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Results for “VASCULAR RESISTANCE”

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PubMed1998

Reduction in pulmonary vascular resistance with long-term epoprostenol (prostacyclin) therapy in primary pulmonary hypertension.

BACKGROUND: Primary (idiopathic) pulmonary hypertension is a progressive, fatal disease. Conventional therapy with anticoagulant and vasodilator drugs may improve symptoms and survival among selected patients, but there is no evidence that the disease can be reversed. METHODS: We evaluated the effects of long-term therapy (i.e., for more than one year) with intravenous epoprostenol (prostacyclin) in patients with advanced primary pulmonary hypertension. The base-line evaluation included an assessment of pulmonary vascular dilation in response to intravenous adenosine. The epoprostenol dose was increased monthly to the maximum tolerated. Long-term therapy was evaluated by measuring improvement in symptoms, exercise capacity, and hemodynamic measures. RESULTS: We evaluated 27 patients with primary pulmonary hypertension over a mean (+/-SD) period of 16.7+/-5.2 months. Intravenous adenosine had a variable effect on pulmonary vascular resistance (mean reduction, 27 percent; range, 0 to 56; P<0.001). Epoprostenol therapy was initiated and the rate of infusion was increased by an average of 2.4 ng per kilogram of body weight per minute each month. Twenty-six of the 27 patients had improvement in symptoms and hemodynamic measures, and overall, pulmonary vascular resistance declined by 53 percent to 7.9+/-3.8 resistance units (P<0.001) at the time of restudy. The long-term effects of epoprostenol exceeded the short-term pulmonary vasodilator response to adenosine in all but one patient. Seven of the eight patients who had minimal pulmonary vasodilation in response to adenosine (mean reduction in resistance units, <20 percent) still had a significant reduction in pulmonary vascular resistance when treated with epoprostenol (mean, 39+/-14 percent; P=0.002). CONCLUSIONS: In primary pulmonary hypertension, long-term therapy with epoprostenol lowers pulmonary vascular resistance beyond the level achieved in the short term with intravenous adenosine. Epoprostenol appears to have sustained efficacy in this disorder.

Adult↗

PubMed1990

The vascular resistance of arterial stenoses in series.

The vascular resistance of stenoses in series has been studied in vitro by use of fiber optic laser Doppler anemometry to measure the cross-sectional areas of the stenoses. Pressure gradients across each of the stenoses were measured while both the severity and the separation of the stenoses were altered. The individual resistances were compared with the combined resistance. Resistance at a stenosis is a nonlinear function of the severity of the stenosis. The resistance is a complex function of the perfusion pressure and the cross-sectional area of the stenosis and cannot be accurately predicted from a single plane angiographic image. With multiple stenoses an approximate assessment of the combined effect can be obtained by summing the value of the resistance for each stenosis but not the degree of the stenoses. The nonlinear relationship of resistance to stenosis severity means that if one stenosis is more severe than the other, the combined effect can be regarded as the same as the effect of the more severe stenosis acting by itself. The distance between the stenoses does not change their combined effect.

Arteries↗

PubMed1991

Effect of hypertonic saline infusion on renal vascular resistance in anesthetized dogs.

Changes in renal vascular resistance (RVR) and their mechanisms were investigated following infusion of 7.5% hypertonic saline (4 ml/kg) in anesthetized dogs. In all animals the left kidney was perfused at a constant perfusion flow (59 +/- 6 ml/min) with heparinized blood using a pulsatile roller pump. Renal perfusion pressure (RPP), systemic blood pressure (SBP), central venous pressure (CVP), and heart rate (HR) were measured simultaneously. Electrical stimulation of renal sympathetic nerves was also performed to evaluate the neurally mediated change in renal vasculature before and after infusion of hypertonic saline. In animals with intact vagi, intravenous administration of hypertonic saline resulted in significant increases in both mean blood pressure (MBP) and CVP, and caused significant decreases in HR and RVR. These effects were not affected by bilateral cervical vagotomy. In both intact and vagotomized animals, changes in RVR in response to renal nerve stimulation were attenuated after infusion of hypertonic saline. These results suggest that reduction in RVR after intravenous infusion of hypertonic saline is not a reflex effect mediated by vagal afferents. Instead, vascular response of the renal artery to hypertonic saline may result from a suppression of neurotransmission from renal sympathetic nerve endings to renal vascular smooth muscle.

