Role of cardiopulmonary baroreflexes during dynamic exercise

To examine the role of cardiopulmonary (CP) mechanoreceptors in the regulation of arterial blood pressure during dynamic exercise in humans, we measured mean arterial pressure (MAP), cardiac output (Q), and forearm blood flow (FBF) during mild cycle ergometer exercise (77 W) in 14 volunteers in the supine position with and without lower-body negative pressure (LBNP). During exercise, MAP averaged 103 +/- 2 mmHg and was not altered by LBNP (-10, -20, or -40 mmHg). Steady-state Q during exercise was reduced from 10.2 +/- 0.5 to 9.2 +/- 0.5 l/min (P less than 0.05) by application of -10 mmHg LBNP, whereas heart rate (97 +/- 3 beats/min) was unchanged. MAP was maintained during -10 mmHg LBNP by an increase in total systemic vascular resistance (TSVR) from 10.3 +/- 0.5 to 11.4 +/- 0.6 U and forearm vascular resistance (FVR) from 17.5 +/- 1.9 to 23.3 +/- 2.6 U. The absence of a reflex tachycardia or reduction in arterial pulse pressure during -10 mmHg LBNP supports the hypothesis that the increase in TSVR and FVR results primarily from the unloading of CP mechanoreceptors. Because CP mechanoreceptor unloading during exercise stimulates reflex circulatory adjustments that act to defend the elevated MAP, we conclude that the elevation in MAP during exercise is regulated and not merely the consequence of differential changes in Q and TSVR. In addition, a major portion of the reduction in FBF in our experimental conditions occurs in the cutaneous circulation. As such, these data support the hypothesis that CP baroreflex control of cutaneous vasomotor tone is preserved during mild dynamic exercise.     

Postural cardiovascular reflexes: comparison of responses of forearm and calf resistance vessels

Simultaneous measurements were made of changes in vascular resistance in the forearm and calf in response to moving from supine to sitting or to head-down tilt. The subjects were healthy male volunteers, 21-63 yr. Blood flows were measured by venous occlusion plethysmography using mercury-in-Silastic strain-gauges. The gauges were maintained at the same level relative to the heart during the postural changes. Arterial blood pressure was measured by auscultation; heart rate was counted from the plethysmograms. Changing from supine to sitting caused a decrease in forearm blood flow from 4.13 +/- 0.14 to 2.16 +/- 0.19 ml.100 ml-1.min-1. Corresponding calf flows were 4.21 +/- 0.32 and 4.40 +/- 0.59 ml.100 ml-1.min-1. There was no change in mean arterial blood pressure, and heart rate increased by 8.0 +/- 1.5 beats/min. Arrest of the circulation of both legs with occlusion cuffs on the thighs before sitting, to prevent pooling of blood in them, reduced the degree of forearm vasoconstriction. Neck suction (40 Torr) during sitting, to oppose the decrease in transmural pressure at the carotid sinuses, inhibited the vasoconstriction. During a 30 degrees head-down tilt, there was a dilatation of forearm but not of calf resistance vessels. A Valsalva maneuver caused a similar constriction of both vascular beds. Thus, when changes in vascular resistance in forearm and calf are compared, the major reflex adjustments to changes in posture take place in the forearm.     

Sympathetic nerve activity in arm and leg muscles during lower body negative pressure in humans

Nonhypotensive lower body negative pressure (LBNP) is reported to decrease forearm but not calf blood flow as measured by strain-gauge plethysmography. This suggests that unloading of cardiopulmonary receptors increases sympathetic outflow to arm but not to leg. To test this hypothesis we measured muscle sympathetic nerve activity (MSA) in the arm (radial nerve) and leg (peroneal nerve) simultaneously during LBNP. In eight healthy subjects, we measured heart rate, blood pressure, and radial and peroneal MSA during LBNP at 10 and 20 mmHg. There was no difference between radial and peroneal MSA at rest, and there were successive parallel increases of MSA in both nerves during LBNP at 10 and 20 mmHg. These data indicate that there are nearly identical increases of sympathetic outflow to the arm and leg during mild to moderate degrees of orthostatic stress.     

