeneity in shock and small-volume resuscitation in pigs with coronary stenosis

Kleen, Martin, Martin Welte, Peter Lackermeier, OliverHabler, Gregor Kemming, and Konrad Messmer. Myocardial blood flowheterogeneity in shock and small-volume resuscitation in pigs withcoronary stenosis. J. Appl. Physiol.83(6): 1832-1841, 1997.We analyzed the effects of shock andsmall-volume resuscitation in the presence of coronary stenosis onfractal dimension (D) and spatialcorrelation (SC) of regional myocardial perfusion. Hemorrhagic shockwas induced and maintained for 1 h. Pigs were resuscitated withhypertonic saline-dextran 60 [HSDex, 10% of shed blood volume(SBV)] or normal saline (NS; 80% of SBV). Therapy was continuedafter 30 min with dextran (10% SBV). At baseline, D was 1.39 ± 0.06 (mean ± SE;HSDex group) and 1.34 ± 0.04 (NS group). SC was 0.26 ± 0.07 (HSDex) and 0.26 ± 0.04 (NS). Left anterior descending coronaryartery stenosis changed neither D norSC. Shock significantly reduced D(i.e., homogenized perfusion): 1.26 ± 0.06 (HSDex) and 1.23 ± 0.05 (NS). SC was increased: 0.41 ± 0.1 (HSDex) and 0.48 ± 0.07 (NS). Fluid therapy with HSDex further decreasedD to 1.22 ± 0.05, whereas NS didnot change D. SC was increased by bothHSDex (0.56 ± 0.1) and NS (0.53 ± 0.06). At 1 h afterresuscitation, SC was constant in both groups, andD was reduced only in the NS group(1.18 ± 0.02). We conclude that hemorrhagic shock homogenizedregional myocardial perfusion in coronary stenosis and that fluidtherapy failed to restore this.

     

Ultrasound evaluation of piglet diaphragm function before and after fatigue

Kocis, Keith C., Peter J. Radell, Wayne I. Sternberger, JaneE. Benson, Richard J. Traystman, and David G. Nichols. Ultrasound evaluation of piglet diaphragm function before and after fatigue. J. Appl. Physiol. 83(5):1654-1659, 1997.Clinically, a noninvasive measure of diaphragmfunction is needed. The purpose of this study is to determine whetherultrasonography can be used to 1)quantify diaphragm function and 2)identify fatigue in a piglet model. Five piglets were anesthetized withpentobarbital sodium and halothane and studied during the followingconditions: 1) baseline (spontaneous breathing); 2) baseline + CO₂ [inhaledCO₂ to increase arterial PCO₂ to 50-60 Torr (6.6-8kPa)]; 3) fatigue + CO₂ (fatigue induced with 30 minof phrenic nerve pacing); and 4)recovery + CO₂ (recovery after 1 hof mechanical ventilation). Ultrasound measurements of the posteriordiaphragm were made (inspiratory mean velocity) in the transverseplane. Images were obtained from the midline, just inferior to thexiphoid process, and perpendicular to the abdomen. M-mode measures weremade of the right posterior hemidiaphragm in the plane just lateral tothe inferior vena cava. Abdominal and esophageal pressures weremeasured and transdiaphragmatic pressure (Pdi) was calculated duringspontaneous (Sp) and paced (Pace) breaths. Arterial blood gases werealso measured. Pdi(Sp) and Pdi(Pace)during baseline + CO₂ were 8 ± 0.7 and 49 ± 11 cmH₂O, respectively, anddecreased to 6 ± 1.0 and 27 ± 7 cmH₂O,respectively, during fatigue + CO₂. Mean inspiratory velocityalso decreased from 13 ± 2 to 8 ± 1 cm/s during theseconditions. All variables returned to baseline during recovery + CO₂. Ultrasonography can beused to quantify diaphragm function and identify piglet diaphragm fatigue.