Animals↗

PubMed1990

Effects of nitrendipine and hypoxia on pulmonary vascular resistance in experimental emphysema.

We evaluated the hemodynamic effects of nitrendipine, a dihydropyridine Ca2+ channel blocker, and hypoxia in intact dogs with emphysema produced by treatments with aerosolized papain. We also determined the effects of emphysema, chronic Ca2+ channel blocker treatment, and acute hypoxia on the distribution of vascular resistance in isolated left lower lobes. Pulmonary vascular resistance was increased (4 +/- 1 mm Hg/L/min) in the animals studied 6 months after receiving 4 weekly treatments with papain compared with control animals (2.6 +/- 0.6 mm Hg/L/min, p less than 0.05), and this effect of emphysema was blunted with chronic nitrendipine, 3 mg/kg twice a day (3.1 +/- 0.9 mm Hg/L/min). Both at baseline and at 6 months, hypoxia-induced increases in pulmonary vascular resistance were abolished by nitrendipine. The total pulmonary pressure gradient (delta Pt) was partitioned into pressure gradients across arterial (delta Pa), middle (delta Pm), and venous (delta Pv) vessels by occlusions performed during normoxia (PIO2 = 200 mm Hg) and hypoxia (PIO2 = 30 mm Hg). Papain-treated animals had elevated delta Pt compared with that in control animals because of an increased delta Pv (9.7 +/- 1.1 mm Hg versus 5.2 +/- 0.4 mm Hg in control animals, p less than 0.05). In contrast, only delta Pm was increased with papain + nitrendipine (2.6 +/- 1.0 mm Hg versus 0.2 +/- 0.3 mm Hg in control animals, p less than 0.05). An increase in the downstream pressure gradient was also observed when lobes from animals with emphysema were studied under conditions of reverse perfusion. Hypoxic responses were similar in the control and papain groups, with increases in delta Pa and delta Pm.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1975

Estimation of non-autonomic and autonomic components of iliac bed vascular resistance in renal hypertensive rabbits.

Iliac bed vascular resistance (IVR) was measured before and after pharmacological block of the autonomic effectors in unanaesthetized renal hypertensive and normotensive rabbits with previously implanted Doppler flowmeters. This permitted partitioning the resting IVR into a non-autonomic component (ie, steady-state IVR after block) and an autonomic component (ie, resting IVR minus non-autonomic IVR). When IVR was measured at the same mean arterial pressure (MAP) before and after block in each animal, the increase in estimated non-autonomic IVR accounted entirely for the rise in resting IVR in renal hypertensive rabbits. However, if IVR measurements after block were made at a lower MAP than before block, the estimated non-autonomic and autonomic components were both significantly increased in renal hypertensive rabbits. It is concluded that in the latter experiment non-autonomic IVR in renal hypertension was underestimated, whilst the autonomic component was overestimated. The rise in non-autonomic IVR in renal hypertension was partly due to structural changes in the iliac bed, since IVR remained higher in hypertensive than in normotensive rabbits after abolishing smooth muscle tone with vasodilator drugs.

Animals↗

PubMed1988

Increase of pulmonary vascular resistance during cold provocation in patients with variant angina.

This study was performed to evaluate pulmonary vascular reactivity in patients with angiographically documented coronary vasospasm. Right heart catheterization was performed in 8 subjects with vasospastic angina without evidence of Raynaud's phenomenon: heart rate, systemic and pulmonary arterial pressure as well as cardiac output were determined at rest, during cold provocation and after 20 minutes recovery. Data were obtained both before and during treatment with nifedipine. During cold provocation pulmonary vascular resistance was elevated significantly (P less than 0.02 compared with baseline); systemic vascular resistance tended to increase; nifedipine blunted both vasoconstrictor effects. Our results indicate an abnormal vascular response of the pulmonary arteries to cold provocation in patients with symptomatic coronary artery spasm and suggest a primary vasospastic disorder with coronary and pulmonary manifestation.

Adult↗

PubMed2002

Effects of dilutional and modified ultrafiltration in plasma endothelin-1 and pulmonary vascular resistance after the Fontan procedure.

