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Biomedical subjects

S F Vatner

Publications and source records attributed to S F Vatner.

At least 217 records · Page 12Linked to original sources
PubMed1981

Interaction of carotid chemoreceptor and pulmonary inflation reflexes in circulatory regulation in conscious dogs.

The interaction of carotid chemoreceptor and pulmonary inflation reflex control of peripheral and coronary vasoactivity and myocardial contractility was examined in conscious dogs. Stimulation of carotid chemoreceptors resulted in an increase in rate and depth of respiration, an increase in myocardial contractility, and more intense vasoconstriction in the iliac than in the mesenteric, renal, or cerebral beds. The coronary bed responded primarily with vasodilation. The increase in rate and depth of respiration stimulated pulmonary inflation reflexes, which in turn were partially responsible for the coronary vasodilation, but also attenuated the positive inotropic response and even reversed the initial peripheral vasoconstriction to a period of significant vasodilation.

Blood Pressure↗
PubMed1980

Sympathetic regulation of the cerebral circulation by the carotid chemoreceptor reflex.

The effects of carotid chemoreceptor reflex stimulation (intracarotid injection of nicotine 0.2 microgram/kg) were examined in conscious dogs on the cerebral circulation, using the radioactive microsphere technique to measure cerebral blood flow. In intact dogs (n = 18) with ventilation controlled, carotid chemoreceptor reflex stimulation increased (P less than 0.01) mean arterial pressure by 36 +/- 5% (SE) and calculated cerebral vascular resistance by 58 +/- 13%, whereas cerebral blood flow fell by 7 +/- 6% (NS). After bilateral cervical sympathectomy (n = 9), carotid chemoreceptor reflex stimulation induced significantly different (P less than 0.01) effects on cerebral blood flow, which rose by 42 +/- 8%, and cerebral vascular resistance, which did not change. To determine whether the difference in effect was due to the sympathectomy or merely to the repetition of the stimulus, another group of dogs (sham; n = 6) that had intact sympathetic nerves were studied a second time. In "sham" dogs, the repeat response to carotid chemoreceptor stimulation also induced significantly different effects from those in dogs with sympathectomy. After general anesthesia with sodium pentobarbital, or after section of the ipsilateral carotid sinus nerve, carotid chemoreceptor stimulation with nicotine, 0.2 microgram/kg, failed to induce a detectable hemodynamic effect. Thus, in the conscious dog, stimulation of the carotid chemoreceptor reflex elicits significant sympathetically mediated vasoconstriction in cerebral vessels.

Animals↗
PubMed1980

Correlation between acute reductions in myocardial blood flow and function in conscious dogs.

Decreases in regional endocardial function (ultrasonic dimension technique) and blood flow (radioactive microsphere technique) were correlated in 14 conscious dogs with acute graded levels of coronary stenosis. Coronary stenosis affected overall ventricular function only slightly, but induced gradual reductions in regional blood flow (BF) and segment length (SL) shortening in the ischemic zone. The relationship was best fit by an exponential function relating % change in SL to % change in BF; i.e., SL(% delta) = -161.6 e -0.047BF(% delta) (r = 0.92). In 14 segments, where no change in function was observed, blood flow fell by 6 +/- 1%. However, 10--20% reductions of blood flow impaired function significantly. Severe reduction of blood flow was required to reduce function completely. In 12 segments exhibiting paradoxical motion, blood flow fell by 95 +/- 2%, a value greater (P < 0.01) than in four akinetic segments, i.e., those with no shortening or lengthening (-82 +/- 4%). These data, which show on one hand that only 10-20% reductions in blood flow impair function significantly and that, on the other hand, severe reductions in blood flow are required to abolish active shortening completely, indicate sensitive coupling between blood flow and function in the conscious dog with acute myocardial ischemia.

Animals↗
PubMed1980

Alpha adrenergic vasoconstriction and nitroglycerin vasodilation of large coronary arteries in the conscious dog.

