Effects of prostaglandin F2 alpha and prostacyclin on pulmonary microcirculation in the cat

In pulmonary microcirculation, using a new X-ray television system, we measured the effects of prostaglandin F2 alpha (PGF2 alpha) and prostacyclin on the internal diameter (ID), flow velocity, volume flow, and transit times of a contrast medium in small arteries (Ta) and veins (Tv) in anesthetized cats. The ID of the arteries and veins ranged from 100 to 500 micron. PGF2 alpha, 0.3, 1, and 3 micrograms/kg, predominantly decreased ID on the arterial side in a dose-dependent manner but increased flow velocity 27-62%. Consequently, volume flow was kept relatively constant. With PGF2 alpha, Ta and Tv were decreased 18-41% and 4-15%, respectively. Prostacyclin, 2 and 4 micrograms/kg, uniformly dilated the ID of small arteries 9-16% but did not change small veins. With prostacyclin, flow velocity was unchanged or decreased, whereas volume flow was increased significantly, 27-32%. No significant changes of Ta and Tv were observed in response to prostacyclin. When both prostaglandins, PGF2 alpha and prostacyclin, were administered, they canceled each other with respect to the ID of small pulmonary arteries. Prostacyclin also prevented the PGF2 alpha-induced vasoconstriction of the pulmonary venous microcirculation.     

Nonuniform effects of histamine on small pulmonary vessels in cats

In in vivo cat lung, using an X-ray TV system, we analyzed responses in internal diameter (ID), flow velocity, and volume flow of arteries and veins (100-500 microns ID) to histamine (8-15 micrograms/kg iv) under three conditions. With histamine alone, three types of ID response (constriction, dilatation, and no change) occurred in parallel-arranged arteries. Relative frequency and magnitude of constriction were maximum in arteries of 300-400 micron ID, whereas those of dilatation were maximum in arteries of 100-200 micron ID. In veins, relatively uniform constriction occurred. Under H2-blockade, histamine caused greater constriction than that with histamine alone in arteries and veins of 300-500 micron ID. Under beta-blockade, with histamine, ID of all vessels decreased significantly below the ID sizes under the above two conditions, and no dilatation occurred. In two parallel arteries that showed opposite ID changes to histamine, flow velocity increased, but volume flow decreased in a constricted artery while it increased in a dilated one. Those data indicated that, with histamine, qualitatively and quantitatively nonuniform ID response was induced in both parallel- and series-arranged small pulmonary arteries and, in turn, produced heterogeneous flow distribution. Factors to cause the nonuniformity may be partly explained by difference in density of H2- and beta-receptors in vascular walls.     

Effects of regional alveolar hypoxia and hypercapnia on small pulmonary vessels in cats

Using an X-ray TV system, we analyzed responses in the internal diameter (ID), flow velocity, and volume flow in small pulmonary vessels (100-600 microns ID) during unilobar hypoxia and hypercapnia in cats. In the hypoxic and hypercapnic lobes, the ID reduced in proportion to the degree of hypoxia and hypercapnia, respectively. The ID reduction was larger in the arteries than in the veins for a given stimulus. In the arteries, the ID reduced nonuniformly in the series-arranged vessels in response to both stimuli. The percentage ID reduction was maximal in the arteries of 200-300 microns ID, in which it was 21, 26, 28, and 36% with 5% O2, 0% O2, 5% CO2, and 10% CO2 inhalations, respectively. On the other hand, in the veins, uniform ID reduction occurred for a given stimulus. In the contralateral normoxic lobe, the ID did not change significantly. In both hypoxic and hypercapnic lobes, the flow velocity and volume flow of the small arteries decreased, with 5% O2, by 18 and 40%, respectively, and, with 5% CO2, by 23 and 50%, respectively. In contrast, in the normoxic lobe, they increased significantly during 5% O2 and 5% CO2 inhalations. We concluded that regional alveolar hypoxia and hypercapnia induced a local vasoconstriction particularly in the small arteries of 200-300 microns ID and decreased the flow velocity and volume flow in the same lung region.     