Vascular responses in forearm and calf to contralateral static exercises

Ten normal subjects performed a 90-s isometric exercise [20, 30, and 40% of maximal voluntary contraction (MVC) of the flexor muscle of the right index finger or quadriceps muscle of the right leg. Contralateral forearm and calf blood flows (strain gauge plethysmography) and arterial blood pressure (auscultation) were measured simultaneously. Each exercise caused a decrease in forearm vascular resistance and a progressive increase in calf resistance. These changes were greatest with the 40% MVC. With finger exercise at 20 and 40% MVC, the percentage decreases in forearm vascular resistance from control were 12.3 and 22.7%, respectively (P less than 0.01). Similar decreases (9.5 and 24.9%, respectively; P less than 0.01) were noted with exercise of the quadriceps muscle. By contrast, the corresponding increases in calf vascular resistance were greater (P less than 0.01) with quadriceps exercise (13.3 and 55.4%, respectively) than with finger exercise (6.0 and 36.0%). Arrest of the circulation to the exercising muscles just before the exercise ended caused an abrupt increase in forearm vascular resistance and a decrease in calf resistance. These studies provide further evidence of the heterogeneity of responses of forearm and calf resistance vessels to certain cardiovascular stimuli.     

Does the pressor response to ischemic exercise improve blood flow to contracting muscles in humans?

The purpose of this study was to determine in humans 1) the gain for the reflex pressor response that occurs when perfusion pressure to rhythmically contracting muscles is reduced and 2) whether the pressor response improves blood flow to the contracting muscles. Six normal subjects performed light, moderate, and heavy rhythmic forearm contractions (30/min) with the forearm enclosed in a Plexiglas box. Pressure in the box was increased 10 mmHg each minute up to 50 mmHg to reduce transmural pressure in the arterial system of the forearm. Mean arterial pressure (MAP) was measured continuously. During light exercise no reflex increase in MAP occurred until box pressure was 50 mmHg. During moderate and heavy exercise MAP began to increase with only 10- to 20-mmHg increases in box pressure. The slope of this increase was 3.5-3.9 mmHg per 10 mmHg of box pressure (approximately 60% of that in dogs). In a further study on six subjects a deep vein draining the active forearm muscles was cannulated and deep venous O2 saturation measured to assess how a 50-mmHg increase in box pressure and subsequent reflex increase in MAP altered blood flow to the contracting muscles during heavy rhythmic exercise. The increase in box pressure reduced blood flow to contracting forearm muscles by 20-25% and was followed by a 19-mmHg increase in MAP that did not appear to improve perfusion of the active muscles. This finding was unexpected, because studies in dogs suggest that the pressor response to rhythmic exercise with restricted muscle blood flow can improve perfusion of the active muscles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Aging and the skin blood flow response to the unloading of baroreceptors during heat and cold stress.

Control of skin blood flow (SkBF) is on the efferent arm of both thermoregulatory and nonthermoregulatory reflexes. To what extent aging may affect the SkBF response when these two reflex systems interact is unknown. To determine the response of aged skin to the unloading of baroreceptors in thermoneutral, cold stress, and heat stress conditions, sequential bouts of nonhypotensive lower body negative pressure (LBNP) were applied at -10, -20, and -30 mmHg in 14 young (18-25 yr) and 14 older (63-78 yr) men. SkBF was measured by laser-Doppler velocimetry (averaged over 2 forearm sites), and data are expressed as percentage of maximal cutaneous vascular conductance (%CVC(max)). Total forearm blood flow was measured by venous occlusion plethysmography, and forearm vascular conductance (FVC) was calculated as the ratio of forearm blood flow to mean arterial pressure. In young men, all three intensities of LBNP in thermoneutrality decreased FVC significantly (P < 0.05), but FVC at -10 mmHg did not change in the older men. There were no significant LBNP effects on %CVC(max). Application of LBNP during cold stress did not significantly change %CVC(max) or FVC in either age group. During heat stress, -10 to -30 mmHg of LBNP decreased FVC significantly (P < 0.05) in both age groups, but these decreases were attenuated in the older men (P < 0.05). %CVC(max) decreased at -30 mmHg in the younger men only. These results suggest that older men have an attenuated skin vasoconstrictor response to the unloading of baroreceptors in heat stress conditions. Furthermore, the forearm vasoconstriction elicited by LBNP in older men reflects that of underlying tissue (i.e., muscle) rather than that of skin, whereas -30 mmHg LBNP also decreases SkBF in young hyperthermic men.     