The effects of methoxamine and nitroglycerin on measurements of large vessel (left circumflex) coronary dimensions were examined in eight conscious dogs using an ultrasonic dimension gauge, and total coronary resistance was calculated from measurements of arterial pressure and coronary blood flow. Methoxamine (50 mug/kg per min), after transiently increasing left circumflex coronary dimensions, induced sustained reductions in left circumflex diameter (9+/-2%) and external (18+/-4%) and internal (27+/-5%) cross-sectional areas, at a time when mean arterial pressure rose by 65+/-5%, left ventricular dP/dt had decreased only slightly, and heart rate and mean coronary blood flow remained at control levels. Calculated large vessel and total coronary resistances rose similarly, i.e., by 108+/-29 and 92+/-14%, respectively. Methoxamine reduced coronary arterial wall stiffness from control at comparable stress levels, although at any common radius, wall stiffness was augmented substantially. Nitroglycerin (25 mug/kg) induced an initial decrease in coronary dimensions along with the fall in arterial pressure. However, left circumflex coronary dimensions then rose, reaching a maximum 5 min later at a time when left circumflex coronary blood flow was reduced and heart rate and left ventricular dP/dt were at control levels. At this time, significantly different effects were observed on large vessel coronary resistance, which fell by 18+/-2%, and on total coronary resistance, which rose by 11+/-4%. Thus, in the conscious dog, large coronary vessels not only react passively to changes in aortic pressure but also undergo substantial active changes. Alpha adrenergic stimulation is sufficiently powerful to reduce cross-sectional area, despite the opposing elevation of distending pressure.

Animals↗
PubMed1980

Cardio-selective beta adrenergic stimulation with prenalterol in the conscious dog.

The effects of cardioselective beta-1 adrenergic agonist, 1-(4-hydroxyphenoxy)-isopropylamino-2-propanol), i.e., prenalterol, were examined on direct and continuous measurements of left ventricular (LV) pressure, diameter, dP/dt, velocity of shortening, arterial pressure, iliac blood flow and heart rate in 10 conscious dogs. Prenalterol was infused on 3 separate days in doses of 1, 2 and 4 micrograms/kg/min for 15 min. The largest dose of the drug increased LV/dP/dt by 70 +/- 7% from 3581 +/- 130, velocity of LV shortening by 27 +/- 4% from 86 +/- 7 mm/sec, heart rate by 51 +/- 9% from 80 +/- 5 beats/min and iliac blood flow by 40 +/- 4% from 134 +/- 15 ml/min and decreased LV end-diastolic diameter by 8 +/- 2% from 35 +/- 2 mm and LV end-systolic diameter by 15 +/- 2% from 24 +/- 2 mm. All these responses were significant, P < .01. Mean arterial pressure did not change. The positive inotropic effects persisted for 1 hr. The lowest dose of the drug studied increased LV dP/dt and velocity but not heart rate. Practolol, a beta-1 adrenergic receptor blocker, prevented the positive inotropic effects and the increases in iliac blood flow indicating that prenalterol exerts its cardiovascular actions primarily by stimulation of beta-1 adrenergic receptors.

Adrenergic beta-Agonists↗
PubMed1979

Depressed responsiveness of the carotid sinus reflex in conscious newborn animals.

The responsiveness of the carotid sinus reflex was evaluated by comparing the effects of bilateral carotid occlusion (BCO) in conscious adult dogs and puppies on measurements of arterial pressure, cardiac output, heart rate, and calculations of total peripheral resistance (TPR). In eight adult dogs, BCO increased mean arterial pressure by 57 +/- 6%, TPR by 48 +/- 5%, and heart rate by 45 +/- 15%. In puppies, BCO induced smaller increases (P less than 0.05) in mean arterial pressure (30 +/- 5%) and TPR (29 +/- 4%), while heart rate did not change. After elimination of opposing vagal and aortic baroreceptor reflexes, the differences in responses to BCO of mean arterial pressure and TPR between adults and newborns were even greater. Thus, the carotid baroreceptor reflex appears to be depressed in the newborn when compared with the fully developed reflex in the normal, conscious adult.

Animals↗
PubMed1979

Depressed responsiveness to vasoconstrictor and dilator agents and baroreflex sensitivity in conscious, newborn lambs.