Diameter and flow velocity changes in small pulmonary vessels due to microembolization

The pulmonary vascular bed was embolized with glass beads in small doses that induced no significant changes in pulmonary arterial pressure in anesthetized cats. We analyzed changes in internal diameter (ID), flow velocity, and volume flow of embolized and nonembolized arteries simultaneously with ID changes of small veins. In embolized arteries, with 180-, 300-, and 500-microns beads, ID constricted maximally in just proximal portions of the plug by 22, 23, and 17%, respectively, but with 840-microns beads, no ID constriction occurred. With 50-microns beads, the maximum ID constriction occurred in arteries of 200-300 microns but not in those of 100-200 microns. The constriction decreased in the upstream larger arteries and disappeared in those greater than 800 microns ID. In the nonembolized arteries no ID change occurred. Veins constricted slightly compared with arteries. By heparin pretreatment, ID constriction was slightly attenuated in arteries and was almost abolished in veins, whereas it was not affected with hexamethonium bromide. At a branching site, volume flow to an embolized artery decreased because of a decrease in ID and flow velocity, whereas volume flow to a nonembolized artery increased because of an increase in flow velocity. We concluded that pulmonary microembolization induced a vasoconstriction chiefly in small pulmonary arteries upstream to the plug. After embolization, blood flow was locally redistributed from an embolized to a nonembolized artery at a branching site. Arterial vasoconstriction may be mediated chiefly by local mechanical factors.     

Total deposition of ultrafine sodium chloride particles in human lungs

The total deposition of monodisperse, 0.026-0.19 micron (dry volume equivalent diameter) sodium chloride particles in the lungs of five healthy subjects, who breathed orally, was measured. For a tidal volume of 1,000 ml and flow rate of 500 ml/s, the percentages deposited were: 37.2 +/- 8.4% (mean +/- SD) for 0.026 micron, 23.8 +/- 3.3% for 0.051 micron, 22.8 +/- 3.1% for 0.096 micron, and 31.8 +/- 6.2% for 0.19 micron particles. The deposition minimum corresponded to a particle size of approximately 0.08 micron. Deposition did not correlate with measures of lung volume or body size but did correlate with forced expired flow rate after 75% of forced vital capacity (FVC) exhaled (FEF 75%/FVC) and with percent-predicted values for FEF 25-75% and FEF 75%. Lengthening the breathing period from 4 to 8 s/breath while maintaining flow rate at 500 ml/s caused an additional 11.3 +/- 3.1% of the inhaled particles to deposit. Sedimentation and diffusion were found to be the principal deposition mechanisms. These hygroscopic particles deposited according to sizes they would attain in air with a relative humidity between 96 and 100%.     

Duplex sonography of arteriovenous fistula in chronic hemodialysis patients

Duplex sonography was used to assess functional features of arteriovenous fistula (AVF) for hemodialysis (HD). Internal diameter (ID), resistance index (RI) and blood flow (BF) velocity in feeding artery and in vein ofAVF, and venous BF volume were analyzed with purpose to determine the normal values. Presumed normal BF velocities are those of clinically well functioning shunts, allowing BF through HD lines of minimally 250 ml/min. Study included 66 nondiabetic HDpatients (30 women, 36 men), mean age 52-13 years, treated by HD for median 61 (4-252) months. Measurements in 47patients with clinically well functioning AVF were as followed: mean arterial ID 5.2 +/- 1.4 mm, median arterial RI 0.3 (0.3-0.9), median arterial BF velocity 1.5 (0.6-3.6) m/s, mean venous ID 7.6 +/- 2.2 mm, median venous RI 0.3 (0.3-0.9), mean venous BF velocity 1.6 +/- 0.7 m/s, and median venous BF volume 530 (120-1890) ml/min. Patients with poor functioning AVF had significantly less arterial ID, higher arterial RI, less venous ID, less venous BF velocity and volume. Duplex sonography findings obtained for clinically estimated well functioning shunt should be considered as normal Doppler values. Blood vessels' morphologic features depend upon age, and older patients have more pronounced changes.     