Plantar vibration improves leg fluid flow in perimenopausal women

Recent studies have indicated that plantar-based vibration may be an effective approach for the prevention and treatment of osteoporosis. We addressed the hypothesis of whether the plantar vibration operated by way of the skeletal muscle pump, resulting in enhanced blood and fluid flow to the lower body. We combined plantar stimulation with upright tilt table testing in 18 women aged 46-63 yr. We used strain-gauge plethysmography to measure calf blood flow, venous capacitance, and the microvascular filtration relation, as well as impedance plethysmography to examine changes in leg, splanchnic, and thoracic blood flow while supine at a 35 degrees upright tilt. A vibrating platform was placed on the footboard of a tilt table, and measurements were made at 0, 15, and 45 Hz with an amplitude of 0.2 g point to point, presented in random order. Impedance-measured supine blood flows were significantly (P = 0.05) increased in the calf (30%), pelvic (26%), and thoracic regions (20%) by plantar vibration at 45 Hz. Moreover, the 25-35% decreases in calf and pelvic blood flows associated with upright tilt were reversed by plantar vibration, and the decrease in thoracic blood flow was significantly attenuated. Strain-gauge measurements showed an attenuation of upright calf blood flow. In addition, the microvascular filtration relation was shifted with vibration, producing a pronounced increase in the threshold for edema, P(i), due to enhanced lymphatic flow. Supine values for P(i) increased from 24 +/- 2 mmHg at 0 Hz to 27 +/- 3 mmHg at 15 Hz, and finally to 31 +/- 2 mmHg at 45 Hz (P < 0.01). Upright values for P(i) increased from 25 +/- 3 mmHg at 0 Hz, to 28 +/- 4 mmHg at 15 Hz, and finally to 35 +/- 4 mmHg at 45 Hz. The results suggest that plantar vibration serves to significantly enhance peripheral and systemic blood flow, peripheral lymphatic flow, and venous drainage, which may account for the apparent ability of such stimuli to influence bone mass.     

Diminished baroreflex control of forearm vascular resistance in physically fit humans

The stimulus-response characteristics of cardiopulmonary baroreflex control of forearm vascular resistance (FVR) were studied in five unfit [UF, maximal O2 consumption (VO2 max) = 38.5 ml X min-1 X kg-1] and six fit (F, VO2 max = 57.0 ml X min-1 X kg-1) subjects. We assessed the relationship between reflex stimulus, i.e., changes in central venous pressure (CVP) and response, i.e., FVR, during selective unloading of the cardiopulmonary mechanoreceptors with lower body negative pressure (0 to -20 mmHg). The linear relationship between FVR and CVP, the gain of this baroreflex, was significantly diminished in the F subjects, -2.42 +/- 0.57 U/mmHg, compared with the UF, -5.15 +/- 0.58 U/mmHg. Both groups, F and UF, had similar resting values for CVP and FVR; thus the diminished gain in F subjects was not simply an artifact resulting from a shift of the set point along the baroreflex stimulus-response curve. We also found a linear relationship between baroreflex gain and total blood volume (r = 0.59, P less than 0.05). We conclude that the gain of this vascular reflex is attenuated in trained individuals and is related to cardiovascular adaptations, such as an increased blood volume, associated with exercise training.     

Venous cuff pressures from 30 mmHg to diastolic pressure are recommended to measure arterial inflow by plethysmography.

Venous occlusion strain gauge plethysmography (VOP) is based on the assumption that the veins are occluded and arterial inflow is undisturbed by the venous cuff pressure. Literature is not clear concerning the pressure that should be used. The purpose of this study was to determine the optimal venous occlusion pressure at which the highest arterial inflow is achieved in the forearm, calf, and leg by using VOP. We hypothesized that, for each limb segment, an optimal (range of) venous cuff pressure can be determined. Arterial inflow in each limb segment was measured in nine healthy individuals by VOP by using pressures ranging from 10 mmHg up to diastolic blood pressure. Arterial inflows were similar at cuff pressures between 30 and 60 mmHg for the forearm, leg, and calf. Arterial inflow in the forearm was significantly lower at 10 mmHg compared with the other cuff pressures. In addition, arterial inflows at 20 mmHg tended to be lower in each limb segment than flow at higher cuff pressures. In conclusion, no single optimum venous cuff pressure, at which a highest arterial inflow is achieved, exists, but rather a range of optimum cuff pressures leading to a similar arterial inflow. Venous cuff pressures ranging from 30 mmHg up to diastolic blood pressure are recommended to measure arterial inflow by VOP.     