     

Femoral arterial injection of adenosine in humans elevates MSNA via central but not peripheral mechanisms

MacLean, D. A., B. Saltin, G. Rådegran, and L. Sinoway. Femoral arterial injection of adenosine in humanselevates MSNA via central but not peripheral mechanisms.J. Appl. Physiol. 83(4):1045-1053, 1997.The purpose of the present study was to examinethe effects of femoral arterial injections of adenosine on musclesympathetic nerve activity (MSNA) under three different conditions.These conditions were adenosine injection alone, adenosine injectionafter phenylephrine infusion, and adenosine injection distal to a thighcuff inflated to arrest the circulation. The arterial injection ofadenosine alone resulted in a fourfold (255 ± 18 U/min) increaseabove baseline (73 ± 12 U/min; P < 0.05) in MSNA with an onset latency of 15.8 ± 0.8 s from thetime of injection. The systemic infusion of phenylephrine resulted in an increase (P < 0.05) in meanarterial pressure of ~10 mmHg and a decrease(P < 0.05) in heart rate of8-10 beats/min compared with baseline values before phenylephrineinfusion. After adenosine injection, the onset latency for the increasein MSNA was delayed to 19.2 ± 2.1 s and the magnitude of increasewas attenuated by ~50% (123 ± 20 U/min) compared with adenosineinjection alone (P < 0.05). When acuff was inflated to 220 mmHg to arrest the circulation and adenosinewas injected into the leg distal to the inflated cuff, there were nosignificant changes in MSNA or any of the other measured variables.However, on deflation of the cuff, there was a rapid increase(P < 0.05) in MSNA, with an onsetlatency of 9.1 ± 0.9 s, and the magnitude of increase (276 ± 28 U/min) was similar to that observed for adenosine alone. These datasuggest that ~50% of the effects of exogenously administered adenosine are a result of baroreceptor unloading due to a drop in bloodpressure. Furthermore, the finding that adenosine did not directlyresult in an increase in MSNA while it was trapped in the leg but thatit needed to be released into the circulation suggests that adenosinedoes not directly stimulate thin fiber muscle afferents in the leg ofhumans. In contrast, it would appear that adenosine exerts its effectsvia some other chemically sensitive pool of afferents.

     

Pulmonary blood flow distribution has a hilar-to-peripheral gradient in awake, prone sheep

Walther, Sten M., Karen B. Domino, Robb W. Glenny, Nayak L. Polissar, and Michael P. Hlastala. Pulmonary blood flow distribution has a hilar-to-peripheral gradient in awake, prone sheep.J. Appl. Physiol. 82(2): 678-685, 1997.We examined the pulmonary blood flow distribution withintravenous fluorescent microspheres (15 µm) in nine prone,unanesthetized, lambs. Lungs flushed free of blood were air-dried attotal lung capacity and sectioned into~2-cm³ pieces. The pieces wereweighed, identified by lobe, and assigned spatial coordinates.Fluorescence was read on a spectrophotometer, and signals werecorrected for piece weight and normalized to mean flow. Pulmonary bloodflow heterogeneity was assessed by using the coefficient of variationof the flow data. The number of pieces (±SD) analyzed were 1,249 ± 150/animal. Heterogeneity of blood flow was 29.5 ± 6.5%(coefficient of variation = SD/mean). Pulmonary blood flow decreasedwith distance from hilus (P < 0.002) but did not change significantly with vertical height. Distance fromthe hilus was the best predictor of pulmonary blood flow (R² = 0.201) and,together with spatial coordinates and lobe, accounted for 33.7 ± 12.0% of blood flow variability. We conclude that pulmonary blood flowin the awake, prone sheep is distributed with a hilar-to-peripheral gradient but no significant vertical gradient.

     

