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At least 217 records · Page 12Linked to original sources

PubMed1977

Increased pulmonary vascular resistance with systemic hypertension. Effect of minoxidil and other antihypertensive agents.

Recent case reports suggest that pulmonary hypertension could be caused by minoxidil, a new potent vasodilating antihypertensive drug. Therefore, we evaluated the incidence and severity of pulmonary hypertension in 110 patients with systemic hypertension. Fourteen patients were treated with minoxidil for 2 to 35 months (mean 19.9 months), 15 were treated with no drugs, and the remaining 81 patients received conventional antihypertensive agents of several types. Pulmonary vascular resistance correlated positively (P is less than 0.05) with systemic vascular resistance. Minoxidil-treated patients with hypertension previously refractory to conventional therapy had slightly lower pulmonary vascular resistance than other hypertensive subjects. There was no correlation between pulmonary vascular resistance and duration of minoxidil therapy or other types of antihypertensive regimens. The positive correlation between pulmonary and systemic vascular resistance suggests the possibility of a causal hypertension relation in the two vascular beds.

Adolescent↗

PubMed1989

Pulmonary vascular resistance after cessation of positive end-expiratory pressure.

This report describes the pulmonary vascular response of infant lamb lung to abrupt cessation of positive end-expiratory pressure (PEEP) during volume-regulated continuous positive-pressure breathing (CPPB). In an intact, endobronchially ventilated preparation, the increase in left lung blood flow (QL) after abrupt cessation of 11 Torr left lung PEEP was found to be gradual, although peak airway pressure (Pmax) fell promptly from 36 to 14 Torr; 49% of the increase in QL occurred greater than 10 s after cessation of PEEP. Recruitment of zone I vasculature that had been created by balloon occlusion of the left pulmonary artery was found to occur promptly after balloon deflation. Isolated neonatal lamb lungs, perfused at constant flow rate, showed similar persistent elevation of pulmonary vascular resistance after cessation of 15 Torr PEEP, although Pmax fell abruptly from 39 to 12 Torr. This hysteresis was eliminated by calcium channel blockade with verapamil, and the magnitude of the change in pulmonary arterial pressure after either application or cessation of PEEP was reduced (25 and 26%, respectively). These observations suggest that, during CPPB, lung stretch alters neonatal pulmonary vascular tone or, by causing calcium channel-dependent lung volume hysteresis, modulates pulmonary vascular resistance. This interaction exaggerates the effect of airway pressure changes on pulmonary vascular resistance during mechanical ventilation.

Animals↗

PubMed1994

Relation between endothelin-1 spillover in the lungs and pulmonary vascular resistance in patients with chronic heart failure.

OBJECTIVES: The aim of this study was to clarify the origin of plasma endothelin-1 and to determine the relation between pulmonary vascular resistance and endothelin-1 secretion in the pulmonary circulation in patients with chronic congestive heart failure. BACKGROUND: Plasma levels of endothelin-1, a potent endothelium-derived vasoconstrictor peptide, are increased in congestive heart failure, but the source has not been clarified. Recent studies have indicated a relation between endothelin-1 and pulmonary hypertension. We therefore evaluated the contribution of endothelin-1 secretion in the pulmonary circulation to the regulation of pulmonary vascular resistance in patients with chronic heart failure. METHODS: A comparison was made of the plasma levels of endothelin-1 between the main pulmonary artery and the pulmonary capillary wedge region, as well as between the femoral artery and the femoral vein in 62 patients with chronic heart failure. Stepwise multivariate regression analysis was used to detect independent predictors of pulmonary vascular resistance among the various vasoconstrictor hormones in these patients. RESULTS: There was no significant difference in plasma endothelin-1 levels between the femoral artery and vein. In contrast, plasma endothelin-1 increased significantly from the main pulmonary artery to the pulmonary capillary wedge region ([mean +/- SEM] 3.1 +/- 0.23 vs. 4.6 +/- 0.36 pg/ml, p < 0.01), and the increase was related to the severity of heart failure. Among the various vasoconstrictor factors, such as plasma active renin concentration, plasma angiotensin II, plasma norepinephrine, femoral venous plasma endothelin-1 and pulmonary endothelin-1 spillover, only endothelin-1 spillover in the lungs showed an independent and significant correlation with pulmonary vascular resistance (r = 0.82, p < 0.001). CONCLUSIONS: The main source of circulating endothelin-1 is not the peripheral vascular bed but the pulmonary vascular bed in patients with chronic heart failure. In addition, endothelin-1 secretion in the lungs may regulate the pulmonary vascular resistance in patients with chronic heart failure. These findings are consistent with a significant role for endogenous endothelin-1 in the pathophysiology of heart failure, especially in the pulmonary circulation.