Potent vasodilator responses to human urotensin-II in human pulmonary and abdominal resistance arteries

The peptide human urotensin-II (hUT-II) and its receptor have recently been cloned. The vascular function of this peptide in humans, however, has yet to be determined. Vasoconstrictor and vasodilator responses to hUT-II were investigated in human small muscular pulmonary arteries [approximately 70 microm internal diameter (ID)] and human abdominal resistance arteries (approximately 200 microm ID). Vasodilator responses were investigated in endothelin-1 (3 nM) precontracted vessels and, in the small pulmonary vessels, compared with the known vasodilators adrenomedullin, sodium nitroprusside, and acetylcholine. In human small pulmonary arteries, hUT-II did not induce vasoconstriction but was a potent vasodilator [-log M concentration causing 50% of the maximum vasodilator effect (pIC(50)) 10.4 +/- 0.5; percentage of reduction in tone (E(max)) 81 +/- 8% (vs. 23 +/- 11% in time controls), n = 5]. The order of potency for vasodilation was human urotensin-II = adrenomedullin (pIC(50) 10.1 +/- 0.4, n = 6) > sodium nitroprusside (pIC(50) 7.4 +/- 0.2, n = 6) = acetylcholine (pIC(50) 6.8 +/- 0.3, n = 6). In human abdominal arteries, hUT-II did not induce vasoconstriction but was a potent vasodilator [pIC(50) 10.3 +/- 0.7; E(max) 96 +/- 8% (vs. 43 +/- 16% in time controls), n = 4]. This is the first report that hUT-II is a potent vasodilator but not a vasoconstrictor of human small pulmonary arteries and systemic resistance arteries.     

Mechanism for pressor response to nonexertional heating in the conscious rat

The purpose of this study was to determine the systemic hemodynamic mechanism(s) underlying the pressor response to nonexertional heat stress in the unrestrained conscious rat. After a 60-min control period [ambient temperature (Ta) 24 degrees C], male Sprague-Dawley rats (260-340 g) were exposed to a Ta of 42 degrees C until a colonic temperature (Tc) of 41 degrees C was attained. As Tc rose from control levels (38.1 +/- 0.1 degrees C) to 41 degrees C, mean arterial blood pressure (carotid artery catheter, n = 33) increased from 124 +/- 2 to 151 +/- 2 mmHg (P less than 0.05). During this period, heart rate increased (395 +/- 5 to 430 +/- 6 beats/min, P less than 0.05) and stroke volume remained unchanged. As a result, ascending aorta blood flow velocity (Doppler flow probe, n = 8), used as an index of cardiac output, did not change from control levels during heating, but there was a progressive Tc-dependent increase in systemic vascular resistance (+30% at end heating, P less than 0.05). This systemic vasoconstrictor response was associated with decreases in blood flow (-31 +/- 9 and -21 +/- 5%) and increases in vascular resistance (94 +/- 16 and 53 +/- 8%; all P less than 0.05) in the superior mesenteric and renal arteries (n = 8 each) and increases in plasma norepinephrine (303 +/- 37 to 1,237 +/- 262 pg/ml) and epinephrine (148 +/- 28 to 708 +/- 145 pg/ml) concentrations (n = 12, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Skin-surface cooling elicits peripheral and visceral vasoconstriction in humans.

Skin-surface cooling elicits a pronounced systemic pressor response, which has previously been reported to be associated with peripheral vasoconstriction and may not fully account for the decrease in systemic vascular conductance. To test the hypothesis that whole body skin-surface cooling would also induce renal and splanchnic vasoconstriction, 14 supine subjects performed 26 skin-surface cooling trials (15-18 degrees C water perfused through a tube-lined suit for 20 min). Oral and mean skin temperature, heart rate, stroke volume (Doppler ultrasound), mean arterial blood pressure (MAP), cutaneous blood velocity (laser-Doppler), and mean blood velocity of the brachial, celiac, renal, and superior mesenteric arteries (Doppler ultrasound) were measured during normothermia and skin-surface cooling. Cardiac output (heart rate x stroke volume) and indexes of vascular conductance (flux or blood velocity/MAP) were calculated. Skin-surface cooling increased MAP (n = 26; 78 +/- 5 to 88 +/- 5 mmHg; mean +/- SD) and decreased mean skin temperature (n = 26; 33.7 +/- 0.7 to 27.5 +/- 1.2 degrees C) and cutaneous (n = 12; 0.93 +/- 0.68 to 0.36 +/- 0.20 flux/mmHg), brachial (n = 10; 32 +/- 15 to 20 +/- 12), celiac (n = 8; 85 +/- 22 to 73 +/- 22 cm.s(-1).mmHg(-1)), superior mesenteric (n = 8; 55 +/- 16 to 48 +/- 10 cm.s(-1).mmHg(-1)), and renal (n = 8; 74 +/- 26 to 64 +/- 20 cm.s(-1).mmHg(-1); all P < 0.05) vascular conductance, without altering oral temperature, cardiac output, heart rate, or stroke volume. These data identify decreases in vascular conductance of skin and of brachial, celiac, superior mesenteric, and renal arteries. Thus it appears that vasoconstriction in both peripheral and visceral arteries contributes importantly to the pressor response produced during skin-surface cooling in humans.     

