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Biomedical subjects

S F Vatner

Publications and source records attributed to S F Vatner.

At least 235 records · Page 13Linked to original sources
PubMed1978

Effects of nitroglycerin on cardiac function and regional blood flow distribution in conscious dogs.

The effects of intravenous infusion of nitroglycerin (NTG), 8 and 32 microgram/kg.min for 7 min, and of sublingual NTG, 1.2 mg, were examined on direct and continuous measurements of systemic, coronary, and regional hemodynamics, left ventricular (LV) dimensions, pressures, and myocardial contractility in conscious dogs. NTG induced sustained reductions in LV dimensions and transient increases in heart rate and dP/dt, and decreases in mean arterial pressure. Initially NTG increased cardiac output and flows to the coronary, mesenteric, renal, and iliac beds, while systemic and regional vascular resistances fell. Later, cardiac output, cardiac work, and mesenteric and iliac flows fell significantly below control, and significant vasoconstriction in the systemic as well as mesenteric, iliac, and coronary beds was observed at a time when LV end-diastolic dimensions were still significantly reduced. Peripheral vasoconstriction was not observed with systemic NTG in deafferented dogs or when NTG, 1 microgram/kg.min, was infused intra-arterially into the iliac bed. Thus, systemic NTG induces a biphasic response consisting of initial arteriolar vasodilation followed by vasoconstriction in the mesenteric, iliac, coronary and systemic beds, which is presumably due to longer lasting effects on preload and to secondary reflex responses to the drug.

Administration, Oral↗
PubMed1978

Extent of utilization of the Frank-Starling mechanism in conscious dogs.

The extent to which an increase in preload increases left ventricular (LV) end-diastolic (ED) diameter (D) was studied in seven conscious dogs instrumented with ultrasonic D transducers and miniature LV pressure (P) gauges. Preload was elevated by three techniques: 1) volume loading with saline infusion, 2) induction of global myocardial ischemia by constricting the left main coronary artery, and 3) infusion of methoxamine. These three interventions increased LVEDP to over 30 mmHg from a control of 10 +/- 1 mmHg. With volume loading, LVEDD rose by only 1.55 +/- 0.39 mm from a control of 44.08 +/- 1.08 mm; with ischemia LVEDD rose by only .96 +/- .29 mm from a control of 42.55 +/- 2.18 mm, while with methoxamine LVEDD rose by only 1.34 +/- 0.38 mm from a control of 43.89 +/- 2.07 mm. In contrast, in the open-chest, anesthetized dog, LVEDD was greatly reduced and volume expansion resulted in a profound increase in LVEDD. Thus, the Frank-Starling mechanism is not an important controlling mechanism in the normal, reclining, conscious animal, since LVEDD appears to be near maximal at rest and does not increase substantially despite striking increases in LVEDP.

Animals↗
PubMed1978

Depression of regional blood flow and wall thickening after brief coronary occlusions.

The effects of a 15-min coronary occlusion and subsequent reperfusion were investigated in conscious dogs previously instrumented for measurement of left ventricular pressure, dP/dt, regional wall thickening, electrograms, and myocardial blood flow. Coronary occlussion reduced overall left ventricular function only slightly but eliminated systolic wall thickening in the ischemic zone and reduced regional myocardial blood flow in the ischemic zone from 1.04 +/- 0.04 to 0.27 +/- 0.02 ml/min per g and the endo/epi flow ratio from 1.23 +/- 0.04 to 0.44 +/- 0.04, while S-T segment elevation increased from 1.1 +/- 0.3 to 8.2 +/- 0.9 mV. After release of the occlusion, S-T segment elevation disappeared within 1 min while reactive hyperemia in the previously occluded artery and a transient increase in cardiac diastolic wall thickness occurred and then subsided by 15 min. In contrast, systolic wall thickening and the endo/epi flow ratio remained significantly depressed for more than 3 h. Thus reperfusion after a 15 minute coronary occlusion results in a prolonged period of reduced regional myocardial blood flow, particularly in the endocardial layers, which correlates with the prolonged depression of regional myocardial shortening and wall thickening.

Animals↗
PubMed1978

Measurement of multiple simultaneous small dimensions and study of arterial pressure-dimension relations in conscious animals.