Adult↗

PubMed1985

Segmental pulmonary vascular resistance in progressive hydrostatic and permeability edema.

We used the in situ blood-perfused left lower lobe preparation of the dog to examine the effect of hydrostatic and permeability edema on the slope and intercept of the vascular pressure-flow (P/Q) relationship and on the longitudinal distribution of vascular resistance with the arterial and venous occlusion technique. Hydrostatic edema (HE) was induced by raising the venous pressure, and permeability edema (PE) was induced with alpha-naphthylthiourea. When the hematocrit (Hct) of the perfusate was kept normal (approximately 40%), HE had no significant effect on either the slope or the intercept of the P/Q relationship or on the distribution of vascular resistance. PE caused a small increase in the intercept of the P/Q relationship and a small rise in the resistance of the vessels in the middle segment. In another series of HE experiments in which Hct was allowed to increase during edema formation, there was a marked increase in vascular resistance. We conclude that edema per se does not increase vascular resistance significantly and that the increases in vascular resistance which were observed previously by other investigators in the isolated lungs may be due to increases in blood hematocrit.

Animals↗

PubMed1985

Testosterone-induced decrement of prostatic vascular resistance in rats is reversed by estrogens.

The function and growth of the rat prostate are stimulated by androgens and inhibited by estrogens. To study the influence of these hormones on the prostatic blood flow, prostatic vascular resistance was measured in castrated adult rats, which were testosterone supplemented and treated with different estrogenic substances. Prostatic blood flow was measured using the microsphere technique. Testosterone supplementation for 8-9 days after castration resulted in decreased vascular resistance in both the ventral and dorsolateral prostates. In testosterone-supplemented rats, treatment for the same period of time with estradiol benzoate, ethinyl estradiol, and diethylstilbestrol induced increased vascular resistance in both the ventral and dorsolateral prostates. However, treatment with estromustine or estramustine did not change prostatic vascular resistance significantly. It was concluded that the testosterone-induced decrease of prostatic vascular resistance was reversed by estradiol, ethinyl estradiol, and diethylstilbestrol, possibly by a direct effect on the prostate.

Animals↗

PubMed2000

Dissociation of muscle sympathetic nerve activity and leg vascular resistance in humans.

We examined the hypothesis that the increase in inactive leg vascular resistance during forearm metaboreflex activation is dissociated from muscle sympathetic nerve activity (MSNA). MSNA (microneurography), femoral artery mean blood velocity (FAMBV, Doppler), mean arterial pressure (MAP), and heart rate (HR) were assessed during fatiguing static handgrip exercise (SHG, 2 min) followed by posthandgrip ischemia (PHI, 2 min). Whereas both MAP and MSNA increase during SHG, the transition from SHG to PHI is characterized by a transient reduction in MAP but sustained elevation in MSNA, facilitating separation of these factors in vivo. Femoral artery vascular resistance (FAVR) was calculated (MAP/MBV). MSNA increased by 59 +/- 20% above baseline during SHG (P < 0.05) and was 58 +/- 18 and 78 +/- 18% above baseline at 10 and 20 s of PHI, respectively (P < 0.05 vs. baseline). Compared with baseline, FAVR increased 51 +/- 22% during SHG (P < 0.0001) but returned to baseline levels during the first 30 s of PHI, reflecting the changes in MAP (P < 0.005) and not MSNA. It was concluded that control of leg muscle vascular resistance is sensitive to changes in arterial pressure and can be dissociated from sympathetic factors.

Adult↗

PubMedDate not supplied

Control of hindlimb vascular resistance in rats chronically sympathectomized with 6-hydroxydopamine.