Coronary artery flow measurement using navigator echo gated phase contrast magnetic resonance velocity mapping at 3.0 T

A validation study and early results for non-invasive, in vivo measurement of coronary artery blood flow using phase contrast magnetic resonance imaging (PC-MRI) at 3.0T is presented. Accuracy of coronary artery blood flow measurements by phase contrast MRI is limited by heart and respiratory motion as well as the small size of the coronary arteries. In this study, a navigator echo gated, cine phase velocity mapping technique is described to obtain time-resolved velocity and flow waveforms of small diameter vessels at 3.0T. Phantom experiments using steady, laminar flow are presented to validate the technique and show flow rates measured by 3.0T phase contrast MRI to be accurate within 15% of true flow rates. Subsequently, in vivo scans on healthy volunteers yield velocity measurements for blood flow in the right, left anterior descending, and left circumflex arteries. Measurements of average, cross-sectional velocity were obtainable in 224/243 (92%) of the cardiac phases. Time-averaged, cross-sectional velocity of the blood flow was 6.8+/-4.3cm/s in the LAD, 8.0+/-3.8cm/s in the LCX, and 6.0+/-1.6cm/s in the RCA.     

Hypercholesterolemia inhibits L-type calcium current in coronary macro-, not microcirculation.

Hypercholesterolemia (HC) is a mary risk factor for the development of coronary heart disease. Coronary ion regulation, especially calcium, is thought to be important in coronary heart disease development; however, the influence of high dietary fat and cholesterol on coronary arterial smooth muscle (CASM) ion channels is unknown. The purpose of this study was to determine the effect of diet-induced HC on CASM voltage-gated calcium current (I(Ca)). Male miniature swine were fed a high-fat, high-cholesterol diet (40% kcal fat, 2% wt cholesterol) for 20-24 wk, resulting in elevated serum total and low-density lipoprotein cholesterol. Histochemistry indicated early atherosclerosis in large coronary arteries. CASM were isolated from the right coronary artery (>1.0 mm ID), small arteries ( approximately 200 microm), and large arterioles ( approximately 100 microm). I(Ca) was determined by whole cell voltage clamp. L-type I(Ca) was reduced approximately 30% by HC compared with controls in the right coronary artery (-5.29 +/- 0.42 vs. -7.59 +/- 0.41 pA/pF) but not the microcirculation (small artery, -8.39 +/- 0.80 vs. -10.13 +/- 0.60; arterioles, -10.78 +/- 0.93 vs. -11.31 +/- 0.95 pA/pF). Voltage-dependent activation was unaffected by HC in both the macro- and microcirculation. L-type voltage-gated calcium channel (Ca(v)1.2) mRNA and membrane protein levels were unaffected by HC. Inhibition of I(Ca) by HC was reversed in vitro by the cholesterol scavenger methyl-beta-cyclodextrin and mimicked in control CASM by incubation with the cholesterol donor cholesterol:methyl-beta-cyclodextrin. These data indicate that CASM L-type I(Ca) is decreased in large coronary arteries in early stages of atherosclerosis, whereas I(Ca) in the microcirculation is unaffected. The inhibition of calcium channel activity in CASM of large coronary arteries is likely due to increases in membrane free cholesterol.     

