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Biomedical subjects

S F Vatner

Publications and source records attributed to S F Vatner.

At least 271 records · Page 15Linked to original sources
PubMed1974

Effects of dobutamine on left ventricular performance, coronary dynamics, and distribution of cardiac output in conscious dogs.

The effects of dobutamine ([+/-]-4-[2-[[3-(p-hydroxyphenyl)-1-methyl propyl] amino] ethyl] pyrocatechol hydrochloride), a new synthetic cardioactive sympathomimetic amine, were examined on direct and continuous measurements of left ventricular (LV) diameter (D), pressures (P), velocity of shortening (V), dP/dt, dP/dt/P, arterial pressure, cardiac output, and regional blood flows in the left circumflex coronary, mesenteric, renal, and iliac beds in healthy, conscious dogs. At the highest dose of dobutamine examined, 40 mug/kg/min, the drug increased dP/dt/P from 65+/-3 to 128+/-4 s(-1) and isolength velocity from 72+/-4 to 120+/-7 mm/s without affecting LV end diastolic D significantly. Mean arterial P rose from 92+/-2 to 104+/-3 mm Hg and heart rate from 78+/-3 to 111+/-7 beats/min, while LV end systolic D fell from 24.1+/-1.4 to 19.9+/-1.8 mm, reflecting a rise in stroke volume from 30+/-4 to 42+/-3 ml. Cardiac output rose from 2.41+/-0.23 to 4.35+/-0.28 liter/min, while calculated total peripheral resistance declined from 0.042+/-0.005 to 0.028+/-0.003 mm Hg/ml/min. The greatest increases in flow and decreases in calculated resistance occurred in the iliac and coronary beds, and the least occurred in the renal bed. Propranolol blocked the inotropic and beta(2) dilator responses while vasoconstricting effects mediated by alpha adrenergic stimulation remained in each of the beds studied. When dobutamine was infused after a combination of practolol and phentolamine, dilatation occurred in each of the beds studied. These observations indicate that dobutamine is a potent positive inotropic agent with relatively slight effects on preload, afterload, or heart rate, and thus may be a potentially useful clinical agent. The one property of this drug which is not ideal is its tendency to cause a redistribution of cardiac output favoring the muscular beds at the expense of the kidney and visceral beds.

Animals↗
PubMed1974

Effects of hemorrhage on regional blood flow distribution in dogs and primates.

The effects of hemorrhage on arterial pressure, blood flows, and resistances in the coronary, mesenteric, renal, and iliac beds of healthy, conscious dogs and intact, tranquilized baboons were studied. Mild nonhypotensive hemorrhage (14+/-2 ml/kg) increased heart rate and mesenteric and iliac resistances slightly but significantly, and decreased renal resistance (-13+/-2%). Moderate hypotensive hemorrhage, 26+/-2 ml/kg, reduced mean arterial pressure (-23+/-2 mm Hg) and blood flows to the mesenteric (-56+/-3%), iliac (-58+/-5%), and coronary (-39+/-4%) vascular beds, and increased heart rate (+89+/-9 beats/min) and resistances in the mesenteric (+73+/-15%), iliac (+102+/-19%), and coronary (+27+/-5%) beds. In contrast to the other beds, renal flow rose 11+/-6% above control and renal resistance fell 31+/-2% below control. Renal vasodilatation with hemorrhage was also observed in five baboons. The increases in mesenteric and iliac resistances were blocked almost completely by phentolamine, while the increase in coronary resistance was only partially blocked by phentolamine. The renal dilatation was not blocked by phentolamine, propranolol, atropine, or tripelennamine, but was prevented by indomethacin, suggesting that this dilatation was mediated by a prostaglandin-like compound. Thus the peripheral vascular responses to hemorrhage involve intense vasoconstriction in the mesenteric and iliac beds. In the normal conscious dog and the intact, tranquilized primate, the renal bed does not share in the augmentation of total peripheral resistance with nonhypotensive and moderate hypotensive hemorrhage, but does with more severe hemorrhage. In fact, renal vasodilatation occurs with nonhypotensive or moderate hypotensive hemorrhage, which can be prevented by blockade of prostaglandin synthetase with indomethacin.

Animals↗
PubMed1974

Effects of catecholamines, exercise, and nitroglycerin on the normal and ischemic myocardium in conscious dogs.

The effects of isoproterenol, norepinephrine, dobutamine, exercise, and nitroglycerin on left ventricular diameter, pressure, velocity of shortening, dP/dt, dP/dt/P, arterial pressure, left circumflex coronary blood flow, and coronary vascular resistance were examined in healthy conscious dogs with normal coronary perfusion and in the same animals after moderate global ischemia had been induced by partial occlusion of the left main coronary artery. In the normal nonischemic heart, all interventions improved left ventricular performance, as evidenced by increases in dP/dt/P and velocity at the same or lower left ventricular end-diastolic diameter. Interventions, which in the normal heart caused large increases in heart rate and myocardial contractility, e.g. isoproterenol and exercise, or which decreased coronary perfusion pressure, e.g. nitroglycerin or isoproterenol, elicited paradoxical responses in moderate global ischemia, i.e., left ventricular enddiastolic diameter and pressure rose, and dP/dt/P and velocity fell substantially. On the other hand, norepinephrine, which increased coronary perfusion pressure along with myocardial contractility but did not increase heart rate, improved left ventricular function. Dobutamine, which did not alter heart rate or arterial pressure substantially while improving myocardial contractility, produced an intermediate response between that of norepinephrine and isoproterenol in the presence of moderate global myocardial ischemia. Thus, interventions that increase myocardial O(2) requirements, by increasing heart rate and myocardial contractility without augmenting coronary perfusion pressure, can produce a paradoxical depression of ventricular function in the presence of global myocardial ischemia.

Adrenergic beta-Agonists↗
PubMed1973

Extent of regulation of the heart's contractile state in the conscious dog by alteration in the frequency of contraction.

The effects of alterations in the frequency of contraction over the range from 94 to 220/min on left ventricular pressure, diameter, and dP/dt were studied in 10 dogs instrumented with ultrasonic diameter ganges and miniature pressure gauges. The same dogs were studied on separate days in the conscious state, after general anesthesia with pentobarbital Na, 30 mg/kg, and in the conscious state after pretreatment with propranolol, 3 mg/kg. End diastolic diameter was maintained constant during alterations in frequency by infusing saline intravenously. The maximum increases in peak dP/dt and dP/dt/P in the conscious state were 14 and 10%, respectively. After anesthesia, raising the frequency of contraction from 122 to 220/min caused maximum increases in peak dP/dt and dP/dt/P of 36 and 30%, respectively. In the conscious state after cardiac depression by propranolol, the maximum increases in peak dP/dt and dP/dt/P were 23 and 23%, respectively. Thus, increasing the frequency of contraction of the normal heart of the conscious dog causes only a slight inotropic effect, but this effect is significantly greater in the presence of myocardial depression produced by anesthesia with pentobarbital Na or in the conscious animal after a myocardial-depressing dose of propranolol.

Anesthesia, General↗