BACKGROUND: Pulmonary vascular resistance (PVR) is closely related with patients' hemodynamics after the Fontan procedure and endothelin-1 (ET-1) may play an important role in pulmonary circulation. Modified ultrafiltration (MUF) is known to remove inflammatory mediators after cardiopulmonary bypass (CPB) surgery. The time courses of plasma ET-1 and PVR were examined before and after the Fontan procedure with MUF. METHODS: Twenty-two patients who underwent the Fontan procedure were divided into two groups: a dilutional ultrafiltration/modified ultrafiltration (DUF/MUF) group (n =11) and a control group (n = 11). Conventional ultrafiltration was performed during CPB in the control group. DUF was performed semicontinuously during CPB and MUF was continued until 15 to 20 minutes after the CPB with polyacrylonitonile membrane in the DUF/ MUF group. The plasma ET-1 concentration was measured before and after CPB, after MUF in the DUF/MUF group, and 6 and 24 hours after CPB. PVR was calculated simultaneously using a thermodilutional catheter. RESULTS: Plasma ET-1 levels increased significantly after CPB in the control group but they did not increase immediately after CPB in the DUF/MUF group. Similarly, PVR increased significantly after CPB in the control group but it did not increase after CPB in the DUF/MUF group and remained low at 6 and 24 hours after CPB. CONCLUSIONS: DUF and MUF suppress the increase in the plasma ET-1 concentration that occurs immediately after the completion of the Fontan procedure and may be an effective intervention for maintaining low PVR after the procedure.

Cardiopulmonary Bypass↗

PubMed1994

Response of right ventricular systolic function to exercise stress: effects of pulmonary vascular resistance on right ventricular systolic function.

To elucidate factors influencing responses of right ventricular systolic function to exercise stress, we evaluated the right ventricular ejection fraction and peak ejection rate with two different loading conditions, atrial septal defect and mitral stenosis, at rest and during exercise by means of gated equilibrium blood pool radionuclide ventriculography. In both atrial septal defect and mitral stenosis, strong correlations between changes in the right ventricular ejection fraction with exercise and pulmonary vascular resistance at rest (r = -0.97, p < 0.001; r = -0.86, p < 0.005: respectively) were found. Significant correlations between changes in the right ventricular peak ejection rate with exercise and pulmonary vascular resistance at rest (r = -0.85, p < 0.05; r = -0.75, p < 0.01: respectively) were found in atrial septal defect and mitral stenosis. Both the right ventricular ejection fraction and peak ejection rate were lower during exercise than at rest when pulmonary vascular resistance at rest was more than 200 dynes.sec.cm-5.m2 in both atrial septal defect and mitral stenosis. In conclusion, right ventricular systolic function responding to exercise stress was influenced by the pulmonary vascular resistance in both atrial septal defect and mitral stenosis.

Adult↗

PubMed1993

[Value of vascular resistance in fetal circulation during normal pregnancy].

The aim of the study is to estimate the values of resistance index (RI) in the arteries of the fetus using color doppler ultrasound. Measurements have been made in aorta, umbilical and medial cerebral artery of the fetus and in arcuate artery of the pregnant women. 50 women have been examined every 4 weeks and another 50 every 6 weeks during normal pregnancy. Resistance index has been calculated based on analyses of flow waves configuration in all of the mentioned arteries. Likeness between curves obtained in women examined every 4 and 6 weeks in obvious. The examination of mean RI values shows that vascular resistance in descending aorta remains constant during the vascular resistance in descending aorta remains constant during the all the period. In arcuate artery vascular resistance falls down until 22 week of pregnancy and then settles on constant level. RI of umbilical artery decreases during pregnancy and in median cerebral artery reaches its peak in 32/34 week of pregnancy.

Aorta↗

PubMed1997

Effect of tumor necrosis factor alpha on vascular resistance, nitric oxide production, and glucose and oxygen consumption in perfused tissue-isolated human melanoma xenografts.

The effect of tumor necrosis factor alpha (TNF-alpha) on vascular resistance, nitric oxide production, and consumption of oxygen and glucose was examined in a perfused tissue-isolated tumor model in nude mice. One experimental group was perfused with heparinized Krebs-Henseleit buffer, a second one was perfused with TNF-alpha (500 microgram/kg) 5 h before perfusion. The vascular resistance increased significantly 5 h after TNF-alpha injection. The increase in vascular resistance did not seem to be mediated by a decrease in tumor nitric oxide production, as determined by perfusate nitrate/nitrite concentrations, but may be due to aggregation of leukocytes, platelets, and erythrocytes and/or endothelial consumption among the three experimental groups. The oxygen consumption was linearly dependent on the amount of available oxygen in the perfusate, whereas the glucose consumption was constant and independent of the glucose delivery rate. The present experiments provide new insights into physiological and metabolic mechanisms of action of TNF- alpha for optimization of future treatment schedules involving TNF-alpha.

