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Brain tissue blood flow was measured precisely by the colored microsphere method during retrograde cerebral perfusion in 10 normothermic mongrel dogs. The average tissue blood flow rates to the cerebral cortex, cerebral medulla, brain stem, cerebellum, and spinal cord during retrograde cerebral perfusion at 25 mm Hg of external jugular venous pressure were 10.5 +/- 10.3, 4.2 +/- 4.6, 11.1 +/- 9.8, 12.3 +/- 8.6, and 9.1 +/- 5.8 ml/min per 100 gm, respectively. The brain was perfused wholly by retrograde cerebral perfusion without lateralization. Total cerebral blood flow was calculated as the sum total rates of blood flow to each area. Total cerebral blood flow during retrograde cerebral perfusion at 25 mm Hg was 7.8 +/- 4.4 ml/min, which represented 3.5% +/- 1.9% of whole body blood flow and one third of the total cerebral blood flow (28.0 +/- 4.2 ml/min) during cardiopulmonary bypass at a flow rate of 1000 ml/min. Oxygen consumption and carbon dioxide elimination by the total cerebrum during retrograde cerebral perfusion at 25 mm Hg were 0.54 +/- 0.23 ml/min and 34 +/- 15 @mmol/min, respectively, or 8.6% +/- 3.6% and 7.0% +/- 3.1% of the corresponding whole body value and represented about one third of that measured during cardiopulmonary bypass (1.21 +/- 0.39 ml/min and 96 +/- 15 @mmol/min). Total cerebral blood flow, total cerebral oxygen consumption, and carbon dioxide elimination increased as the external jugular venous pressure increased from 15 to 25 mm Hg; however, no further increase occurred once the external jugular venous pressure exceeded 25 mm Hg. (J THORAC CARDIOVASC SURG 1995;109:772-9)

The effects of 5-(N,N-dimethyl)amiloride, a potent and specific Na^+-H^+ exchange inhibitor, were investigated in isolated perfused rabbit hearts subjected to ischemia and reperfusion. Phosphorus 31-nuclear magnetic resonance spectroscopy was used to monitor intracellular pH, creatine phosphate, @b-adenosine triphosphate, and inorganic phosphate. After cardioplegic arrest with St. Thomas' Hospital solution, normothermic (37@? C) global ischemia was induced for 45 minutes, and the hearts were reperfused for 50 minutes. Dimethyl amiloride at 10 @mmol/L, which has minimal inotropic and chronotropic effects on the nonischemic heart, was added to the cardioplegic solution. Treatment with dimethyl amiloride reduced the elevation of left ventricular end-diastolic pressure during and after the ischemia and improved the postischemic recovery of developed pressure from 76% +/- 3.2% at 30 minutes of reperfusion in control hearts ( n = 6) up to 99% +/- 1.9% in hearts treated with dimethyl amiloride ( n = 8). Dimethyl amiloride did not affect the decline in intracellular pH during ischemia for up to 30 minutes but enhanced the intracellular acidosis thereafter. The intracellular pH at the end of ischemia was 6.21 +/- 0.05 in control hearts compared with 5.24 +/- 0.17 in hearts treated with dimethyl amiloride ( p < 0.05). During reperfusion, intracellular pH of hearts treated with dimethyl amiloride was less than control for 5 minutes, but subsequent recovery of intracellular pH was similar to control. Treatment with dimethyl amiloride did not affect creatine phosphate breakdown, inorganic phosphate accumulation, and @b-adenosine triphosphate depletion during 45 minutes of ischemia. The creatine phosphate resynthesis and inorganic phosphate reduction during reperfusion were also unaffected. These findings suggest that Na^+-H^+ exchange plays an important role not only during reperfusion but also during ischemia for the development of postischemic cardiac dysfunction most likely by inducing primary Na^+ and secondary Ca^2^+ overload. Specific Na^+-H^+ exchange inhibitors like dimethyl amiloride would have a potential therapeutic profile in cardiac surgery, especially if added before ischemia. (J THORAC CARDIOVASC SURG 1996;112:765-75)

