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At least 19 recordsLinked to original sources
PubMed1977

Dynamics of myocardial oxygen consumption and coronary vascular resistance.

Coronary vascular resistance may be regulated in part by substances whose concentrations are determined by or reflect the rate of myocardial oxygen consumption (e.g., adenosine, vessel wall PO2). We tested this hypothesis by comparing the time course of changes in myocardial oxygen consumption and coronary vascular resistance following 20 beat/min changes in heart rate. Main left coronary arteries of in situ dog hearts were perfused with blood at constant flow. Coronary sinus O2 content was monitored continuously with a densitometer and reflected the time course of changes in oxygen consumption and also the effects of vascular transit between tissue and the coronary sinus. These transit effects were estimated from dye transit curves and added to the time course of changes in coronary perfusion pressure which was proportional to coronary vascular resistance at constant flow. Coronary sinus O2 content changes preceded the adjusted time course of vascular resistance. This supports the hypothesis that coronary vascular resistance is regulated in part by factors closely linked to oxidative metabolism.

Animals↗
PubMed1977

Influence of inhibitors of prostaglandin synthesis on renal vascular resistance and on renal vascular responses to vasopressor and vasodilator agents in the cat.

We determined the effects of indomethacin and meclofenamate, two inhibitors of prostaglandin synthesis, on renal vascular resistance and on renal responses to nerve stimulation, pressor and depressor hormones in the in situ feline kidney under conditions of controlled blood flow. Both inhibitors produced a gradual rise in renal vascular resistance which became maximal 15-20 minutes after administration. The increase in renal resistance after indomethacin was not attenuated during intrarenal infusion of either phentolamine or SQ 20881. Pretreatment with propranolol, in a dose sufficient to inhibit renin secretion, also did not attenuate the increase in renal resistance produced by indomethacin. However, infusion of [Sar1-, Ala8]angiotensin II, an angiotensin II antagonist, did attenuate the indomethacin-induced increase in renal vascular resistance. After indomethacin, the vasoconstrictor response to norepinephrine was enhanced, whereas responses to nerve stimulation and angiotensin were unaffected. Although meclofenamate enhanced renal vascular resistance, its effects on vasoconstrictor responses were inconsistent. After indomethacin, the renal dilator response to bradykinin was enhanced; however, dilator responses to nitroglycerin were unaltered. The present data indicate that the increase in renal vascular resistance after indomethacin does not depend on the adrenergic system but may be dependent on the renin-angiotensin system. The inconsistent effect of the inhibitors of synthesis on renal constrictor responses to nerve stimulation suggests that endogenous prostaglandins do not serve to modulate the effects of the sympathetic nervous system on the feline renal vascular bed. These results also indicate that renal dilator responses to bradykninin are not mediated by prostaglandins in the cat.

Animals↗
PubMed1979

Vertical gradient in regional vascular resistance and pre to post capillary resistance ratios in the dog lung.

The ratios of pre-capillary (Ra) and post-capillary (Rv) resistances to total vascular resistance (RT) were measured at different vertical distances in the lungs of supine dogs. Capillary pressures were estimated as the algebraic sum of the alveolar absorption pressure for Tyrode's solution and the plasma colloid osmotic pressure. Segmental resistance fractions (Ra/RT, Rv/RT) were calculated using the pressure drops between arterial, capillary, and venous pressures at each vertical distance within the lung. In a second group of animals, total vascular resistance was calculated at each lung level using regional blood flow as measured by radiolabelled microspheres and the corresponding regional vascular pressures. The total vascular resistance was lowest in Zone III portions of the lung, but Ra/RT and Rv/RT were constant throughout this zone (n = 22) averaging .63 +/- .02 (SEM) and .37 +/- .02 (SEM, respectively, resulting in Ra/Rv of 1.70). Total vascular resistance increased markedly in Zone II portions of the lung, but the relative contribution of Ra/RT decreased from .62 +/- .07 (SEM) to .45 +/- .05 (SEM). Thus Ra/Rv decreased from 1.70 to .82 in Zone II. The absolute values of pre- and post-capillary resistances were lowest in Zone III but post-capillary resistance increased to a greater degree than pre-capillary resistance up Zone II.

Animals↗
PubMed1979

Renal vascular resistance and reactivity in the spontaneously hypertensive rat.