The effects of vasoconstrictors and vasodilators were compared in conscious, newborn lambs and adult sheep instrumented with electromagnetic flow probes on the ascending aorta and catheters in the thoracic aorta. Methoxamine, angiotensin II, norepinephrine, nitroglycerin and isoproterenol were administered intravenously to evaluate their effects on arterial pressure, cardiac output and systemic vascular resistance (SVR). The difference in response between adults and newborns was most apparent with methoxamine. Methoxamine, 400 micrograms/kg, i.v., which increased mean arterial pressure by 57 +/- 6% and SVR by 278 +/- 27% in newborn lambs, caused greater increases (p less than 0.01) of 81 +/- 8% and 1418 +/- 141%, respectively, in the adults. Responses also differed significantly between newborn and adult animals to norepinephrine, angiotensin II, nitroglycerin and isoproterenol. In a second group of animals in which smaller amounts of methoxamine and isoproterenol were injected directly into the terminal aorta, changes in terminal aortic flow and resistance were examined. Again, both vasoconstrictor and vasodilator responses were more marked in adults than in newborns. Finally, the sensitivity of the arterial baroreceptor reflex was evaluated by comparing the regression of pulse interval (PI) on systolic arterial pressure (SAP) after an intravenous dose of methoxamine in conscious, adult and newborn animals. The PI/SAP slopes in adult sheep, 45.4 +/- 3.5 msec/mm Hg, were significantly greater (p less than 0.01) than in newborn lambs, 11.7 +/- 2.2 msec/mm Hg.

Angiotensin II↗
PubMed1979

Prostaglandin control of the renal circulation in response to hypoxemia in the fetal lamb in utero.

We studied the effects of 10-minute periods of hypoxemia in unanesthetized fetal lambs in utero instrumented for measurements of arterial pressure and renal and iliac blood flows. Fetal hypoxemia, induced by delivering a hypoxic gas mixture to the ewe, was characterized by a reduction in fetal PaO2 from 20.1 +/- 1.4 to 8.8 +/- 1.0 mm Hg (mean +/- SE). The fetus responded with bradycardia and persistent vasoconstriction in the iliac bed throughout the 10-minute period. In contrast, renal resistance rose significantly only at the end of the hypoxemic period. After 5-7 minutes of hypoxemia, when iliac flow had fallen by 40 +/- 4% and iliac resistance had risen by 86 +/- 13%, renal flow and resistance were not changed significantly from control; in fact, we found that renal flow rose substantially at this time in several fetal lambs. After blockade of prostaglandin synthesis with either indomethacin or meclofenamate, renal flow fell after 5-7 minutes of hypoxemia by 36 +/- 5%. The reduction in renal flow and increases in renal resistance were significantly greater than was observed prior to blockade of prostaglandin synthesis. Thus, fetal hypoxemia elicits bradycardia and intense peripheral vasoconstriction reflected by the changes in the iliac bed, with relative sparing of the reanl bed. The relative protection of the renal bed during fetal hypoxemia appears to be related to a mechanism involving prostaglandins, since after blockade of prostaglandin synthesis, hypoxemia results in intense renal vasoconstriction.

Animals↗
PubMed1979

Effects of exerimental right ventricular hypertrophy on myocardial blood flow in conscious dogs.

The effects of right ventricular hypertrophy on the overall and regional distribution of myocardial blood flow in the absence of an elevated coronary arterial driving pressure were evaluated in 18 concscious dogs subjected to a chronic pressure overload of the right ventricle induced by pulmonary artery constriction. The sustained pressure overload for duration of 4--6 wk or 4--5 mo resulted in significant increases in right ventricular mass (45 and 110%, respectively) and right ventricular fiber diameter (22 and 60%, respectively). Moreover, the presence of moderate and severe hypertrophy was associated with marked increases in transmural blood flow per gram to the right ventricle proportional to the observed increases in mass, i.e., of 36 and 109%, respectively, from a normal value of 0.67 +/- 0.04 ml/min per g, whereas left ventricular blood flow remained unaltered from a normal value of 1.00 +/- 0.06 ml/min per g. Despite the large increase in blood flow per gram to moderately and severely hypertrophied right ventricle, no significant changes in the ratio of capillary:muscle fiber number were observe. These data suggest that the development of right ventricular hypertroph is characterized by a sustained compensatory response of the coronary circulation to the augmented work load and mass, and that is not associated with a proliferative response of the vasculature supplying the enlarged ventricle.

Animals↗