1. Vascular resistance was measured after acute surgical denervation in the blood-perfused hind limbs of adult normal rats and rats which had been treated with 6-hydroxydopamine in the first 2 weeks of postnatal life. Vascular resistance was significantly higher in the limbs of 6-hydroxydopamine treated rats. 2. No excess of vasoconstrictor materials was detected when blood from 6-hydroxydopamine treated rats was used to perfuse the hind limbs of untreated rats or other 6-hydroxydopamine treated rats. 3. Hind limb blood vessels of 6-hydroxydopamine treated rats showed increased sensitivity to normal amounts of circulating vasoconstrictors of adrenal origin and to intra-arterial infusions of noradrenaline and angiotensin. 4. Infusion of desipramine into the hindlimb blood vessels of 6-hydroxydopamine treated rats did not increase vasoconstrictor responses to infused noradrenaline. Infusion of desipramine into the limbs of untreated rats increased responses to noradrenaline but these never attained the magnitude and duration of responses seen in limbs of 6-hydroxydopamine treated rats. 5. The increased sensitivity to noradrenaline of hindlimb vessels from 6-hydroxydopamine treated rats could partly be accounted for by an absence of neuronal uptake sites and partly by the development of non-specific post-junctional supersensitivity.

Angiotensin II↗

PubMedDate not supplied

Collateral cerebral vascular resistance in patients with significant carotid stenosis.

This study tests, the hypothesis that asymptomatic patients with hemodynamically significant internal carotid artery stenosis have a lower ipsilateral collateral cerebral vascular resistance and hence greater blood flow than their symptomatic cohorts. We measured internal carotid artery blood flow and cerebral perfusion pressures intraoperatively prior to and after carotid endarterectomy in 35 symptomatic and 10 asymptomatic patients with hemodynamically significant internal carotid artery stenosis. When the stenosis produced 30% or greater reduction in blood flow the calculated nondimensional normalized ratio of collateral cerebral vascular resistance of ipsilateral hemisphere cerebral vascular resistance was 1.15 +/- 0.83 (mean +/- SD) for the 10 asymptomatic patients and 2.98 +/- 1.89 for the 35 symptomatic patients (p = 0.0044). For the subgroup of 22 patients with 50% or greater reduction in internal carotid artery blood flow the resistance ratios were 0.782 +/- 0.541 for the 5 asymptomatic patients and 3.21 +/- 2.26 for the 17 symptomatic patients (p = 0.029). These results suggest that asymptomatic patients with hemodynamically significant internal carotid artery stenoses have a lower collateral cerebral vascular resistance than their symptomatic cohorts. The low collateral resistance may provide an adequate collateral cerebral blood flow to prevent ischemia and symptoms.

Blood Pressure↗

PubMed2004

Phosphodiesterase-3 inhibition prevents the increase in pulmonary vascular resistance following inhaled nitric oxide withdrawal in lambs.

OBJECTIVES: To determine the effects of inhaled nitric oxide on endogenous cyclic adenosine monophosphate in the intact lamb, and to determine the potential role of cyclic adenosine monophosphate in the rebound pulmonary hypertension associated with nitric oxide withdrawal. DESIGN: Prospective, placebo-controlled experimental study. SETTING: University-based basic science research laboratory. SUBJECTS: One-month-old lambs. INTERVENTIONS: Six 1-month-old control lambs, and 6 milrinone- (phosphodiesterase-3 inhibitor) treated lambs, were mechanically ventilated. Inhaled nitric oxide (40 ppm) was administered for 24 hrs and then acutely withdrawn. Sequential peripheral lung biopsies were obtained before, during, and 2 hrs after withdrawing inhaled nitric oxide therapy. MEASUREMENTS AND MAIN RESULTS: In control lambs, initiation of nitric oxide decreased left pulmonary vascular resistance by 29.6%, and withdrawal rapidly increased pulmonary vascular resistance by 77.1% (p <.05). Lung tissue cyclic adenosine monophosphate concentrations decreased by 25.3% during nitric oxide therapy (p <.05). In milrinone-treated lambs, nitric oxide decreased pulmonary vascular resistance by 26.6% (p <.05), but pulmonary vascular resistance was unchanged after acute withdrawal. Lung tissue cyclic adenosine monophosphate concentrations were preserved during nitric oxide therapy. CONCLUSIONS: Inhaled nitric oxide produces potent pulmonary vasodilation by activating soluble guanylate cyclase and increasing smooth muscle cell concentrations of guanosine-3',5'-cyclic monophosphate. However, alterations in endogenous nitric oxide/guanosine-3',5'-cyclic monophosphate during inhaled nitric oxide have been implicated in the clinically significant increases in pulmonary vascular resistance noted upon its acute withdrawal. Previous in vitro data suggest that exogenous nitric oxide/guanosine-3',5'-cyclic monophosphate can also alter cyclic adenosine monophosphate concentrations via their effect on cyclic adenosine monophosphate production and metabolism. The current in vivo study demonstrates that lung tissue cyclic adenosine monophosphate concentrations are decreased during inhaled nitric oxide and suggests a role for decreased cyclic adenosine monophosphate in the rebound pulmonary hypertension noted upon inhaled nitric oxide withdrawal. Milrinone may be a useful adjunct therapy during inhaled nitric oxide to preserve cyclic adenosine monophosphate concentrations and prevent rebound pulmonary hypertension.