Atrial distension in humans during microgravity induced by parabolic flights

Videbaek, Regitze, and Peter Norsk. Atrialdistension in humans during microgravity induced by parabolic flights.J. Appl. Physiol. 83(6):1862-1866, 1997.The hypothesis was tested that human cardiacfilling pressures increase and the left atrium is distended during 20-speriods of microgravity (µG) created by parabolic flights, comparedwith values of the 1-G supine position. Left atrial diameter(n = 8, echocardiography) increasedsignificantly during µG from 26.8 ± 1.2 to 30.4 ± 0.7 mm(P < 0.05). Simultaneously, centralvenous pressure (CVP; n = 6, transducer-tipped catheter) decreased from 5.8 ± 1.5 to 4.5 ± 1.1 mmHg (P < 0.05), and esophageal pressure (EP; n = 6) decreased from1.5 ± 1.6 to 4.1 ± 1.7 mmHg (P < 0.05). Thus transmural CVP(TCVP = CVP  EP; n = 4)increased during µG from 6.1 ± 3.2 to 10.4 ± 2.7 mmHg(P < 0.05). It is concluded thatshort periods of µG during parabolic flights induce an increase inTCVP and left atrial diameter in humans, compared with the resultsobtained in the 1-G horizontal supine position, despite a decrease inCVP.

     

Effects of transient intrathoracic pressure changes (hiccups) on systemic arterial pressure

Mathew, Oommen P. Effects of transient intrathoracicpressure changes (hiccups) on systemic arterial pressure.J. Appl. Physiol. 83(2): 371-375, 1997.The purpose of the study was to determine the effect oftransient changes in intrathoracic pressure on systemic arterialpressure by utilizing hiccups as a tool. Values of systolic anddiastolic pressures before, during, and after hiccups were determinedin 10 intubated preterm infants. Early-systolic hiccups decreasedsystolic blood pressure significantly (P < 0.05) compared with control(39.38 ± 2.72 vs. 46.46 ± 3.41 mmHg) and posthiccups values,whereas no significant change in systolic blood pressure occurredduring late-systolic hiccups. Diastolic pressure immediately after thehiccups remained unchanged during both early- and late-systolichiccups. In contrast, diastolic pressure decreased significantly(P < 0.05) when hiccups occurred during diastole (both early and late). Systolic pressures of the succeeding cardiac cycle remained unchanged after early-diastolic hiccups, whereas they decreased after late-diastolic hiccups. Theseresults indicate that transient decreases in intrathoracic pressurereduce systemic arterial pressure primarily through an increase in thevolume of the thoracic aorta. A reduction in stroke volume appears tocontribute to the reduction in systolic pressure.

     

Almitrine and doxapram decrease fatigue and increase subsequent recovery in isolated rat diaphragm

McGuire, Michelle, Michael F. Carey, and John J. O'Connor.Almitrine and doxapram decrease fatigue and increase subsequent recovery in isolated rat diaphragm. J. Appl.Physiol. 83(1): 52-58, 1997.The effects ofalmitrine bimesylate and doxapram HCl on isometric force produced by invitro rat diaphragm were studied during direct muscle activation at37°C. Doxapram and almitrine ameliorate respiratory failureclinically by indirectly increasing phrenic nerve activity. This studywas carried out to investigate possible direct actions of these agentson the diaphragm before and after fatigue of the fibers. Two age groupsof animals were chosen [6-14 wk (group1) and 50-55 wk (group2)] because it is known that increasing agedecreases a muscle fiber's resistance to fatigue. Muscle strips wereisolated from both group 1 and group 2 and directly stimulated (2-mspulse duration, 5-15 V) to produce twitch tensions of 1.3 and 2.1 N/cm², respectively. At lowconcentrations, doxapram (20 µg/ml) and almitrine (12 µg/ml)had no effect on twitch contraction or 100-Hz tetanic tension. However,40 µg/ml doxapram and 30 µg/ml almitrine increased twitch tensionby 9.0 ± 1.4 and 11.6 ± 1.9%, respectively, in animals ofgroup 2 (n = 5). A fatigue protocol consistingof low-frequency stimulation (30-Hz trains, 250-ms duration every 2 sfor 5 min) caused a reduction of twitch tension in animals ofgroup 1 (48 ± 4% ofcontrol) and group 2 (28 ± 4% ofcontrol). At 90 min postfatigue, the twitch tension recovered to 72 ± 3 and 42 ± 2% of control values ingroup 1 and group2, respectively. In the presence of doxapram (20 µg/ml), there was a significant increase in the recovery of twitchtension at 90 min in group 1 andgroup 2 (84.5 ± 3.2 and 80.1 ± 2.8%, respectively) compared with controls at 90 min postfatigue. Inthe presence of almitrine (12 µg/ml), there was a full recovery fromfatigue in group 1 animals (100% ofcontrol) and a recovery to 95.6 ± 2.1% of control ingroup 2 animals at 90 min. Theseresults demonstrate a significant improvement in the rapidity andmagnitude of recovery from fatigue in the rat diaphragm muscle in thepresence of both doxapram and, especially, almitrine. These effects maybe due to changes in intracellular calcium, ADP/ATP ratios, or oxygenfree radical scavenging.