Renal vascular resistance is elevated in spontaneously hypertensive rats (SHR) when compared to normotensive control Wistar-Kyoto rats (WKY). The present study examined possible determinants of this raised vascular resistance in in situ autoperfused kidneys of pentobarbital-anesthetized, 12- to 16-wk-old SHR and WKY. Over a wide range of arterial pressures (30--100 mmHg) renal blood flow was consistently higher in WKY than in SHR. This relative flow difference was unchanged by acute renal denervation, with renal vascular resistance decreasing approximately 20% in both strains. Changes in renal vascular resistance to renal nerve stimulation and the administration of intra-arterial vasoactive hormones also were assessed. Vascular responses to renal nerve stimulation, tyramine, angiotensin II, and acetylcholine were similar in kidneys of the two strains, but reactivity to norepinephrine was significantly less in kidneys of SHR. It was concluded that elevated renal vascular resistance in the SHR does not result from an excessive neurogenic influence on the renal vasculature or from vascular hyperreactivity to norepinephrine or angiotensin II.

Acetylcholine↗
PubMed1979

Carotid and cardiopulmonary baroreceptor control of splanchnic and forearm vascular resistance during venous pooling in man.

1. This study evaluated the contribution of carotid and cardiopulmonary baroreceptors to reflex splanchnic and forearm vascular adjustments during venous pooling in man. We compared (a) responses to lower body suction which produces venous pooling with (b) responses to lower body suction plus simultaneous application of neck suction. The rationale was that simultaneous application of neck suction, which stretches carotid baroreceptors, would minimize the contribution of carotid baroreceptors to circulatory adjustments produced by lower body suction.2. Lower body suction at 40 mmHg decreased central venous pressure and arterial pulse pressure and increased forearm vascular resistance (plethysmography), splanchnic vascular resistance (indocyanine green dye clearance), and heart rate. Simultaneous application of neck suction prevented the tachycardia and most of the splanchnic vasoconstriction during lower body suction, but did not significantly attenuate the forearm vasoconstriction.3. The major findings in this study are first, that the splanchnic vasoconstrictor response during venous pooling is mediated primarily through carotid baroreceptors, and secondly, that carotid and cardiopulmonary baroreceptors produce strikingly contrasting and non-uniform regional vascular responses during venous pooling. Cardiopulmonary baroreceptors exert the predominant influence on forearm vascular resistance, but appear to have only a minor influence on splanchnic vascular resistance. Carotid baroreceptors produce most of the splanchnic vasoconstriction during venous pooling. but have a minor role in the forearm vasoconstriction.

Abdomen↗
PubMed1977

Cardiovascular correlates of attention in normal and psychiatrically disturbed children. Blood pressure, peripheral blood flow, and peripheral vascular resistance.

Blood pressure, peripheral blood flow, and peripheral vascular resistance were measured in normal adults and children and in children with autism and severe disturbances in personality development while the individuals were engaged in a variety of attentional tasks. The tasks were designed to elicit outward direction of attention (and intake of sensory input) or inward direction of attention (and relative rejection of external sensory input). During tasks involving sensory rejection, normal adults and normal children showed increased blood flow and decreased peripheral vascular resistance; with sensory intake, blood flow was decreased and resistance was increased. The most severely impaired children showed little alteration in their physiological response to task requirements. Autistic children had higher mean blood flow and lower peripheral vascular resistance than normal children and adults. Some autistic children characteristically may be in a state of sensory rejection associated with generally higher levels of arousal or defense against environmental bombardment.

Adolescent↗
PubMed1977

Effects of increased intracranial pressure on pulmonary vascular resistance of fetal and neonatal goats.

The effects of increased intracranial pressure on the pulmonary circulation were investigated in fetal and neonatal goats. Pulmonary vascular resistance and systemic arterial pressure increased with elevation of intracranial pressure in neonatal animals. Alpha-adrenergic blockade completely eliminated both of these responses. The response of the fetal pulmonary circulation was unlike that seen in the postnatal animal. Although there was a slight elevation of pulmonary vascular resistance initially, the predominant response was a decrease in resistance. The decrease in fetal pulmonary vascular resistance was unaffected by phenoxybenzamine, but reversed by propranolol. After the beta-adrenergic blockade, increased intracranial pressure produced an increase in pulmonary vascular resistance. Similarly, ventilation of fetal lungs resulted in an increase in pulmonary vascular resistance after increased intracranial pressure. These results demonstrate for the first time that pulmonary vascular resistance may be altered in fetal and neonatal animals by increasing intracranial pressure. The elevation of pulmonary vascular resistance after elevated intracranial pressure must be due to an active pulmonary vascular constriction.

Age Factors↗
PubMed1977

Reflex changes in hindlimb and renal vascular resistance in response to distention of the isolated pulmonary arteries of the dog.