Administration, Inhalation↗

PubMed1996

Effects of intra-arterial infusion of insulin on control of forearm vascular resistance in normotensive and hypertensive subjects.

In this article, I will review the recent progress in the relationship between hyperinsulinemia and control of vascular resistance. I particularly focus on effects of intra-arterial infusion of insulin on control of resting forearm vascular resistance and on vascular reactivity to vasoconstrictor agents in normotensive and hypertensive subjects. In conclusion, the physiological levels of local hyperinsulinemia may decrease resting forearm vascular resistance in some normotensive subjects but not in all. Insulin-induced vasodilation may be due to the production of prostacyclin but not due to nitric oxide. Hyperinsulinemia attenuates vasoconstriction induced by phenylephrine and angiotensin II in normotensive subjects. Although acute intra-venous infusion of insulin activates the sympathetic nerve system, it may not elevate blood pressure in normotensive subjects possibly due to above mentioned anti-vasoconstrictor effects of insulin. In contrast, insulin-induced anti-vasoconstrictor mechanisms may be lost in hypertensive subjects, which may result in hypertension.

Blood Vessels↗

PubMed1996

RSR-13, an allosteric effector of hemoglobin, increases systemic and iliac vascular resistance in rats.

Tissue O2 delivery in excess of metabolic demand may be a factor in the development of high vascular resistance in experimental models of volume-expanded hypertension. This hypothesis was previously tested in rats with an exchange transfusion of red blood cells treated with inositol hexaphosphate or an intravenous infusion of RSR-4, allosteric effectors of hemoglobin. The binding of these drugs with hemoglobin effect a conformational change in the molecule, such that the affinity for O2 is reduced. However, in both preparations, the changes in vascular resistance could have been nonspecific. The present studies used intravenous infusions of RSR-13, which did not share some of the problematic characteristics of RSR-4 and inositol hexaphosphate. Conscious instrumented rats (an electromagnetic flow probe on ascending aorta or an iliac, mesenteric, or renal Doppler flow probe) were studied for 6 h after an RSR-13 infusion of 200 mg/kg in 15 min. This dose significantly increased arterial P50 (PO2 at which hemoglobin is 50% saturated) from 38 +/- 0.8 to 58 +/- 1.4 mmHg at 1 h after the start of the infusion. In the 3rd h cardiac output fell significantly from a control value of 358 +/- 33 to 243 +/- 24 ml.kg-1.min-1 and total peripheral resistance significantly increased from 0.31 +/- 0.03 to 0.43 +/- 0.04 mmHg.ml-1.kg.min. Cardiac output and P50 returned toward control over the next few hours. Neither cardiac output nor total peripheral resistance changed in the group of rats receiving vehicle alone. In a separate group of rats, iliac flow decreased significantly to 60% of control and iliac resistance increased to 160% of control. Iliac flow increased significantly in the group of rats that received vehicle only. Although the mechanism of these changes has not been established, these results suggest that a decreased O2 affinity leads to an increased total peripheral resistance and regional vascular resistance and support the hypothesis that O2 plays a role in the metabolic autoregulation of blood flow.

Allosteric Regulation↗

PubMed1976

The effects of increased blood viscosity on pulmonary vascular resistance.

The isolated left lower lobes of 15 dogs' lungs were perfused by means of a roller pump with blood at hematocrit values ranging from 31 to 80 per cent. Pressure-flow curves were constructed at blood flow rates from one half to three times the normal flow for the left lower lobe at each hematocrit level. The perfusion pressure was normalized with reference to the normal hematocrit(38 to 48 per cent) and normal blood flow for the left lower lobe (20 ml. per kilogram per minute). From these normalized pressure-flow curves, normalized resistance-flow curves were constructed at different mean hematocrit levels. Regression lines were drawn relating normalized pulmonary vascular resistance to hematocrit at different rates of pulmonary blood flow which might be found in patients with congenital heart disease. It was found that pulmonary vascular resistance rose in an exponential fashion as the hematocrit was increased, and that the blood viscosity determined both the shape of the resistance-flow curve and magnitude of the increase in resistance to pulmonary blood flow, especially when the pulmonary blood flow was less than normal and the hematocrit was greater than 54 per cent. The family of regression lines relating pulmonary vascular resistance to hematocrit at different flow rates may be used clinically in patients with congenital heart disease and polycythemia to determine if an elevated pulmonary vascular resistance is due to increased blood viscosity or obstructive pulmonary vascular disease. It is concluded that an increased blood viscosity due to polycythemia significantly alters the pulmonary hemodynamics of patients with congenital heart disease with either increased or decreased pulmonary blood flow. Increased blood viscosity may play an important part in the early initiation and development of pulmonary arteriosclerosis in patients with transposition of the great arteries.