     

Alignment of microvascular units along skeletal muscle fibers of hamster retractor

Emerson, Geoffrey G., and Steven S. Segal. Alignment ofmicrovascular units along skeletal muscle fibers of hamster retractor.J. Appl. Physiol. 82(1): 42-48, 1997.When muscle fibers contract, blood flow requirements increasealong their entire length. However, the organization of capillaryperfusion along muscle fibers is unclear. The microvascular unit (MVU)is defined as a terminal arteriole and the group of capillaries itsupplies. We investigated whether neighboring MVUs along the fiber axis perfused the same group of muscle fibers by using the parallel-fibered retractor muscle. Hamsters were anesthetized and perfused with Microfilto visualize MVUs relative to muscle fibers. Fields of study, whichencompassed five to seven neighboring MVUs along a muscle fiber, werechosen from the interior of muscles and along muscle edges. On average,MVUs were 1 mm in length, 0.50 mm in width, and 0.1 mm deep; segmentsof ~30 fibers were contained in this tissue volume of 0.05 mm³ (20 MVUs/mg muscle). The totaldistance across muscle fibers encompassed by a pair of MVUs isdesignated "union" (U); the fraction of this distance common toboth MVUs is designated "intersection" (I). The ratio of I to Ufor the widths of neighboring MVUs provides an index of MVU alignmentalong muscle fibers (e.g., I/U = 1.0 indicates complete alignment,where the fibers perfused by one MVU are the same as those perfused bythe neighboring MVU). We found that I/U along muscle edges (0.71 ± 0.02) was greater (P < 0.05) thanthe ratio measured within muscles (0.66 ± 0.02). A model predicteda maximum I/U of 0.58 with random MVU alignment. Thus measured valueswere closer to random than to complete alignment. These findingsindicate that an increase in blood flow along muscle fibers requiresthe perfusion of many MVUs and imply that vasodilation is coordinatedamong the parent arterioles from which corresponding MVUsarise.

     

Measurement of pulmonary blood flow by fractal analysis of flow heterogeneity in isolated canine lungs

Barman, Scott A., Laryssa L. McCloud, John D. Catravas, andIna C. Ehrhart. Measurement of pulmonary blood flow by fractalanalysis of flow heterogeneity in isolated canine lungs. J. Appl. Physiol. 81(5):2039-2045, 1996.Regional heterogeneity of lung blood flow can bemeasured by analyzing the relative dispersion (RD) of mass(weight)-flow data. Numerous studies have shown that pulmonary bloodflow is fractal in nature, a phenomenon that can be characterized bythe fractal dimension and the RD for the smallest realizable volumeelement (piece size). Although information exists for theapplicability of fractal analysis to pulmonary blood flow in wholeanimal models, little is known in isolated organs. Therefore, thepresent study was done to determine the effect of blood flow rate onthe distribution of pulmonary blood flow in the isolated blood-perfusedcanine lung lobe by using fractal analysis. Four different radiolabeledmicrospheres (¹⁴¹Ce,⁹⁵Nb,⁸⁵Sr, and⁵¹Cr), each 15 µm in diameter,were injected into the pulmonary lobar artery of isolated canine lunglobes (n = 5) perfused at fourdifferent flow rates ( flow1 = 0.42 ± 0.02 l/min;flow2 = 1.12 ± 0.07 l/min;flow 3 = 2.25 ± 0.17 l/min; flow 4 = 2.59 ± 0.17 l/min), and the pulmonary blood flow distribution was measured. Theresults of the present study indicate that under isogravimetric bloodflow conditions, all regions of horizontally perfused isolated lunglobes received blood flow that was preferentially distributed to themost distal caudal regions of the lobe. Regional pulmonary blood flowin the isolated perfused canine lobe was heterogeneous and fractal innature, as measured by the RD. As flow rates increased, fractal dimension values (averaging 1.22 ± 0.08) remained constant, whereas RD decreased, reflecting more homogeneous blood flowdistribution. At any given blood flow rate, high-flow areas of the lobereceived a proportionally larger amount of regional flow, suggestingthat the degree of pulmonary vascular recruitment may also be spatially related.