Functional asymmetry in carotid sinus cardiac reflexes in humans

The reflex cardiac response to activation (CBA) and inactivation (CBI) of the left and right carotid baroreceptors was studied in 30 healthy subjects, aged between 24 and 38 years. The CBA was evoked by applying negative pressure (from -20 to -60 mmHg) for 10 s to the left and right carotid sinus regions separately or both together, using two small neck capsules. The CBI was produced by applying left and right positive neck pressure (from 20 to 60 mmHg) for 10 s. The blood flow velocity was measured non-invasively with a Doppler scanner placed in the suprasternal notch. Blood flow acceleration was calculated and used as an indication of left cardiac contractility. Heart rate was measured continuously. Differences were found between right and left carotid sinus responses to CBA and CBI. The maximal response of the R-R interval was significantly greater during right CBA than during left CBA (the average gain: R-R.mmHg-1 2.69 ms.mmHg-1 and 1.75 ms.mmHg-1, respectively). Also, the reflex CBI response was significantly greater for the right (3.16 ms.mmHg-1) than for the left (2.22 ms.mmHg-1). The reflex decrease/increase in blood-flow acceleration in response to CBA/CBI was significantly greater during left than during right-sided activation/inactivation. It is suggested that the functional asymmetry was related to differences in right/left-sided cardiac innervation as well as to central ipsilateral projection of the carotid baroreceptor afferents to the nuclei tractus solitarii.     

Rapid blunting of sympathetic vasoconstriction in the human forearm at the onset of exercise.

The purpose of this study was to test the hypothesis that sympathetic vasoconstriction is rapidly blunted at the onset of forearm exercise. Nine healthy subjects performed 5 min of moderate dynamic forearm handgrip exercise during -60 mmHg lower body negative pressure (LBNP) vs. without (control). Beat-by-beat forearm blood flow (Doppler ultrasound), arterial blood pressure (finger photoplethysmograph), and heart rate were collected. LBNP elevated resting heart rate by approximately 45%. Mean arterial blood pressure was not significantly changed (P = 0.196), but diastolic blood pressure was elevated by approximately 10% and pulse pressure was reduced by approximately 20%. At rest, there was a 30% reduction in forearm vascular conductance (FVC) during LBNP (P = 0.004). The initial rapid increase in FVC with exercise onset reached a plateau between 10 and 20 s of 126.6 +/- 4.1 ml. min(-1). 100 mmHg(-1) in control vs. only 101.6 +/- 4.1 ml. min(-1). 100 mmHg(-1) in LBNP (main effect of condition, P = 0.003). This difference was quickly abolished during the second, slower phase of adaptation in forearm vascular tone to steady state. These data are consistent with a rapid onset of functional sympatholysis, in which local substances released with the onset of muscle contractions impair sympathetic neural vasoconstrictor effectiveness.     

Reflex constriction of human limb resistance vessels to head-down neck flexion

The effect of head-down neck flexion on forearm and calf blood flow was determined in 10 healthy male subjects. The subject lay prone, with the neck slightly extended and the chin resting on a soft-padded support at the edge of the table. The chin support was then removed, and the subject maximally flexed and lowered the neck. This was followed by return to the initial position. Neck flexion caused a rapid decrease in blood flow in both forearm and calf; at 30 s this averaged 39 and 35%, respectively. The flow in both forearm and calf gradually recovered as the neck flexion was sustained and approached the control values at the end of 10 min. The blood flow at the ankle was unchanged, indicating that the decrease occurred in the skeletal muscles. The arterial blood pressure and heart rate were unchanged; thus the decrease in flow was due to vasoconstriction. The fact that the decrease was evident as soon as the head was lowered indicated that it was nervously mediated. Neither contraction of the flexor muscles of the neck nor venous congestion of the head, in the absence of the head-down position, altered the blood flow. Although the mechanism of the decrease in flow has not been determined, the studies demonstrate that in response to certain stimuli, the resistance vessels in the skeletal muscles of the forearm and calf undergo a similar nervously mediated vasoconstriction.     