This paper describes the development of several important modifications that were incorporated into the ultrasonic, transit-time dimension system in order to obtain multiple simultaneous, instantaneous, and continuous measurements of the external dimensions of the aorta and its major branches in conscious, unrestrained animals. At operation a pair of small piezoelectric crystals was sutured to arterial adventitia, and a miniature pressure gauge was implanted in the vessel at the same cross-sectional plane. After recovery from surgery, wall motion was not altered appreciably and scarring was minimal. This technique allows long-term monitoring of aortic pressure-dimension relations and is applicable for small (fetal and neonatal) as well as large (adult dogs and sheep) animals. When vessel wall thickness is measured, stress-radius analysis can be performed so as to compute vascular elastic stiffness as a function of stress. Moreover, the suitability for radiotelemetry of the pressure and dimension signals measured with this technique enables the study of these parameters in unrestrained animals, e.g., during spontaneous severe exercise.

Angiotensins↗
PubMed1978

Hemodynamic effects of intravenous sodium nitroprusside in the conscious dog.

The hemodynamic effects of 7 min i.v. sodium nitroprusside (NP) were studied in conscious dogs previously instrumented for measurement of arterial pressure, cardiac output, regional blood flow distribution, left ventricular (LV) pressure, and internal dimensions. Nitroprusside, 25 microgram/kg/min, reduced mean arterial pressure by 23 +/- 3%. Cardiac output increased initially by 39 +/- 7% and returned toward control by the end of the infusion. Regional blood flows increased initially; the relative rise was greatest in the coronary (+ 225 +/- 39%), intermediate in the mesenteric (+ 98 +/- 23%) and iliac (+ 38 +/- 6%), and least in the renal (+ 10 +/- 3%) bed. By the end of the infusion period the vasodilation was unchanged in the iliac bed, less intense in the coronary and mesenteric, while in the iliac bed, blood flow was reduced and resistance was actually increased by 33 +/- 11% above control. A generalized vasonconstriction ensued after cessation of infusion. In contrast, when the drug was administered intra-arterially to the iliac bed, arterial pressure did not fall and only iliac vasodilation was observed. Peak cardiac effects were characterized by increases in heart rate and LV dP/dt, along with marked reduction in LV end-systolic diameter (- 13 +/- 2%), and in end-diastolic diameter (-17 +/- 2%) and pressure. LV end-diastolic diameter fell even heart rate was maintained at a constant rate by pacing. Thus, in the conscious dog, NP reduced LV dimensions substantially, while inducing changes in peripheral beds. The differences in these effects depend on interactions between the direct effects of NP and the opposing effects of reflex adjustments which appear sufficiently powerful to result in net constriction of the iliac bed late during the infusion.

Animals↗
PubMed1978

Effects of a cardiac glycoside in combination with propranolol on the ischemic heart of conscious dogs.

The effects of coronary occlusion and of subsequent propranolol and ouabain administration were examined in 12 conscious dogs. Overall left ventricular (LV) function was assessed by measurement of LV pressure and dP/dt, and regional myocardial function was assessed by measurements of segment length (SL), velocity of SL shortening and regional myocardial "work," i.e., pressure-length loops in normal and moderately and severely ischemic zones. Regional intramyocardial electrograms were measured at the same sites as function along with regional myocardial blood flow as determined by the radioactive microsphere technique. Coronary occlusion resulted in graded loss of function from the normal to severely ischemic zones, along with graded flow reductions and graded elevation of the ST segment. Propranolol, 1 mg/kg, depressed overall LV function and function in the normal zone more than in ischemic zones. Propranolol reduced flow to the normal zone and increased flow to ischemic zones, while not affecting ST-segment elevation significantly. In the presence of occlusion and propranolol, ouabain, 20 microgram/kg, improved overall LV function as well as regional function in the normal, moderately ischemic and severely ischemic zones. In addition, ouabain reduced ST elevation and increased blood flow further in moderately and severely ischemic zones. Most strikingly, ouabain returned normal systolic shortening to eight severely ischemic segments which were previously akinetic.

