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Cardiopulmonary bypass results in a "euthyroid sick" state. Recently, interest has focused on the relationship between low serum triiodothyronine levels and postoperative cardiovascular hemodynamics. The present study was undertaken to more clearly define the acute effects of triiodothyronine on myocardial mechanics and energetics after hypothermic global ischemia using an ex-vivo canine heart preparation to model the clinical condition. Experiments were performed on isolated hearts subjected to hyperkalemic arrest with 90 minutes of hypothermic (10 degrees C) ischemia. Isolated hearts were cross-perfused by euthyroid support dogs in which triiodothyronine levels spontaneously decreased by 65% to 75% (p < 0.01) after the initiation of cross-perfusion. In nine heart preparations, triiodothyronine (Triostat) was given as a bolus dose (0.2 micrograms/kg) after 1 hour of baseline data collection with a subsequent measurable rise in serum triiodothyronine levels (p < 0.01). In six postischemic hearts, reverse triiodothyronine was given as a 0.2 micrograms/kg bolus. Triiodothyronine was also administered to a group of eight nonischemic, continuously perfused isolated hearts. Intrinsic myocardial contractility was assessed by analysis of the preload recruitable stroke work area, energetic efficiency from the myocardial oxygen consumption-pressure-volume area relationship, and coronary vascular resistance from analysis of coronary flow and perfusion pressure. Acute administration of triiodothyronine to postischemic hearts improved the preload recruitable stroke work area from 9.5 +/- 1.42 to 14.9 +/- 2.03 x 10(7) erg/ml, a 56% increase from baseline (p < 0.001), but had no effect on the preload recruitable stroke work area of the nonischemic hearts. The inotropic response resulting from triiodothyronine treatment did not alter the myocardial oxygen consumption-pressure-volume area relationship. Triiodothyronine treatment was associated with significantly decreased coronary resistance and increased coronary flow through a range of diastolic loading conditions in the postischemic hearts. The biologically inactive thyroid hormone metabolite reverse triiodothyronine was without effect on any of the measured parameters. On the basis of these results, we conclude that the low triiodothyronine state of cardiopulmonary bypass can be reproduced in this isolated heart model and that acute triiodothyronine treatment results in a unique inotropic action manifest only in the postischemic reperfused myocardium and is accomplished without oxygen wasting effects.

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The beneficial hemodynamic effects of IABP are critically dependent on balloon timing relative to the diastolic phase of the cardiac cycle. A microprocessor-based controller has been developed to implement real-time automation of IABP using P-R intervals to regulate balloon deflation and systolic time intervals to trigger balloon inflation in a semi-automatic fashion. Experiments were performed on anesthetized open-chest dogs. Simultaneous measurement of aortic pressure and flow, coronary flow, and left ventricular pressure were recorded. Muscle segment lengths in normal and ischemic border zones were also measured from implanted pairs of endocardial ultrasonic dimension gages. P-waves were obtained from atrial cardiograms, and heart sounds were detected using a special filtering circuit. Both signals were input together with ECG to automate IABP timing. Systolic time intervals were calculated in real-time. IABP efficacy was assessed from changes in aortic flow, coronary flow, tension time index, end diastolic pressure, and the endocardial viability ratio. Comparisons were made between automated and manual timing set by a certified technician. Results indicate that automated timing yielded equivalent hemodynamic enhancement with greater ease of adjustment. A closed-loop control scheme is proposed which allows complete automatic device operation and the capability to rapidly achieve the optimum of any directly measurable hemodynamic variable.

No abstract