We describe a preparation that uses a constant flow, right heart bypass for perfusion of an isolated pouch of the main pulmonary arteries at controlled pressures, and show that increments in pressure in the pulmonary arterial pouch are accompanied by increases in systemic vascular resistance and in hindlimb vascular resistance. These changes are demonstrated over the whole range of 5-120 cm H2O pressure in the pulmonary arterial pouch. In contrast there are no significant changes in renal vascular resistance or heart rate. We find that changing the temperature of the perfusate in the pulmonary arterial pouch from 37 degrees C to 30 degress C is associated with a decrease in systemic vascular resistance. Furthermore, the effects of raising the pulmonary arterial pouch pressure and of cooling are abolished by cervical vagotomy. These findings suggest that there is a tonic reflex vasoconstrictor tone generated by the activity of receptors lying in or close to the walls of the pulmonary artery. These findings also suggest that the differential effects on systemic vascular resistance and renal resistance may provide one mechanism by which changes in blood volume may lead to appropriate changes in renal solute excretion.

Animals↗
PubMed1979

The age factor in blood flow in the calf and in vascular resistance at rest and in reactive hyperaemia.

The blood flow and vascular resistance in the calf were studied in two groups of healthy subjects (mean ages 22 and 49 years) at rest and in reactive hyperaemia produced by five minutes' ischaemia of the lower limb. The blood flow was determined by venous occlusive plethysmography and vascular resistance was computed from the mean blood pressure measured by auscultation on the arm and from the blood flow in the calf, at rest and during reactive hyperaemia. The resting flow and blood flows throughout practically the whole time of hyperaemia were found to be significantly smaller in young individuals. The maximal flow was significantly lower, the maximal flow time was significantly prolonged in young subjects. The recovery time and repayment of the flow debt in the two groups were the same. Vascular resistance in the calf was significantly greater in young subjects, both at rest and during dilatation. We assume from the results that the capacity of the arterial system in the lower limbs is significantly smaller in young individuals.

Adolescent↗
PubMed1978

Effects of beta-adrenergic blocking agents on peripheral vascular resistance.

The effects of the beta-adrenergic blocking agents propranolol, pindolol, atenolol, bunitrolol, and methypranol on the vascular resistance of isolated perfused hindlimbs of rats were investigated. At concentrations of 0.01 microgram/ml in the perfusate dl-propranolol and pindolol significantly increased vascular resistance by blockade of beta2-receptor mediated vasodilatation, whereas atenolol, bunitrolol and methypranol had no effect on peripheral resistance at this concentration. With increasing concentrations up to 10 microgram/ml all drugs, with the exception of atenolol, caused vasodilatation. We conclude that the specificity of beta-blocking agents can be established in the isolated perfused hindlimb vasculature of rats through its effect on vascular resistance. The lack of inhibition of vascular beta2-receptors at low concentrations of atenolol and also bunitrolol and methypranol show relative selectivity for beta1-receptors. The differential effects of beta-adrenergic agents on vascular resistance may have significance for the clinical use of the drugs.

Adrenergic beta-Antagonists↗
PubMed1975

Effects of alveolar and perfusion hypoxia and hypercapnia on pulmonary vascular resistance in the lamb.

The effects of ventilatory hypoxia and hypercapnia and perfusion hypoxia and hypercapnia on pulmonary vascular resistance were studied in the intact lamb using right heart techniques to isolate and perfuse the left lower lobe. Ventilatory hypoxia increased vascular resistance in the left lower lobe by constricting predominantly vessels upstream from small lobar veins, presumably small arteries. The response to hypoxia was not blocked by phentolamine and diphenhydramine in doses that markedly decreased pressor responses to norepinephrine and histamine in the lung. Perfusion hypoxia did not alter vascular resistance in the perfused lobe. Ventilatory hypercapnia increased vascular resistance in the lung by constricting mainly upstream vessels, whereas perfusion hypercapnia decreased resistance by dilating upstream vessels. These data indicate that histamine and catecholamines are not involved in the response to alveolar hypoxia. These results suggest that the sensor site for ventilatory hypoxia is close to the alveolus since the response is unrelated to lobar arterial Po2. It is concluded that systemic reflexes are not necessarily involved in the response of the pulmonary vascular bed to ventilatory hypoxia or hypercapnia and that the magnitude and rapidity of this response suggest that it may represent an important local mechanism for the control of ventilation-perfusion relationships in this species.

Animals↗
PubMed1976

Comparison of alpha-MSH and several vasoactive substances on vascular resistance in the feline mesenteric vascular bed.