Dynamic capacitance of epicardial coronary arteries in vivo

The dynamic capacitance of epicardial coronary arteries (i.d. greater than or equal to 0.4 mm) in vivo was assessed from the volume stiffness and volume of these arteries. The volume stiffness was derived from the pressure wave front velocity as determined in dogs by measuring the delay time between the pressure pulses recorded proximal and distal to a segment of the anterior descending branch of the left coronary artery. The pressure pulse was generated elsewhere in the arterial system during diastole. The volume of the epicardial coronary arteries was calculated from the lengths and diameters as measured in araldite casts, making corrections for in-vitro/in-vivo differences in dimensions. The dynamic capacitance of the right coronary artery, and the anterior descending and circumflex branches of the left coronary artery at an arterial pressure of 13.3 kPa and a frequency between 7 and 30 Hz was found to be 0.0024 +/- 0.0013, 0.0062 +/- 0.0028 and 0.0079 +/- 0.0035 mL/kPa (mean +/- SD), respectively. The total capacitance of the epicardial coronary arteries was calculated to be (0.007 mL/kPa)/100 g, which is small as compared to the total capacitance of the coronary vasculature, including the intramyocardial compartment, which is in the order of (0.5 mL/kPa)/100 g [1].     

Length-tension relationships of small arteries, veins, and lymphatics from the rat mesenteric microcirculation

The passive and active length-tension relationships of isolated rat mesenteric lymphatics ( approximately 150 microm ID), and adjacent small arteries ( approximately 240 microm) and veins ( approximately 275 microm) were compared under isometric conditions using a wire myograph. About 60% of the lymphatic vessels developed spontaneous contractions in physiological saline solution at nominal preload. To maximally activate smooth muscle, 145 mM K(+) + 5 x 10(-5) M norepinephrine was used for arteries, and 145 mM K(+) + 1 x 10(-6) M substance P was used for lymphatics and veins. In response, arteries exhibited monotonic force development to a plateau level, whereas lymphatics and veins showed biphasic force development, consisting of a transient force peak followed by partial relaxation to a plateau over approximately 5 min. The passive and the active length-tension curves were similar in shape among all three vessels. However, the maximal active tension of arteries (3.4 +/- 0.42 mN/mm) was significantly greater than peak active tension (0.59 +/- 0.04 mN/mm) or plateau tension (0.20 +/- 0.04 mN/mm) in small veins and greater than peak active tension (0.34 +/- 0.02 mN/mm) or plateau tension (0.21 +/- 0.02 mN/mm) in lymphatics. Maximal active medial wall stress was similar between lymphatics and veins but was approximately fivefold higher in small arteries. For lymphatics, the pressure calculated from the optimal preload was significantly higher than that found previously in isobaric studies of isolated lymphatics, suggesting the capacity to operate at higher than normal pressures for increased responsiveness. Our results represent the first mechanical comparisons of arterial, venous, and lymphatic vessels in the same vasculature.     

Superior vena caval blood flow velocities in adults: a Doppler echocardiographic study

Superior vena caval blood flow velocity was measured in 30 normal adults (age 20-65, mean 36 yr). The flow velocities were measured by pulsed Doppler echocardiography, using a Duplex system with the transducer at the right supraclavicular fossa, approximating a 0 degrees Doppler angle. Four distinct flow waveforms were found during each cardiac cycle: A, a small retrograde flow during right atrial contraction (peak flow velocity 12.4 +/- 2.2 cm/s); B, a small antegrade flow during right atrial relaxation (15.7 +/- 5.0 cm/s); S, a large antegrade flow during ventricular systole (35.2 +/- 7.3 cm/s); and D, a large antegrade flow during ventricular diastole (23.2 +/- 3.1 cm/s). The wave duration was inversely related to heart rate. The peak flow velocities of the S and D waves were inversely related to the patients' ages. This study provides recognition of the pattern and range of normality essential to extension of this noninvasive technique to the diagnosis of pathological conditions.     

Influence of coronary artery diameter on eNOS protein content

The purpose of this study was to test the hypothesis that the content of endothelial nitric oxide synthase (eNOS) protein (eNOS protein/g total artery protein) increases with decreasing artery diameter in the coronary arterial tree. Content of eNOS protein was determined in porcine coronary arteries with immunoblot analysis. Arteries were isolated in six size categories from each heart: large arteries [301- to 2,500-microm internal diameter (ID)], small arteries (201- to 300-microm ID), resistance arteries (151- to 200-microm ID), large arterioles (101- to 150-microm ID), intermediate arterioles (51- to 100-microm ID), and small arterioles(<50-microm ID). To obtain sufficient protein for analysis from small- and intermediate-sized arterioles, five to seven arterioles 1-2 mm in length were pooled into one sample for each animal. Results establish that the number of smooth muscle cells per endothelial cell decreases from a number of 10 to 15 in large coronary arteries to 1 in the smallest arterioles. Immunohistochemistry revealed that eNOS is located only in endothelial cells in all sizes of coronary artery and in coronary capillaries. Contrary to our hypothesis, eNOS protein content did not increase with decreasing size of coronary artery. Indeed, the smallest coronary arterioles had less eNOS protein per gram of total protein than the large coronary arteries. These results indicate that eNOS protein content is greater in the endothelial cells of conduit arteries, resistance arteries, and large arterioles than in small coronary arterioles.     