     

Irregularities and power law distributions in the breathing pattern in preterm and term infants

Unlike olderchildren, young infants are prone to develop unstable respiratorypatterns, suggesting important differences in their control ofbreathing. We examined the irregular breathing pattern in infants bymeasuring the time interval between breaths ("interbreathinterval"; IBI) assessed from abdominal movement during 2 h of sleepin 25 preterm infants at a postconceptional age of 40.5 ± 5.2 (SD) wk and in 14 term healthy infants at a postnatal age of 8.2 ± 4 wk. In 10 infants we performed longitudinal measurements on twooccasions. We developed a threshold algorithm for the detection of abreath so that an IBI included an apneic period and potentially someperiods of insufficient tidal breathing excursions (hypopneas). Theprobability density distribution (P) of IBIs follows a power law,P(IBI)~IBI,with the exponent  providing a statistical measurement of the relative risk of insufficient breathing. With maturation,  increased from 2.62 ± 0.4 at 41.2 ± 3.6 wk to 3.22 ± 0.4 at47.3 ± 6.4 wk postconceptional age, indicating a decrease in longhypopneas (for paired data P = 0.002). The statisticalproperties of IBI were well reproduced in a model of the respiratoryoscillator on the basis of two hypotheses:1) tonic neural inputs to the respiratory oscillator are noisy; and2) the noise explores a criticalregion where IBI diverges with decreasing tonic inputs. Accordingly,maturation of infant respiratory control can be explained by the tonicinputs moving away from this critical region. We conclude thatbreathing irregularities in infants can be characterized by , whichprovides a link between clinically accessible data and theneurophysiology of the respiratory oscillator.

     

Contribution of abdomen and legs to central blood volume expansion in humans during immersion

Johansen, Lars Bo, Thomas Ulrik Skram Jensen, Bettina Pump,and Peter Norsk. Contribution of abdomen and legs to central bloodvolume expansion in humans during immersion. J. Appl.Physiol. 83(3): 695-699, 1997.The hypothesis wastested that the abdominal area constitutes an important reservoir forcentral blood volume expansion (CBVE) during water immersion inhumans. Six men underwent 1) water immersion for 30 min (WI),2) water immersion for 30 min withthigh cuff inflation (250 mmHg) during initial 15 min to exclude legsfrom contributing to CBVE (WI+Occl), and3) a seated nonimmersed control with15 min of thigh cuff inflation (Occl). Plasma protein concentration andhematocrit decreased from 68 ± 1 to 64 ± 1 g/l and from 46.7 ± 0.3 to 45.5 ± 0.4%(P < 0.05), respectively, during WIbut were unchanged during WI+Occl. Left atrial diameter increased from27 ± 2 to 36 ± 1 mm (P < 0.05) during WI and increased similarly during WI+Occl from 27 ± 2 to 35 ± 1 mm (P < 0.05). Centralvenous pressure increased from 3.7 ± 1.0 to 10.4 ± 0.8 mmHg during WI (P < 0.05) butonly increased to 7.0 ± 0.8 mmHg during WI+Occl(P < 0.05). In conclusion, the dilution of blood induced by WI to the neck is caused by fluid from thelegs, whereas the CBVE is caused mainly by blood from theabdomen.

