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Biomedical subjects

A J Manganaro

Publications and source records attributed to A J Manganaro.

7 recordsLinked to original sources
PubMed1981

Detrimental effects of premature use of inotropic drugs to discontinue cardiopulmonary bypass.

Ten dogs underwent 45 minutes of normothermic ischemic arrest. After 15 minutes of reoxygenation, none could support the systemic circulation independently. In five dogs, we could discontinue bypass (cardic output 70 to 100 cc/kg/min) by giving dopamine (10 to 30 mcg/kg/min). In five other dogs, total cardiopulmonary bypass was prolonged for an additional 30 minutes and no dopamine was given. During control and at 15 and 45 minutes after aortic unclamping, we measured myocardial blood flow (microspheres), metabolism (oxygen uptake and lactate), water content (wet/dry weight), left ventricular compliance (intraventricular balloon), and performance (isovolumetric and Starling function curves). Dogs treated with prolonged bypass showed progressive improvement in ventricular compliance, function, and water content and did not require inotropic drugs when bypass was discontinued 45 minutes after ischemia. In contrast, dogs receiving dopamine exhibited more myocardial edema (3.3% versus 1.7% water gain), worse ventricular compliance (18% versus 55% recovered at 25 ml left ventricular volume), poorer contractility (58% versus 70% recovery of +dP/dt), generated 50% less stroke work at a left atrial pressure of 25 mm Hg (0.25 versus 0.52 gm/kg), failed to augment oxygen uptake to meet the metabolic demands of the working heart (11% versus 45% increase in oxygen uptake), and required continued inotropic support to discontinue extracorporeal circulation. We conclude that (1) limited prolongation of total bypass enhances recovery from ischemic damage and (2) use of inotropic drugs to prematurely discontinue extracorporeal circulation will impede recovery by accentuating myocardial edema and further decreasing ventricular compliance, performance, and oxygen utilization.

Animals↗
PubMed1980

Reversal of ischemic damage with amino acid substrate enhancement during reperfusion.

Twenty dogs underwent 15 minutes of normothermic ischemic arrest and 30 minutes of reperfusion while on cardiopulmonary bypass. In 10 control dogs, the reperfusate blood was not modified. In 10 other dogs, the aorta was reclamped and the heart reperfused for 5 minutes with blood containing L-glutamate (0.026M). We measured coronary blood flow (microspheres), left ventricular (LV) metabolism [O2 content, adenosine triphosphate (ATP)], LV compliance (intraventricular balloon), and LV performance (balloon and Starling curves) before and 30 minutes after ischemia. Fifteen minutes of ischemic arrest produced significant depression in contractility and oxidative metabolism. L-Glutamate infusion resulted in higher oxygen uptakes (9.7 versus 6.9 cc/100 gm/min) and allowed more complete recovery of ATP content (80% versus 67%). Glutamate-treated hearts had more complete recovery in the rate of contraction, +dP/dt, (96% versus 68%), and relaxation, --dP/dt (99% versus 72%), the best recovery of compliance (74% versus 88%), and complete (100%) recovery of stroke work index (1.55% versus 0.87% gm - m/kg). We conclude that the addition of L-glutamate to reperfusate blood reverses ischemic damage. We suspect that l-glutamate acts by replenishing Krebs' cycle intermediates lost during ischemia, thereby stimulating oxidative metabolism and enhancing ATP production.

Adenosine Triphosphate↗
PubMed1979

Reversal of ischemic damage with secondary blood cardioplegia.

After severe ischemic injury, it is usually necessary to prolong bypass to enhance recovery. This study tests the hypothesis that the best reversal of ischemic damage is achieved by briefly rearresting the postischemic heart with a continuous infusion of an oxygenated cardioplegic solution (secondary blood cardioplegia) during the period when bypass must be prolonged. Twenty dogs underwent 45 minutes of normothermic ischemic arrest. Fifteen minutes after unclamping, no heart could support the systemic circulation. In all dogs, oxygen demands were lowered by extending bypass for 30 minutes. In 10 of these dogs, demands were further lowered by rearresting the heart for 5 minutes with a continuous infusion of a 37 degrees C blood cardioplegic solution (K+28 mEq/L; pH 7.6; Ca++ 1 mEq/L) at a pressure of 50 mm Hg. Hearts treated with secondary blood cardioplegia showed greater recovery in the rate of contraction (-dP/dt 75% versus 62%, p less than 0.05) and relaxation (-dP/dt 76% versus 58%, p less than 0.05), better recovery of compliance (85% versus 51%, p less than 0.05), a higher stroke work index (0.72 versus 0.50 gm-m/Kg, p less than 0.05), and more ability to augment oxygen uptake (85% versus 45%, p less than 0.05) to meet the demands of the working heart than hearts treated by prolonging bypass alone. We conclude that rearresting the heart with a brief, continuous infusion of a blood cardioplegic solution results in more complete reversal of ischemic damage than possible by prolongation of a bypass alone. We believe that the increased recovery with secondary cardioplegia results from diversion of delivered oxygen toward reparative processes rather than its being expended needlessly on electromechanical work during the time when bypass must be prolonged.

Animals↗