Animals↗

PubMed2001

Vascular resistance in human muscle flaps.

Important differences in free muscle flap survival have been reported in the setting of long arterial and venous vein grafts. The authors provide insight into the etiology of flap failure by addressing the following question: Do differences in flap type result in clinically significant different vascular resistances and consequently anastomotic patency? A total of 15 human flaps were studied intraoperatively: 9 gracilis, 3 rectus abdominis, and 3 latissimus dorsi. The muscle was isolated on a single pedicle and hemodynamic stability was ensured. The venous pedicle was then divided. A timed collection of effluent was used to determine flow. Vascular resistance was calculated by dividing the change in pressure by the flow, and standardizing this for temperature and hematocrit. Average vascular resistance and standard deviation for the gracilis, rectus, and latissimus flaps was 10.34 +/- 7.77 mmHg per milliliter per minute, 2.79 +/- 1.50 mmHg per milliliter per minute, and 3.17 +/- 1.05 mmHg per milliliter per minute respectively. An inverse relationship between muscle vascular resistance and flap mass was found (p < 0.001). This indicates that larger muscles have less vascular resistance. The decreased resistance gives rise to higher flow rates and, as a result, potentially improved vein graft patency. The clinical implication is that a larger flap should be used when high flow-through is critical. The role of flap vascular territory makeup continues to be pursued.

Abdominal Muscles↗

PubMed1997

Effects of endothelin ETA receptor antagonism with PD 156707 on hemodynamics and renal vascular resistance in rabbits.

The objective of this study was to determine the in vivo effectiveness of the selective endothelin ETA receptor antagonist PD 156707 (sodium 2-benzo[1,3]dioxol-5-yl-4-(4-methoxy-phenyl)-4-oxo-3-(3,4,5-trimet hoxy- benzyl)-but-2-enoate). Effectiveness was defined by the ability of the compound to block increases in renal vascular resistance and mean arterial blood pressure induced by an intravenous bolus of 0.3 nmol/kg of human endothelin-1 in pentobarbital anesthetized rabbits. Different groups of rabbits received hour long intravenous infusions of PD 156707 at doses of 0.003, 0.01, 0.03 or 0.3 mg/kg per h. During baseline conditions, mean arterial blood pressure, heart rate, renal blood flow, and renal vascular resistance were similar among the groups. The intravenous bolus of endothelin-1 significantly decreased mean arterial blood pressure (82 +/- 3 mmHg to 65 +/- 3 mmHg, P < 0.05) and increased renal vascular resistance (2.8 +/- 0.3 mmHg/ml per min to 9.2 +/- 1.1 mmHg/ml per min, P < 0.05) in untreated control animals. At doses of 0.3 and 0.03 mg/kg per h, PD 156707 virtually abolished endothelin-1 induced increases in renal vascular resistance, but did not affect the endothelin-1 induced decrease in mean arterial blood pressure. At 0.01 and 0.003 mg/kg per h, PD 156707 also inhibited endothelin-1 induced increases in renal vascular resistance but the effects were less striking, leading to the conclusion that the minimum effective intravenous dose of the compound in rabbits is in the range of 0.01-0.03 mg/kg per h. The results of this study demonstrate that PD 156707 is an extremely potent and highly selective endothelin ETA receptor antagonist. In addition, this study demonstrates the utility of renal vascular resistance as an in vivo bioassay for evaluating the selective vascular effects of endothelin receptor antagonists in this species.

Animals↗

PubMed1982

Relationship between regional lung volume and regional pulmonary vascular resistance.