Animals↗

PubMed1999

Comparison of alterations in fetal regional arterial vascular resistance in appropriate-for-gestational-age singleton, twin and triplet pregnancies.

The objective of this longitudinal study was to evaluate alterations in fetal vascular resistance of fetal peripheral arteries with advancing gestation in singleton appropriate-for-gestational-age (S-AGA), twin appropriate-for-gestational-age (Tw-AGA) and triplet appropriate-for-gestational-age (Tri-AGA) infants. Colour Doppler flow imaging and pulsed Doppler ultrasonographic examinations were performed on 35 S-AGA, 52 Tw-AGA and 12 Tri-AGA fetuses. The pulsatility index for middle cerebral artery (MCAPI), umbilical artery (UAPI), descending aorta (DAPI), splenic artery (SAPI), renal artery (RAPI) and femoral artery (FAPI) was measured as vascular resistance every 2 weeks after 15 weeks of menstrual age until delivery. Optimal models and normal ranges for pulsatility index for each artery in each group were generated. The alterations in various fetal regional arterial pulsatility indices with advancing gestational age showed no significant differences in S-AGA, Tw-AGA and Tri-AGA infants, respectively. These results suggest that there is no significant difference for regional arterial vascular resistance in AGA fetuses among singleton, twin, and triplet pregnancies, whereas there was a slight difference in fetal growth pattern among singleton, twin, and triplet pregnancies described in our previous investigation.

Adult↗

PubMed1999

Systemic blockade of the endothelin-B receptor increases peripheral vascular resistance in healthy men.

Endothelin-1 (ET-1) is an important mediator of vascular tone in humans, and a number of endothelin receptor antagonists are currently in clinical development as vasodilator agents. While the vasoconstrictor role of the ETA receptor is undisputed, the role of the ETB receptor remains unclear. Hemodynamic effects of systemic doses of the ETB-selective antagonist BQ-788 were investigated in 5 healthy male volunteers (age range, 33 to 48 years) in a placebo-controlled, four-way crossover study. After a 15-minute infusion of BQ-788 (3, 30, or 300 nmol/min) or placebo, plasma ET-1 and big ET-1, blood pressure, heart rate, cardiac index, and stroke index were measured. Total peripheral vascular resistance was calculated from cardiac index and mean arterial pressure. Hemodynamic data are expressed as maximum, placebo-corrected, percentage change from baseline following BQ-788 (300 nmol/min) and were examined by ANOVA. Plasma ET-1 increased by 3.7+/-1.2 pg/mL (maximum at 15 minutes, P=0.02), whereas there was no significant change in plasma big ET-1. Although BQ-788 had no effect on mean arterial pressure, there was a reduction in heart rate (13+/-7% at 50 minutes; P=0.002), cardiac index (17+/-5% at 40 minutes; P<0. 0001), and stroke index (8+/-4% at 40 minutes; P=0.002) and an increase in total peripheral vascular resistance (24+/-5% at 40 minutes; P<0.0001). The selective ETB receptor antagonist BQ-788 causes peripheral vasoconstriction in healthy volunteers, suggesting that the overall balance of effects of endogenous ET-1 at the vascular ETB receptor favors vasodilatation. Further investigation is now clearly required to address whether selective ETA or combined ETA/ETB receptor blockade will be more effective in the clinical setting.

Adult↗

PubMed1987

Effect of edema on segmental vascular resistance in isolated lamb lungs determined by micropuncture.