Animals↗
PubMed1978

Initial myocardial adjustments to brief periods of ischemia and reperfusion in the conscious dog.

The changes in left ventricular (LV) dynamics induced by brief periods of ischemia (100 seconds) and subsequent reperfusion were analyzed in conscious dogs. Global LV ischemia, induced by partially occluding the left main coronary artery, reduced LV flow homogeneously and impaired LV function as reflected by decreases in LV stroke "work" (89 +/- 4% M +/- SE), systolic shortening (72 +/- 4%), velocity of shortening (56 +/- 6%), LV systolic pressure (34 +/- 5%), and dP/dt (59 +/- 6%). Regional LV ischemia, induced by occluding either the left circumflex or anterior descending coronary artery completely, reduced flow to the ischemic segment (82 +/- 3%) while decreasing segment work (96 +/- 5%), shortening (82 +/- 3%), and velocity of shortening (70 +/- 5%), with minimal depression of overall LV function. In both groups the extent of shortening was reduced more rapidly and greater (P less than 0.01) than shortening velocity. Moreover, with localized ischemia, segment work was reduced more (P less than 0.01) than shortening. With reperfusion, a transient overshoot in function above preischemic control levels was observed in both groups (global work increased by 60 +/- 12% and regional work by 28 +/- 4% above control). This overshoot was not dependent on adrenergic mechanisms, but was prevented by inhibiting reactive hyperemia. Thus myocardial ischemia induces a dissociation between extent and rate of myocardial shortening. A further dissociation between shortening and work is apparent with regional ischemia. After reperfusion there is a transient overshoot in function which appears to be dependent upon the associated reactive hyperemia.

Animals↗
PubMed1978

Effects of a cardiac glycoside on regional function, blood flow, and electrograms in conscious dogs with myocardial ischemia.

We studied the effects of coronary occlusion and of subsequent ouabain administration on regional myocardial function, flow, and electrograms in 14 conscious dogs. Coronary occlusion resulted in a graded loss of regional function as reflected by measurements of segment length (SL), velocity of SL shortening and myocardial "work" from the normal to severely ischemic zones, along with graded flow (radioactive microsphere technique) reductions and graded elevation of the regional S-T segment. Ouabain, 20 microgram/kg, improved function in the normal zone, in which stroke shortening rose by 0.23 +/- 0.07 mm (mean +/- SE) and "work" rose by 30.2 +/- 9.5 mm Hg-mm. In moderately ischemic segments, stroke shortening rose by 0.60 +/- 0.05 mm and "work" rose by 58.1 +/- 6.1 mm Hg-mm. In the majority of severely ischemic segments, stroke shortening and "work" also increased; the average effect in all severely ischemic segments was an increase in stroke shortening of 0.35 +/- 0.10 mm and in "work" of 31.5 +/- 9.9 mm Hg-mm. In addition, ouabain reduced S-T elevation by 0.90 +/- 0.20 mV in moderately ischemic zones and by 3.14 +/- 0.35 mV in severely ischemic zones, and increased flow by 28 +/- 6% and 46 +/- 9% in moderately and severely ischemic zones, respectively. All these changes were significant, P less than 0.01. Thus, ouabain caused an improvement in perfusion of ischemic tissue, which was associated with significant enhancement of stroke shortening and "work." Most strikingly, ouabain returned normal systolic shortening to 10 severely ischemic segments which previously were akinetic.

Animals↗
PubMed1978

Effects of coronary artery reperfusion on myocardial infarct size calculated from creatine kinase.