We have examined the relationship between regional pulmonary vascular resistance (PVRr) and regional lung volume (VLr) to determine whether the decrease in blood flow in the dependent lung (zone 4) was related to lung volume. Regional blood flow (Qr) was measured with radiolabeled macroaggregates at functional residual capacity (FRC) and at transpulmonary pressure of 10 cmH2O (PL10) in 10 anesthetized supine dogs. VLr was determined at FRC by measuring lung density in frozen lung slices and was calculated at PL10 using each dog's pressure-volume curve. We found that when PVRr was expressed as a function of VLr there was not a single relationship between the two. Instead we found two separate U-shaped curves, one at FRC and one at PL10 indicating that the increased vascular resistance at the lung base remained when the lung volume was made uniform by inflation to PL10. This suggests that there is no simple relationship between VLr and PVRr.

Animals↗

PubMed1996

Age-related and vasomotor stimuli-induced changes in renal vascular resistance detected by Doppler ultrasound.

Indirect measurement of renal vascular resistance by duplex Doppler waveform analysis was evaluated in relation to aging and some pathophysiological conditions. Baseline renal resistive index (RRI) (peak systolic frequency shift - lowest diastolic frequency shift/peak systolic frequency shift) was measured in healthy controls aged 20 to 85 years by analyzing the blood flow velocity waveform of interlobar arteries. RRI changes induced by sympathetic activation (cold pressor test and handgrip test) or by fluid load were evaluated. Both repeatability and reproducibility were very good, as the intra and interoperator variations were all less than their reproducibility coefficients. RRI showed a significant increase with aging (ANOVA P < .001), particularly evident in subjects older than 50 years. Both the cold pressor test and handgrip test induced in all the subjects (n = 16) a significant increase in RRI (P < .001), from 0.59 +/- 0.04 to 0.69 +/- 0.04 (12 +/- 6%) for the cold pressor test and from 0.57 +/- 0.03 to 0.66 +/- 0.03 (15 +/- 2%) for the handgrip test. In eight subjects intravenous fluid load (0.25 mL/kg/min of 0.9% NaCl for 120 min) caused a significant decrease in RRI (P < .001), from 0.62 +/- 0.02 to 0.53 +/- 0.01 (17 +/- 2%), which was inversely related to mean blood pressure rise (r = 0.71, P < .001). These data show that pulsed wave Doppler analysis is an accurate method for an indirect evaluation of changes in renal vascular resistance induced by common vasomotor stimuli.

Adult↗

PubMed1995

[Quantification and monitoring of vascular resistance in the lower limbs by the Doppler method (animal model)].

The object of this study was to define and validate a non-invasive method of evaluation and monitoring of vascular resistances in the leg. Blood flow velocity was measured by Doppler ultrasound in an animal model (ewe) with similar blood flow characteristics in the lower limb as man and allowing access to the required invasive measurements for validation of the method (pressure and flow). Vascular resistances distal to the measuring point (femoral, for example) were assessed using the resistance index R = D/S, S being the peak systolic deflection and D that of diastolic reflux of the Doppler spectral analysis of flow in the femoral artery. The values and variations of this resistance index were compared with the vascular resistances calculated from measurements of pressure and flow at the point of Doppler sampling and expressed in mmHg/ml/min. Femoral flow was measured by Doppler ultrasound (Doppler-echo), and mean pressure by an arterial catheter introduced into the abdominal aorta. Compression of the lower limb veins induced a venous return resulting in a reduction of cardiac output and femoral flow. During compression, femoral flow decreased by an average of 29% (p < 0.001) although mean pressure and heart rate did not change significantly. The femoral resistance index (Rf) increased by an average of 37.5% (p < 0.01) and vascular resistances increased by 45.9% (p < 0.01). Injection of 1 mg adrenaline induced peripheral vasoconstriction with an increase in blood pressure and a decrease in heart rate and femoral flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1982

Forearm vascular resistance in the upper and lower quintiles of blood pressure in adolescent boys: The Muscatine Study.

Nineteen 16 year old white boys whose systolic blood pressures were in the upper (r = 9) and lowest (r = 10) quintile of the distribution in two school surveys in 1975 and 1977 were selected. In 1979 forearm blood flow, blood pressure and heart rate were measured at rest, and during peak reactive hyperemia. Minimal forearm vascular resistance during peak reactive hyperemia was used to assess the structural contribution to vascular resistance. At rest the high quintile group again had significantly higher blood pressures than the low quintile group but their forearm vascular resistance was not significantly different. The high quintile group showed significantly higher minimal forearm vascular resistance at peak reactive hyperemia. The latter observation suggests that there is a difference in the structural contribution to forearm vascular resistance in adolescents with blood pressure in the upper versus lower quintile of the distribution.

Adolescent↗