We have studied the mechanical effects of fluid accumulation on the pulmonary vasculature in 28 isolated blood perfused lungs of newborn lambs. Vascular resistance in the pulmonary arteries, microvessels, and veins was determined by micropuncture measurement of microvascular pressures, and regional distribution of blood flow in the lungs was determined using radiolabelled microspheres both before and after the development of varying degrees of hydrostatic edema. Edema was induced by raising venous pressure. During measurements, alveolar and venous pressures were kept constant at 7 and 8 cm H2O, respectively, as well as lung blood flow (540 +/- 107 ml/min). All vascular pressures were referenced to the superior surface of the lung, site of all micropunctures. Active vasomotor changes were eliminated by addition of papaverine to the perfusate. Under baseline nonedematous conditions in the absence of vasomotor tone, 17% of the total pressure drop was in arteries, 41% was in microvessels, and 42% was in veins. With the development of alveolar edema (80 +/- 13% weight gain), there was no change in total or segmental vascular resistance, but after 148 +/- 97% weight gain, total pulmonary vascular resistance increased by 74%. Segmental pressure drop increased in arteries by 172% and in microvessels by 132% but decreased by 22% in the venous segment. Regional distribution of blood flow remained unchanged. Possible mechanisms for increased resistance to blood flow may be compression of small arterioles and venules (less than 20 micron diameter) by liquid cuffs and/or occlusion of microvessels by the weight of alveolar liquid.

Animals↗

PubMed2004

Angiotensin-(1-7) modulates vascular resistance and sympathetic neurotransmission in kidneys of spontaneously hypertensive rats.

OBJECTIVE: Angiotensin (Ang)-(1-7) generated from Ang I and II is reported to act as an endogenous angiotensin-converting enzyme (ACE) inhibitor and angiotensin type 1 (AT1)-receptor antagonist in vitro and in vivo. Ang-(1-7) has been suggested to play an important role in hypertension. METHODS AND RESULTS: Therefore, we tested whether Ang-(1-7) differentially modulates vascular resistance and neurotransmission in isolated kidneys of spontaneously hypertensive rats stroke prone (SHR-SP) and Wistar-Kyoto rats (WKY). Ang-(1-7) was administered in three concentrations (0.1, 1 and 10 micromol/l) to prevent Ang I- and Ang II-induced pressor responses and facilitation of noradrenaline release. There were indeed concentration-dependent strain differences. Ang-(1-7) prevented Ang I- and Ang II-mediated changes in vascular resistance more potently in SHR-SP than in WKY by inhibiting ACE and by blocking AT1-receptors. Ang-(1-7) by itself had no influence on renal vascular tone in both strains. Ang-(1-7) inhibited Ang I-mediated facilitation of noradrenaline release more potently than Ang II-mediated facilitation of noradrenaline release. Ang-(1-7) by itself enhanced noradrenaline release from SHR-SP, but not from WKY kidneys. CONCLUSION: Ang-(1-7) had a greater impact on Ang I and Ang II modulation of renal vascular resistance in SHR-SP than in normotensive rats. Furthermore, Ang-(1-7) by itself has facilitatory presynaptic effects on noradrenaline release but no postsynaptic effects on renal vascular resistance in SHR-SP. Since plasma levels of Ang-(1-7) accumulate during ACE-inhibitor or AT1-receptor antagonist therapy, Ang-(1-7) could contribute to antihypertensive effects of these agents.

Angiotensin I↗

PubMed1995

Cerebral blood flow, vascular resistance, and oxygen metabolism in acute brain trauma: redefining the role of cerebral perfusion pressure?

OBJECTIVES: To evaluate normal or high cerebral perfusion pressure in relation to cerebral blood flow and oxygen metabolism, as well as other multivariate cerebral hemodynamic and metabolic interrelationships, in acute brain trauma in humans. DESIGN: Prospective, observational study. SETTING: Neuroscience intensive care unit of a university hospital. PATIENTS: Adults (n = 66) with severe acute brain trauma (Glasgow Coma Scale scores from 4 to 8), undergoing multivariate physiologic studies involving cerebral perfusion pressure, cerebral blood flow, cerebral metabolic rate of oxygen consumption, total hemoglobin content, arterio-jugular oxygen content difference, and cerebral vascular resistance, along with other routine procedures. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Statistical analysis did not demonstrate any correlation between cerebral perfusion pressure and cerebral blood flow, between cerebral perfusion pressure and arterio-jugular oxygen content difference, and between cerebral perfusion pressure and cerebral metabolic rate of oxygen consumption, over a broad spectrum of perfusion pressures ranging from 60 to 130 mm Hg. In contrast, a significant negative correlation was found between cerebral vascular resistance and cerebral blood flow, where higher values of cerebral vascular resistance were associated with lower blood flow levels, and vice versa. CONCLUSIONS: In severe acute brain trauma, cerebral hemodynamic and oxygen metabolic variables are not necessarily correlated with normal or even high levels of cerebral perfusion pressure. Under these circumstances, cerebral vascular resistance (not perfusion pressure) is more closely correlated with different patterns of cerebral blood flow and metabolism.