Propranolol and serotonin removal in lung injury

Indicator dilution technique was used to study effects of reduced vascular volume or acute injury on removal of low doses of [3H]propranolol and [14C]serotonin (5-hydroxytryptamine, 5-HT) by perfused rabbit lung. Glass-bead (500 micron) embolization doubled pulmonary arterial pressure (Ppa) at flow rates of 20, 50, and 100 ml/min, decreased volume of distribution by approximately 50%, and increased pulmonary vascular resistance by at least 60%. Before embolization, (flow rate 20 ml/min) removal of [3H]propranolol and [14C] 5-HT was 89 +/- 2 and 75 +/- 5%, respectively, and was unaltered by changes in flow rate. However, after embolization, [3H]propranolol and [14C]5-HT removal decreased in a flow-dependent manner, reaching 28 +/- 4 and 1 +/- 3% (P less than 0.05), respectively, at a flow rate of 100 ml/min. When phorbol myristate acetate (PMA, 200 nM) was perfused (50 ml/min) through the lungs for 15 min, Ppa increased from 13 +/- 1 to 25 +/- 2 cmH2O (P less than 0.05), whereas [3H]propranolol removal decreased from 92 +/- 1 to 75 +/- 5% (P less than 0.05) and [14C]5-HT removal decreased from 73 +/- 3 to 46 +/- 8% (P less than 0.05). The PMA also caused vasoconstriction, which could be partially blocked by adding papaverine (500 microM) to the perfusion medium. Under the latter conditions, Ppa increased to 19 +/- 1 cmH2O and [3H]propranolol removal was unaffected. However, the combination of PMA and papaverine reduced [14C]5-HT removal from 64 +/- 4 to 19 +/- 3%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cellular composition of the cyclic corpus luteum of the cow

The cellular composition of CL from 6 cows on approximately Day 12 of the oestrous cycle, after synchronization with cloprostenol, was studied by ultrastructural morphometry. Point-count measurements of volume density (mean +/- s.d.) showed that large luteal cells occupied 40.2 +/- 7.0% of the luteal tissue, and small luteal cells 27.7 +/- 6.3%. Of the total of 393.4 +/- 52.0 x 10(3) cells per mm3 of luteal tissue, large luteal cells made up only 3.5% and small luteal cells 26.7%, a ratio of 1:7.6. Endothelial cells/pericytes, at 52.3%, were the most numerous cell type. The mean volume per large luteal cell was 29.6 +/- 6.3 x 10(3) microns 3, while that of small luteal cells was 2.7 +/- 0.4 x 10(3) microns 3. In spherical form, these volumes would represent mean diameters of 38.4 microns and 17.2 microns respectively, and are consistent with published measurements on dispersed luteal cells. However, the values for cell numbers are much higher than published values based on luteal tissue dispersion, suggesting that dispersion may result in substantial and possibly selective losses of luteal cells.     

Differences in cardiac microcirculatory wave patterns between the proximal left mainstem and proximal right coronary artery