The effects of alpha-MSH and several other vasoactive substances on the mesenteric vascular bed were studied in the anesthetized cat under conditions of controlled blood flow. Intra-arterial injections of alpha-MSH in doses of 10, 30, and 100 mug resulted in significant dose-related decreases in mesenteric arterial perfusion pressure but little or no effect on systemic arterial pressure. The vasodilator response to alpha-MSH was breif in duration and resistance to flow was decreased 10, 18, and 26 percent at 10, 30, and 100 mug. These significant changes after alpha-MSH were of a much smaller magnitude than were observed after prostaglandins E1 and E2, isoproterenol, bradykinin or glyceryl trinitrate and differed completely from the increased resistance after angiotensin II and norepinephrine.

Angiotensin II↗
PubMed1979

Contribution of prostaglandins to the regulation of pulmonary vascular resistance in adult cats and dogs.

In order to determine the role of prostaglandins in the regulation of pulmonary vascular resistance, we investigated effects of prostaglandin cyclo-oxygenase inhibition by indomethacin (2 mg/kg), meclofenamate (2 mg/kg), and aspirin (40 mg/kg) upon canine and feline pulmonary vasoconstriction caused by two stimuli: acute hypoxia (6% O2) and exogenous PGF2 alpha. Measurements were made utilizing an open chest, pump-perfused, in situ lung preparation. Cat pulmonary vasculatures were more responsive to hypoxia and PGF2 alpha than were dog's. In dogs, indomethacin, meclofenamate, and aspirin all increased pulmonary vascular resistance and augmented pulmonary vasoconstrictor responses to hypoxia and PGF2 alpha. Neither indomethacin, meclofenamate, nor aspirin affected baseline pulmonary vascular resistance of cats. Aspirin and indomethacin augmented pulmonary vasoconstriction in the cat. Meclofenamate was without effect. Further, although aspirin and indomethacin strongly inhibited pulmonary vascular pressor responses to exogenous arachidonic acid, meclofenamate decreased pulmonary responses to arachidonic acid very little. All three inhibitors nearly abolished systemic responses to arachidonic acid in the cat. Exogenous PGI2 infusion decreased pulmonary vascular resistance in the cat. Prostaglandin cyclo-oxygenase activity produces a vasodilator influence, probably PGI2, in the canine pulmonary vasculature that may be significant in protecting the animal from pulmonary hypertension and its consequences. The role of the prostaglandin system in the feline pulmonary vasculature appears to be qualitatively similar, but quantitatively less, than in the dog.

Animals↗
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↗
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↗
PubMed1979

Humoral regulation of vascular resistance after 30 days of pulmonary artery constriction.

In an earlier study of guinea pigs with constriction of the pulmonary artery (PA) for 30 days, hindquarters' vascular resistance was maintained primarily by humoral mechanisms. In the present study, we investigated the contribution of circulating catecholamines, angiotensin II, and other constrictor stimuli to hindquarters' vascular resistance by observing vasodilator responses to specific competitive antagonists. Pressure-flow curves indicated vascular resistances in isolated, perfused, sympathectomized hindquarters of anesthetized guinea pigs. Phentolamine produced significantly greater (P less than 0.05) vasodilatation in animals with constriction of pulmonary artery than in sham animals [Sar1-Ala8]angiotensin II produced no vasodilation in either group. After alpha-adrenergic blockade, papaverine produced similar vasodilatation and similar final perfusion pressures in both groups. It appears that circulating catecholamines and augmented vasoconstrictor responsiveness to norepinephrine are totally responsible for the increased humoral regulation of vascular resistance in this experimental model of right ventricular hypertrophy.

Angiotensin II↗
PubMed1977

Coronary vascular resistance during halothane anesthesia.

To study the effect of halothane on the coronary circulation, the circumflex diastolic coronary vascular resistance was measured in the working heart and total mean coronary resistance (TCR) in the isolated nonworking heart of the dog during administration of 100 per cent oxygen and during administration of 2--3 per cent halothane in oxygen. In the working heart, when the diastolic aortic pressure was kept at a nearly control level, halothane induced decreases of 12 per cent in circumflex diastolic coronary vascular resistance and 18 per cent in left ventricular arteriovenous oxygen content difference and no significant change in diastolic coronary blood flow. This effect occurred in spite of the absence of any significant change of myocardial oxygen consumption. In the nonworking beating, arrested or fibrillating heart, halothane induced a decrease of 24 per cent in total mean coronary resistance. Since the decrease in circumflex diastolic coronary vascular resistance in the working heart connot be attributed to myocardial hypoxia and since the results in the isolated nonworking heart eliminate the influences of mechanical and neurohumoral factors on coronary resistance, it is concluded that the observed decrease in resistance is probably due to vasodilation produced by a direct action of halothane on the coronary vessels. This effect was not modified by beta-adrenergic blockade.

Animals↗