Dynamic autoregulation of cutaneous circulation: differential control in glabrous versus nonglabrous skin

The purpose of this project was to test the hypothesis that, independent of neural control, glabrous and nonglabrous cutaneous vasculature is capable of autoregulating blood flow. In 10 subjects, spectral and transfer function analyses of arterial pressure and skin blood flow (laser-Doppler flowmetry) from glabrous (palm) and nonglabrous (forearm) regions were performed under three conditions: baseline, ganglionic blockade via intravenous trimethaphan administration, and trimethaphan plus oscillatory lower body negative pressure (LBNP; -5 to -10 mmHg) from 0.05 to 0.07 Hz. Oscillatory LBNP was applied to regenerate mean arterial pressure variability that was abolished by ganglionic blockade. Ganglionic blockade was verified by an absence of a heart rate response to a Valsalva maneuver. Spectral power and transfer function gain between blood pressure and skin blood flow were calculated in this oscillatory frequency range (0.05-0.07 Hz). Within this frequency range, ganglionic blockade significantly decreased spectral power of blood flow in both the forearm and palm, whereas regeneration of arterial blood pressure oscillations significantly increased spectral power of forearm blood flow but not palm blood flow. During oscillatory LBNP, transfer function gain between blood pressure and skin blood flow was significantly elevated at the forearm (0.28 +/- 0.03 to 0.53 +/- 0.02 flux units/mmHg; P < 0.05) but was reduced at the palm (4.7 +/- 0.5 to 1.2 +/- 0.1 flux units/mmHg; P < 0.05). These data show that independent of neural control of blood flow, glabrous skin has the ability to buffer blood pressure oscillations and demonstrates a degree of dynamic autoregulation. Conversely, these data suggest that nonglabrous skin has diminished dynamic autoregulatory capabilities.     

Changes in regional blood volume and blood flow during static handgrip

Increased blood pressure (BP) and heart rate during exercise characterizes the exercise pressor reflex. When evoked by static handgrip, mechanoreceptors and metaboreceptors produce regional changes in blood volume and blood flow, which are incompletely characterized in humans. We studied 16 healthy subjects aged 20-27 yr using segmental impedance plethysmography validated against dye dilution and venous occlusion plethysmography to noninvasively measure changes in regional blood volumes and blood flows. Static handgrip while in supine position was performed for 2 min without postexercise ischemia. Measurements of heart rate and BP variability and coherence analyses were used to examine baroreflex-mediated autonomic effects. During handgrip exercise, systolic BP increased from 120 +/- 10 to 148 +/- 14 mmHg, whereas heart rate increased from 60 +/- 8 to 82 +/- 12 beats/min. Heart rate variability decreased, whereas BP variability increased, and transfer function amplitude was reduced from 18 +/- 2 to 8 +/- 2 ms/mmHg at low frequencies of approximately 0.1 Hz. This was associated with marked reduction of coherence between BP and heart rate (from 0.76 +/- 0.10 to 0.26 +/- 0.05) indicative of uncoupling of heart rate regulation by the baroreflex. Cardiac output increased by approximately 18% with a 4.5% increase in central blood volume and an 8.5% increase in total peripheral resistance, suggesting increased cardiac preload and contractility. Splanchnic blood volume decreased reciprocally with smaller decreases in pelvic and leg volumes, increased splanchnic, pelvic and calf peripheral resistance, and evidence for splanchnic venoconstriction. We conclude that the exercise pressor reflex is associated with reduced baroreflex cardiovagal regulation and driven by increased cardiac output related to enhanced preload, cardiac contractility, and splanchnic blood mobilization.     

Effects of lower body negative pressure on sympathetic discharge to leg muscles in humans

Recent studies indicate that nonhypotensive orthostatic stress in humans causes reflex vasoconstriction in the forearm but not in the calf. We used microelectrode recordings of muscle sympathetic nerve activity (MSNA) from the peroneal nerve in conscious humans to determine if unloading of cardiac baroreceptors during nonhypotensive lower body negative pressure (LBNP) increases sympathetic discharge to the leg muscles. LBNP from -5 to -15 mmHg had no effect on arterial pressure or heart rate but caused graded decreases in central venous pressure and corresponding large increases in peroneal MSNA. Total MSNA (burst frequency X mean burst amplitude) increased by 61 +/- 22% (P less than 0.05 vs. control) during LBNP at only -5 mmHg and rose progressively to a value that was 149 +/- 29% greater than control during LBNP at -15 mmHg (P less than 0.05). The major new conclusion is that nonhypotensive LBNP is a potent stimulus to muscle sympathetic outflow in the leg as well as the arm. During orthostatic stress in humans, the cardiac baroreflex appears to trigger a mass sympathetic discharge to the skeletal muscles in all of the extremities.     