     

Recovery of diaphragmatic function in awake sheep after two approaches to thoracic surgery

Imanaka, Hideaki, William R. Kimball, John C. Wain, MasajiNishimura, Kenichi Okubo, Dean Hess, and Robert M. Kacmarek. Recovery of diaphragmatic function in awake sheep after two approaches to thoracic surgery. J. Appl.Physiol. 83(5): 1733-1740, 1997.Video-assistedthoracoscopic surgery (VATS) is replacing thoracotomy, but no study hasaddressed the extent or duration of VATS-induced diaphragmaticalteration. We hypothesized that VATS would impair diaphragmaticfunction less and return diaphragmatic function faster thanthoracotomy. In eight sheep, sonomicrometers were randomly implanted onthe right costal diaphragm via VATS or thoracotomy. Diaphragmaticresting length, shortening fraction, and respiratory function weremeasured weekly during quiet breathing (QB) andCO₂ rebreathing for 4 wk. ForVATS, shortening fraction was smallest onpostoperative days 1 (POD 1) (6.4 ± 3.4 and12.9 ± 8.7% during QB and 10%CO₂ rebreathing, respectively) and7 (6.3 ± 3.4 and 16.9 ± 4.0%during QB and 10% CO₂rebreathing, respectively) and recovered by 3 wk (13.2 ± 1.8 and28.9 ± 8.0% during QB and 10%CO₂ rebreathing, respectively).For thoracotomy, shortening fraction at 10%CO₂ rebreathing was smaller onPODs 1, 7, 14 (15.9 ± 7.1, 13.6 ± 5.4, and 19.0 ± 6.9%) than onPOD 28 (29.9 ± 8.2%), but notduring QB on POD 1 or7 (7.5 ± 3.8 and 3.4 ± 2.6%)compared with POD 28 (10.7 ± 8.7%). Shortening fraction did not differ between surgeries. There wasno group difference in minute ventilation, respiratory rate,transdiaphragmatic pressure, or esophageal and gastric pressures. Inconclusion, although shortening fraction recovered faster for VATS,this translated into insignificant functional differences.

     

Ultrasound Doppler estimates of femoral artery blood flow during dynamic knee extensor exercise in humans

Rådegran, G. Ultrasound Dopplerestimates of femoral artery blood flow during dynamic knee extensorexercise in humans. J. Appl. Physiol.83(4): 1383-1388, 1997.Ultrasound Doppler has been used tomeasure arterial inflow to a human limb during intermittent staticcontractions. The technique, however, has neither been thoroughlyvalidated nor used during dynamic exercise. In this study, the inherentproblems of the technique have been addressed, and the accuracy wasimproved by storing the velocity tracings continuously and calculatingthe flow in relation to the muscle contraction-relaxation phases. Thefemoral arterial diameter measurements were reproducible with a meancoefficient of variation within the subjects of 1.2 ± 0.2%. Thediameter was the same whether the probe was fixed or repositioned atrest (10.8 ± 0.2 mm) or measured during dynamic exercise. The bloodvelocity was sampled over the width of the diameter and the parabolicvelocity profile, since sampling in the center resulted in anoverestimation by 22.6 ± 9.1% (P < 0.02). The femoral arterial Doppler blood flow increased linearly(r = 0.997, P < 0.001) with increasing load [Doppler blood flow = 0.080 · load (W) + 1.446 l/min] and was correlated positively with simultaneousthermodilution venous outflow measurements(r = 0.996, P < 0.001). The two techniques werelinearly related (Doppler = thermodilution · 0.985 + 0.071 l/min; r = 0.996, P < 0.001), with a coefficient ofvariation of ~6% for both methods.

     