Despite having almost identical origins and similar perfusion pressures, the flow-velocity waveforms in the left and right coronary arteries are strikingly different. We hypothesized that pressure differences originating from the distal (microcirculatory) bed would account for the differences in the flow-velocity waveform. We used wave intensity analysis to separate and quantify proximal- and distal-originating pressures to study the differences in velocity waveforms. In 20 subjects with unobstructed coronary arteries, sensor-tipped intra-arterial wires were used to measure simultaneous pressure and Doppler velocity in the proximal left main stem (LMS) and proximal right coronary artery (RCA). Proximal- and distal-originating waves were separated using wave intensity analysis, and differences in waves were examined in relation to structural and anatomic differences between the two arteries. Diastolic flow velocity was lower in the RCA than in the LMS (35.1 +/- 21.4 vs. 56.4 +/- 32.5 cm/s, P < 0.002), and, consequently, the diastolic-to-systolic ratio of peak flow velocity in the RCA was significantly less than in the LMS (1.00 +/- 0.32 vs. 1.79 +/- 0.48, P < 0.001). This was due to a lower distal-originating suction wave (8.2 +/- 6.6 x 10(3) vs. 16.0 +/- 12.2 x 10(3) W.m(-2).s(-1), P < 0.01). The suction wave in the LMS correlated positively with left ventricular pressure (r = 0.6, P < 0.01) and in the RCA with estimated right ventricular systolic pressure (r = 0.7, P = 0.05) but not with the respective diameter in these arteries. In contrast to the LMS, where coronary flow velocity was predominantly diastolic, in the proximal RCA coronary flow velocity was similar in systole and diastole. This difference was due to a smaller distal-originating suction wave in the RCA, which can be explained by differences in elastance and pressure generated between right and left ventricles.     

Internal carotid flow velocity with exercise before and after acclimatization to 4,300 m.

Cerebral blood flow and O2 delivery during exercise are important for well-being at altitude but have not been studied. We expected flow to increase on arrival at altitude and then to fall as O2 saturation and hemoglobin increased, thereby maintaining cerebral O2 delivery. We used Doppler ultrasound to measure internal carotid artery flow velocity at sea level and on Pikes Peak, CO (4,300 m). In an initial study (1987, n = 7 men) done to determine the effect of brief (5-min) exercises of increasing intensity, we found at sea level that velocity [24.8 +/- 1.4 (SE) cm/s rest] increased by 15 +/- 7, 30 +/- 6, and 22 +/- 8% for cycle exercises at 33, 71, and 96% of maximal O2 uptake, respectively. During acute hypobaric hypoxia in a decompression chamber (inspired PO2 = 83 Torr), velocity (23.2 +/- 1.4 cm/s rest) increased by 33 +/- 6, 20 +/- 5, and 17 +/- 9% for exercises at 45, 72, and 98% of maximal O2 uptake, respectively. After 18 days on Pikes Peak (inspired PO2 = 87 Torr), velocity (26.6 +/- 1.5 cm/s rest) did not increase with exercise. A subsequent study (1988, n = 7 men) of the effect of prolonged exercise (45 min at approximately 100 W) found at sea level that velocity (24.8 +/- 1.7 cm/s rest) increased by 22 +/- 6, 13 +/- 5, 17 +/- 4, and 12 +/- 3% at 5, 15, 30, and 45 min.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationship between tracheal mucosal thickness and vascular resistance in dogs

We have measured changes in tracheal mucosal thickness and tracheal vascular resistance in the dog. A probe was used to detect changes in height with time of the tracheal epithelium relative to an underlying cartilage. Tracheal vascular resistance was determined by perfusing a cranial tracheal artery at constant flow and measuring inflow pressure. Various drugs injected close-arterially were tested in 20 greyhounds anesthetized with pentobarbital sodium. Bradykinin, histamine, and methacholine significantly (P less than 0.01) decreased vascular resistance (-39.3 +/- 3.7, -47.3 +/- 4.2, and -22.5 +/- 5.2%, respectively) and increased the thickness of the mucosa (119.0 +/- 25.0, 61.9 +/- 25.0, and 46.3 +/- 6.4 micron). Substance P, vasoactive intestinal peptide, prostaglandin F2 alpha, and prostaglandin E, had large vasodilator actions (-31.4 +/- 5.0, -34.3 +/- 2.2, -21.9 +/- 2.8, and -31.5 +/- 2.4%) but only small effects on mucosal thickness (12.3 +/- 3.9, 13.0 +/- 3.4, 16.7 +/- 6.5, and 8.7 +/- 2.9 micron, respectively). Phenylephrine hydrochloride increased vascular resistance (19.8 +/- 1.7%) and decreased mucosal thickness (-23.9 +/- 3.1 micron). Thus airway vascular resistance and mucosal thickness always change in opposite directions, but drugs have different relative actions on the two variables. Even with large vasodilatations, the absolute changes in mucosal thickness were small and were unlikely to have an appreciable effect on tracheal airway resistance.