Autonomic and vascular responses to reduced limb perfusion.

The purpose of this study was to examine hemodynamic responses to graded muscle reflex engagement in human subjects. We studied seven healthy human volunteers [24 +/- 2 (SE) yr old; 4 men, 3 women] performing rhythmic handgrip exercise [40% maximal voluntary contraction (MVC)] during ambient and positive pressure exercise (+10 to +50 mmHg in 10-mmHg increments every minute). Muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP), and mean blood velocity were recorded. Plasma lactate, hydrogen ion concentration, and oxyhemoglobin saturation were measured from venous blood. Ischemic exercise resulted in a greater rise in both MSNA and MAP vs. nonischemic exercise. These heightened autonomic responses were noted at +40 and +50 mmHg. Each level of positive pressure was associated with an immediate fall in flow velocity and forearm perfusion pressure. However, during each minute, perfusion pressure increased progressively. For positive pressure of +10 to +40 mmHg, this was associated with restoration of flow velocity. However, at +50 mmHg, flow was not restored. This inability to restore flow was seen at a time when the muscle reflex was clearly engaged (increased MSNA). We believe that these findings are consistent with the hypothesis that before the muscle reflex is clearly engaged, flow to muscle is enhanced by a process that raises perfusion pressure. Once the muscle reflex is clearly engaged and MSNA is augmented, flow to muscle is no longer restored by a similar rise in perfusion pressure, suggesting that active vasoconstriction within muscle is occurring at +50 mmHg.     

Vasoconstriction during venous congestion: effects of venoarteriolar response, myogenic reflexes, and hemodynamics of changing perfusion pressure

We dissected the relative contribution of arteriovenous hemodynamics, the venoarteriolar response (VAR), and the myogenic reflex toward a decrease in local blood flow induced by venous congestion. Skin blood flow (SkBF) was measured in 12 supine subjects via laser-Doppler flowmetry 1) over areas of forearm and calf skin, in which the VAR was blocked by using eutectic mixture of local anesthetics (EMLA sites) and 2) over the contralateral forearm or calf skin (control sites), using two different techniques: limb dependency of 23-37 cm below the heart and cuff inflation to 40 mmHg. During limb dependency, SkBF decreased at the control sites, whereas it remained unchanged at the EMLA sites. In contrast, during cuff inflation, SkBF decreased at the control sites and also decreased at the EMLA sites. The percent change in SkBF from baseline was greater during cuff inflation than limb dependency at both the control sites and the EMLA sites. Estimated skin vascular resistance remained unchanged at the EMLA sites during cuff inflation, as well as limb dependency. Thus the decrease in SkBF during venous congestion with cuff inflation is not solely due to the cutaneous VAR but also to a reduction in local perfusion pressure. The VAR is therefore most specifically quantified by venous congestion induced by limb dependency, rather than cuff inflation. Finally, from both techniques, we calculated that during venous congestion induced by limb dependency (calf), approximately 45% of the nonbaroreflex vasoconstriction is induced by the VAR and approximately 55% by the myogenic reflex.     

Calf blood flow during prolonged tilt in idiopathic dilated cardiomyopathy and after cardiac transplantation