Acute Disease↗

PubMed1983

Effects of hydralazine and nitroprusside on cardiopulmonary function when a decrease in cardiac output complicates a short-term increase in pulmonary vascular resistance.

We investigated the short-term cardiopulmonary effects of nitroprusside and hydralazine when cardiac output (CO) was reduced by a short-term increase in pulmonary vascular resistance (PVR). In six anesthetized, ventilated dogs, small autologous blood clots, injected over 1 to 2 hr, increased right ventricular afterload. When CO had fallen approximately 40%, dogs were treated with nitroprusside and subsequently with hydralazine. Both drugs reduced biventricular filling pressures (p less than .05), but only hydralazine increased CO and stroke volume (p less than .05). Although mean blood pressure and pulmonary artery pressure remained constant with hydralazine, systemic vascular resistance and PVR decreased (p less than .01). In contrast, although nitroprusside reduced blood pressure and systemic vascular resistance (p less than .01), it did not affect PVR and pulmonary artery pressure. When CO is significantly reduced because of a short-term increase in PVR, hydralazine may be superior to nitroprusside in improving cardiopulmonary function.

Animals↗

PubMed1985

Effect of environmental hypothermia on vitelline artery blood pressure and vascular resistance in the stage 18, 21, and 24 chick embryo.

We studied the effect of environmental hypothermia on arterial blood pressure, dorsal aortic blood flow, and vascular resistance in stage 18, 21, and 24 chick embryos. The arterial pressure was measured with a servonull micropressure system. Mean dorsal aortic blood flow was calculated from pulsed-Doppler measurement of mean dorsal aortic blood velocity and dorsal aortic diameter. Vascular resistance was calculated by dividing mean vitelline arterial blood pressure by dorsal aortic blood flow. Sequential data were obtained at temperatures of 34.7, 31.1, and 34.1 degrees C. At stage 21, the vitelline arterial blood pressure decreased from 0.82 +/- 0.03 (means +/- SEM) to 0.72 +/- 0.03 mm Hg on cooling and increased from 0.66 +/- 0.05 to 0.87 +/- 0.06 mm Hg on rewarming (p less than 0.05). At stage 21, mean dorsal aortic blood flow decreased from 0.49 +/- 0.02 to 0.33 +/- 0.02 mm3/s with cooling and increased from 0.34 +/- 0.02 to 0.47 +/- 0.02 mm3/s with rewarming. The vascular resistance in stage 21 embryos increased after cooling from 1.68 +/- 0.19 to 2.23 +/- 0.39 mm Hg/mm3/s (means +/- 95% confidence interval). The changes were similar in stage 18 and 24 embryos. We conclude that the reduction of vitelline artery blood pressure resulted from a decrease in cardiac output. In addition, we noted that the vitelline arterial vascular bed can constrict in response to hypothermia prior to autonomic innervation. These changes in hemodynamics may be a teratogenic mechanism for hypothermia-induced cardiac defects in the chick embryo.

Animals↗

PubMed1997

Contribution of red blood cell aggregation to venous vascular resistance in skeletal muscle.

The effects of red blood cell aggregation on venous vascular resistance and conductance were examined in the cat lateral gastrocnemius muscle. During perfusion with blood of normal hematocrit, venous conductance fell linearly by 41% when blood flow was reduced from 5 to 1 ml x min(-1) x 100 g tissue(-1) and increased linearly by 155% when flow was increased from 5 to 20 ml x min(-1) x 100 g tissue(-1). This effect was not seen when the muscle was perfused with an acellular solution of 12% Dextran 40 in Ringer solution and was greatly reduced or absent with a nonaggregating suspension of red blood cells in Ringer solution + Dextran 40. Also, the venous vascular conductance at a control flow of 5 ml x min(-1) x 100 g tissue(-1) during perfusion with the nonaggregating red blood cell suspension was twice that with normal blood of the same hematocrit. The effect of flow on venous conductance was significantly reduced when red blood cell aggregation was increased by addition of Dextran 250 to the blood (200 mg/kg body wt) and was also reduced in animals with systemic hematocrit >50%. These findings suggest that red blood cell aggregation contributes importantly to venous vascular resistance in resting muscle.

Animals↗