The effects of coronary artery reperfusion at 1 and 3 h after occlusion on infarct size (IS) in the conscious dog were compared with a second group of dogs that were not reperfused (24 h occlusion). Infarct size was calculated from creatine kinase (CK) appearing in blood samples (IS(s)) and myocardial CK depletion (IS(m)), and determined from gross and histological inspection of the pathological tissue (IS(p)). Under both conditions, IS(m) correlated well with IS(p). In dogs with 24-h coronary occlusions, IS(s) correlated well with IS(m) (IS(s) = 14.26 + 1.18 x IS(m), r = 0.92). In reperfused dogs, the relationship remained linear but was altered (IS(s) = 15.33 + 2.07 x IS(m), r = 0.89). The slope was significantly greater, P <0.05, than that observed for dogs that were not reperfused, suggesting that more CK appeared in serum per gram of infarct. Similarly, significantly different relationships were observed in the reperfused and nonreperfused dogs, when IS(s) was compared with IS(p). Moreover, the configuration of the serial blood CK curve was changed significantly by reperfusion. In dogs with a 24-h occlusion, CK rose gradually to a peak at 11.4+/-0.5 h. In dogs reperfused at 3 h, CK rose sharply at 3 h and reached a peak at 6.8+/-0.5 h, significantly earlier (P <0.01) than occurred in dogs reperfused at 1 h, i.e., when the peak occurred at 4.2+/-0.4 h. The rapid appearance of CK in blood after reperfusion at 1 and 3 h suggested a washout phenomena. Thus, reperfusion alters the shape of the serial blood CK curve and results in a different linear relationship between calculated and measured infarct size, resulting in greater recovery of CK in blood per unit of infarcted myocardium.

Animals↗
PubMed1978

Control of the myocardial contractile state by carotid chemo- and baroreceptor and pulmonary inflation reflexes in conscious dogs.

The effects of carotid chemoreceptor stimulation with intracarotid injections of either nicotine, 0.2 mug/kg, or cyanide, 2 mug/kg, were compared with the effects of bilateral carotid occlusion on left ventricular (LV) pressure, dP/dt, and diameter in conscious dogs instrumented with ultrasonic diameter gauges and miniature pressure gauges. With heart rate maintained constant, carotid chemoreceptor stimulation increased mean arterial pressure by 27+/-3%, LV and diastolic diameter by 4+/-0.9% and LV dP/dt by 21+/-2%. With ventilation controlled during succinylcholine infusion, carotid chemoreceptor stimulation increased mean arterial pressure by 43+/-2% and dP/dt by 37+/-5%, values significantly greater, P < 0.01, than were observed in dogs with spontaneous ventilation. Similarly, in dogs with spontaneous ventilation after vagotomy, carotid chemoreceptor stimulation also increased dP/dt by a greater amount, i.e., by 48+/-9%. The increases in LV end diastolic diameter were not affected significantly by either cholinergic blockade with atropine or beta adrenergic blockade with propranolol. Although cholinergic blockade did not affect the inotropic or pressor responses significantly, beta adrenergic blockade attenuated the pressor response and essentially abolished the inotropic response. Bilateral carotid occlusion increased mean arterial pressure and LV end diastolic diameter by similar amounts to those observed with chemoreceptor stimulation, but increased dP/dt significantly less, P < 0.02, i.e., by 13+/-2%. As was observed with chemoreceptor stimulation, inotropic responses were not affected significantly by cholinergic blockade, but were essentially abolished by beta adrenergic blockade. Thus, in the conscious dog with heart rate constant, carotid chemoreceptor stimulation induces a clear positive inotropic effect, which is greater in the absence of the attenuating influences of pulmonary inflation reflexes, and for an equal elevation in arterial pressure appears to exert a greater increase in myocardial contractility than does carotid baro-receptor unloading.

Animals↗
PubMed1978

Effects of anesthesia on cardiovascular control mechanisms.

The manner in which general anesthesia affects circulatory control was studied by examining the effects of commonly employed anesthetics on left ventricular function and distribution of cardiac output, and the extent to which responses to physiological and pharmacological stimuli are modified by general anesthesia. While commonly employed anesthetics affect almost every aspect of the circulatory system, the importance of general anesthesia on the circulation tends to be underestimated by considering only its direct effects. More important is the modification of the organism's integrative response to any perturbation. Major differences often directionally opposite, in responses of conscious and anesthetized animals were found for reflex control of the circulation, effects of hemorrhage and alterations in preload and after load. In addition, commonly employed pharmacologic agents, e.g., cardiac glycosdies, catecholamines, and morphine sulfate exerted differing actions in the conscious and anesthetized states. Thus, while it is generally held that the overall responses to complex physiological functions such as exercise or eating can be best described in the intact, conscious organism, the importance of conducting any experiment involving integrative control of the circulation in the conscious organism should also be recognized.

Anesthesia, General↗