In severe congestive heart failure (CHF), abnormal reflex control of calf blood flow during brief head-up tilt that appears to normalize after transplantation (HTX) may be present during prolonged observation also. Therefore, we studied the effect of prolonged (30 min) 50 degrees head-up tilt on calf skeletal muscle blood flow measured by the local (133)Xe washout method in CHF and after HTX and in patients with the presence vs. absence of native right atrium (+PNA and -PNA, respectively). During brief head-up tilt, skeletal muscle blood flow increased 13 +/- 42% in 9 severe CHF patients in contrast to a -28 +/- 22% decrease (P < 0.01) in 11 control subjects, -24 +/- 30% decrease in 15 moderate CHF patients (P < 0.05), -25 +/- 14% decrease in 12 patients with recent HTX (P < 0.01), and -21 +/- 24% decrease in 8 patients with distant HTX (P = 0.06). However, during sustained tilt, blood flow declined to similar levels of that in the other groups in severe CHF. HTX -PNA vs. +PNA showed blunted skeletal muscle vasomotor control (P < 0.05) and a higher systolic blood pressure (139 +/- 14 vs. 125 +/- 15 mmHg, P < 0.05) and heart rate (92 +/- 10 vs. 83 +/- 8 beats/min, P < 0.05). Thus paradox vasodilatation of calf skeletal muscle in severe CHF is present only during brief but not prolonged tilt. This may be one explanation of the rare presence of orthostatic intolerance in CHF and implies only a minor possible role for the abnormality in edema pathogenesis. Removal of all right atrium in HTX has an important hemodynamic impact that may possibly affect later clinical outcome.     

Local vasoconstriction in spinal cord-injured and able-bodied individuals.

Local vasoconstriction plays an important role in maintaining blood pressure in spinal cord-injured individuals (SCI). We aimed to unravel the mechanisms of local vasoconstriction [venoarteriolar reflex (VAR) and myogenic response] using both limb dependency and cuff inflation in SCI and compare these with control subjects. Limb blood flow was measured in 11 male SCI (age: 24-55 yr old) and 9 male controls (age: 23-56 yr old) using venous occlusion plethysmography in forearm and calf during three levels of 1) limb dependency, and 2) cuff inflation. During limb dependency, vasoconstriction relies on both the VAR and the myogenic response. During cuff inflation, the decrease in blood flow is caused by the VAR and by a decrease in arteriovenous pressure difference, whereas the myogenic response does not play a role. At the highest level of leg dependency, the percent increase in calf vascular resistance (mean arterial pressure/calf blood flow) was more pronounced in SCI than in controls (SCI 186 +/- 53%; controls 51 +/- 17%; P = 0.032). In contrast, during cuff inflation, no differences were found between SCI and controls (SCI 17 +/- 17%; controls 14 +/- 10%). Percent changes in forearm vascular resistance in response to either forearm dependency or forearm cuff inflation were equal in both groups. Thus local vasoconstriction during dependency of the paralyzed leg in SCI is enhanced. The contribution of the VAR to local vasoconstriction does not differ between the groups, since no differences between groups existed for cuff inflation. Therefore, the augmented local vasoconstriction in SCI during leg dependency relies, most likely, on the myogenic response.     

Effects of indomethacin on cardiac output distribution in normal and asphyxiated piglets

We determined the effect of breathing 9% CO2/10% O2/81% N2 (asphyxia) on cardiac output distribution (microspheres) in 4-5 day old unanesthetized, chronically instrumented piglets prior to and following intravenous indomethacin administration. Thirty minutes of asphyxia caused PaCO2 to increase from 35 +/- 2 mmHg to 66 +/- 2 mmHg, PaO2 to decrease from 73 +/- 4 mmHg to 41 +/- 1 mmHg, and pH to decrease from 7.52 +/- 0.05 to 7.21 +/- 0.07. Arterial pressure was increased slightly but cardiac output was not changed significantly. Asphyxia caused blood flow to the brain, diaphragm, liver, heart, and adrenal glands to increase while causing decreases in blood flow to the skin, small intestine, and colon. Blood flows to the stomach and kidneys tended to decrease, but the changes were not significant. Treatment with indomethacin during asphyxia did not alter arterial pressure or cardiac output but decreased cerebral blood flow to the preasphyxiated level and decreased adrenal blood flow about 20%. Indomethacin did not alter blood flow to any other systemic organ. At this time the piglet was allowed to breathe air for 2.5 hr undisturbed. Two and a half hours after indomethacin administration, blood flows to all organs returned to the preasphyxia control levels with the exception of cerebral blood flow which was reduced (93 +/- 13 to 65 +/- 7 ml/100 g X min). Three hours after indomethacin administration, the cerebral hyperemia caused by asphyxia was less (134 +/- 17 ml/100 g X min) than prior to indomethacin (221 +/- 15 ml/100 g X min). Indomethacin did not alter the asphyxia-induced changes to any other systemic organ.(ABSTRACT TRUNCATED AT 250 WORDS)