Cerebral vasomotor reactivity at high altitude in humans

The purpose of this study was twofold:1) to determine whether at highaltitude cerebral blood flow (CBF) as assessed during CO₂ inhalation and duringhyperventilation in subjects with acute mountain sickness (AMS) wasdifferent from that in subjects without AMS and2) to compare the CBF as assessedunder similar conditions in Sherpas at high altitude and in subjects atsea level. Resting control values of blood flow velocity in themiddle cerebral artery (V_MCA), pulseoxygen saturation (Sa_O2), andtranscutaneous PCO₂ were measured at4,243 m in 43 subjects without AMS, 17 subjects with AMS, 20 Sherpas,and 13 subjects at sea level. Responses ofCO₂ inhalation andhyperventilation onV_MCA,Sa_O2, and transcutaneous PCO₂ were measured, and the cerebralvasomotor reactivity (VMR = V_MCA/PCO₂)was calculated as the fractional change ofV_MCA per Torrchange of PCO₂, yielding ahypercapnic VMR and a hypocapnic VMR. AMS subjects showeda significantly higher resting controlV_MCA than didno-AMS subjects (74 ± 22 and 56 ± 14 cm/s, respectively;P < 0.001), andSa_O2 was significantly lower (80 ± 8 and 88 ± 3%, respectively; P < 0.001). Resting control V_MCA values inthe sea-level group (60 ± 15 cm/s), in the no-AMS group, and inSherpas (59 ± 13 cm/s) were not different. Hypercapnic VMR valuesin AMS subjects were 4.0 ± 4.4, in no-AMS subjects were 5.5 ± 4.3, in Sherpas were 5.6 ± 4.1, and in sea-level subjects were 5.6 ± 2.5 (not significant). Hypocapnic VMR values were significantly higher in AMS subjects (5.9 ± 1.5) compared with no-AMS subjects (4.8 ± 1.4; P < 0.005) but werenot significantly different between Sherpas (3.8 ± 1.1) and thesea-level group (2.8 ± 0.7). We conclude that AMS subjects havegreater cerebral hemodynamic responses to hyperventilation, higherV_MCAresting control values, and lower Sa_O2 compared with no-AMSsubjects. Sherpas showed a cerebral hemodynamic patternsimilar to that of normal subjects at sea level.     

Segmental body composition assessed by bioelectrical impedance analysis and DEXA in humans

Bracco, David, Daniel Thiébaud, René L. Chioléro, Michel Landry, Peter Burckhardt, and Yves Schutz.Segmental body composition assessed by bioelectrical impedanceanalysis and DEXA in humans. J. Appl.Physiol. 81(6): 2580-2587, 1996.The present study assessed the relative contribution of each body segment to wholebody fat-free mass (FFM) and impedance and explored the use ofsegmental bioelectrical impedance analysis to estimate segmental tissuecomposition. Multiple frequencies of whole body and segmentalimpedances were measured in 51 normal and overweight women. Segmental tissue composition was independentlyassessed by dual-energy X-ray absorptiometry. The sum ofthe segmental impedance values corresponded to the whole body value(100.5 ± 1.9% at 50 kHz). The arms and legs contributed to 47.6 and 43.0%, respectively, of whole body impedance at 50 kHz, whereas they represented only 10.6 and 34.8% of total FFM, asdetermined by dual-energy X-ray absorptiometry. The trunk averaged10.0% of total impedance but represented 48.2% of FFM. For eachsegment, there was an excellent correlation between the specificimpedance index(length²/impedance) and FFM(r = 0.55, 0.62, and 0.64 for arm,trunk, and leg, respectively). The specific resistivity was in asimilar range for the limbs (159 ± 23 cm for the arm and 193 ± 39 cm for the leg at 50 kHz) but was higher for the trunk (457 ± 71 cm). This study shows the potential interest of segmental bodycomposition by bioelectrical impedance analysis and provides specificsegmental body composition equations for use in normal and overweightwomen.

     

Systemic and pulmonary hemodynamic responses to normal and obstructed breathing during sleep

Schneider, H., C. D. Schaub, K. A. Andreoni, A. R. Schwartz,R. L. Smith, J. L. Robotham, and C. P. O'Donnell. Systemic andpulmonary hemodynamic responses to normal and obstructed breathing during sleep. J. Appl. Physiol. 83(5):1671-1680, 1997.We examined the hemodynamic responses to normalbreathing and induced upper airway obstructions during sleep in acanine model of obstructive sleep apnea. During normal breathing,cardiac output decreased (12.9 ± 3.5%,P < 0.025) from wakefulness tonon-rapid-eye-movement sleep (NREM) but did not change from NREM torapid-eye-movement (REM) sleep. There was a decrease(P < 0.05) in systemic (7.2 ± 2.1 mmHg) and pulmonary (2.0 ± 0.6 mmHg) arterial pressures fromwakefulness to NREM sleep. In contrast, systemic (8.1 ± 1.0 mmHg,P < 0.025), but not pulmonary,arterial pressures decreased from NREM to REM sleep. During repetitiveairway obstructions (56.0 ± 4.7 events/h) in NREM sleep, cardiacoutput (17.9 ± 3.1%) and heart rate (16.2 ± 2.5%) increased(P < 0.05), without a change instroke volume, compared with normal breathing during NREM sleep. Duringsingle obstructive events, left (7.8 ± 3.0%,P < 0.05) and right (7.1 ± 0.7%, P < 0.01)ventricular outputs decreased during the apneic period. However, left(20.7 ± 1.6%, P < 0.01) andright (24.0 ± 4.2%, P < 0.05)ventricular outputs increased in the postapneic period because of anincrease in heart rate. Thus 1) thesystemic, but not the pulmonary, circulation vasodilates during REMsleep with normal breathing; 2)heart rate, rather than stroke volume, is the dominant factormodulating ventricular output in response to apnea; and3) left and right ventricular outputs oscillate markedly and in phase throughout the apnea cycle.

     

Angiogenesis in bronchial circulatory system after unilateral pulmonary artery obstruction

Charan, Nirmal B., and Paula Carvalho. Angiogenesis inbronchial circulatory system after unilateral pulmonary artery obstruction. J. Appl. Physiol. 82(1):284-291, 1997.We studied the effects of left pulmonary artery(LPA) ligation on the bronchial circulatory system (BCS) by using asheep model. LPA was ligated in the newborn lambs soon after birth(n = 8), and when the sheep were ~3yr of age anatomic studies revealed marked angiogenesis in BCS.Bronchial blood flow and cardiac output were studied by placing flowprobes around the bronchial and pulmonary arteries in four adult sheep.After LPA ligation, bronchial blood flow increased from 35 ± 6 to134 ± 42 ml/min in ~3 wk (P < 0.05). We also studied gas-exchange functions of BCS ~3 yr after the ligation of LPA in newborn lambs (n = 4) and used a control group (n = 12)in which LPA was ligated acutely. In the left lung,O₂ uptake after acute ligation was16 ± 3 ml/min and was similar to the chronic model, whereasCO₂ output in the control group was 27 ± 3 ml/min compared with 79 ± 12 ml/min in the chronic preparation (P < 0.05).We conclude that LPA ligation causes marked angiogenesis in BCS that iscapable of performing some gas-exchange functions.

     

Fetal sheep adrenal blood flow responses to hypoxemia after splanchnicotomy using fluorescent microspheres

Buchwalder, Lynn F., Michelle Lin, Thomas J. McDonald, andPeter W. Nathanielsz. Fetal sheep adrenal blood flow responses tohypoxemia after splanchnicotomy using fluorescent microspheres. J. Appl. Physiol. 84(1): 82-89, 1998.Adrenal gland blood flow (ABF) increases during hypoxemia infetal sheep, but regulation of ABF is poorly understood. The purpose ofthis study was to determine the effects of splanchnic nerve section onfetal ABF responses to hypoxemia using the fluorescent microsphere (FM) technique. At 125 days of gestation, 14 unanesthetized fetal sheep [bilateral splanchnicotomy (Splx,n = 6) and control (Cont,n = 8)] were injectedwith FM before and at 60 min ofN₂-induced hypoxemia (~40%decrease in fetal arterial PO₂).Adrenal tissue and reference blood samples were digested and filtered, and FM dye was extracted for spectrometer analysis. Baseline whole, medullary, and cortical ABF for the Cont group were similar to published values using radioactive microspheres and did not differ fromSplx values. Hypoxemia increased whole, medullary, and cortical ABF(mean ± SE) from baseline for the Cont group by 281 ± 35, 258 ± 31, and 496 ± 81% (P < 0.05). The increase for the Splx group was attenuated compared with theCont group (P < 0.05) for whole andmedullary ABF (139 ± 27 and 43 ± 27%) but not cortical ABF(326 ± 91%). We conclude that1) the FM technique is valid formeasuring fetal ABF and 2) in fetalsheep the splanchnic nerve is not necessary to maintain basal ABF butplays an important role in regulating the hypoxemia-induced increase inABF through the medullary, but not cortical, ABF response.