Objective: This study compared the cerebral microcirculation during retrograde cerebral perfusion with that during antegrade cardiopulmonary bypass under normothermic and hypothermic conditions. Methods: Brain tissue blood flow was measured with the hydrogen-clearance and colored microsphere (15 and 50 @mm) methods during antegrade cardiopulmonary bypass and retrograde cerebral perfusion. Measurements were performed during normothermia (37^o C), moderate hypothermia (28^o C) and deep hypothermia (20^o C) in groups of mongrel dogs (n = 8). Results: During antegrade cardiopulmonary bypass, the microsphere method showed a significant decrease in cerebral blood flow as body temperature decreased (40.1 +/- 20.8 ml/min/100 gm at 37^o C, 16.2 +/- 18.0 ml/min/100 gm at 20^o C with 50 @mm microspheres) At 20^o C, the cerebral blood flow measured with the 15 @mm microspheres was significantly lower than that assessed with the hydrogen-clearance method (11.3 +/- 7.0 vs 24.8 +/- 7.0 ml/min/100 gm). During retrograde cerebral perfusion, the microsphere method also showed a significant decrease in cerebral blood flow with cooling. At 37^o C, the cerebral blood flow measured with the 15 @mm microspheres (0.8 +/- 0.7 mI/min/100 gm) was significantly lower than that assessed with the hydrogen-clearance method (10.1 +/- 3.5 ml/min/100 gm). At both 28^o and 20^o C, the hydrogen-clearance method showed significantly higher cerebral blood flow (10.1 +/- 5.8 and 8.2 +/- 3.7 ml/min/100 gm) than did the 50 @mm microspheres (1.8 +/- 0.6 and 1.0 +/- 0.8 ml/min/100 gm) and 15 @mm microspheres (0.23 +/- 0.14 and 0.18 +/- 0.15 ml/min/100 gm). Conclusion: (1) Cerebral blood flow that shunts to capillaries is increased during antegrade cardiopulmonary bypass under deep hypothermia. (2) During retrograde perfusion, the majority of the blood flow shunts away from brain capillaries, even under normothermic conditions, and blood flow through large venoarterial shunts increases as body temperature decreases, Although the cerebral microcirculation during retrograde perfusion is decreased, retrograde perfusion provides some degree of oxygenation to the body. (J Thorac Cardiovasc Surg 1997;114:440-7)

The effect of dynamic cardiac compression on left ventricular contractile efficiency was assessed in terms of the pressure-volume relationship and myocardial oxygen consumption. In 11 excised cross-circulated dog hearts, the ventricle was directly compressed during systole (dynamic cardiac compression). Measurements for pressure-volume area (a measure of total mechanical energy), external work, and myocardial oxygen consumption were done before and during dynamic cardiac compression. Dynamic cardiac compression increased pressure-volume area by 28% +/- 17% (mean plus or minus the standard deviation) and external work by 24% +/- 20% (p = 0.0000185 and 0.0000212, respectively) at given end-diastolic and stroke volumes without affecting myocardial oxygen consumption. As a result, the oxygen cost of pressure-volume area, that is, the slope of the myocardial oxygen consumption-pressure-volume area relationship, significantly decreased by 16% +/- 13% (p = 0.0000135) whereas the pressure-volume area-independent myocardial oxygen consumption was unchanged. Then, contractile efficiency, that is, the reciprocal of the slope of the myocardial oxygen consumption-pressure-volume area relationship in joules significantly improved from 45% +/- 8% to 53% +/- 13% (p = 0.0000437). When the native myocardial oxygen consumption-pressure-volume area relationship was assessed by subtracting the dynamic cardiac compression pressure applied to the heart, the slope of the myocardial oxygen consumption-pressure-volume area relationship returned to the control level. This indicates that the contractile efficiency of the native heart was not affected by dynamic cardiac compression. We conclude that dynamic cardiac compression enhances left ventricular pump function by improving the contractile efficiency of the overall heart leaving the energetics of the native heart unchanged. (J Thorac Cardiovasc Surg 1997;113:923-31)

Objective: Cardiomyoplasty is a surgical procedure to support the failing heart, in which a burst-stimulated latissimus dorsi muscle flap is transposed and wrapped around the ventricles. The effect of dynamic cardiac compression, implemented as cardiomyoplasty, on left ventricular performance remains controversial; the mechanism by which clinical symptoms are improved remains unclear. To investigate the mechanism for improvement of patients' symptoms, it is important to evaluate the effects of cardiomyoplasty on left ventricular energetics and on left ventricular systolic and diastolic function. We therefore evaluated the efficiency of energy transfer from the native pressure-volume area to external work under conditions of 1:3 skeletal muscle burst pacing in an animal model with chronic heart failure. Methods: In seven Merino-Wether sheep, cardiomyoplasty was performed after stable heart failure was induced by staged coronary embolizations (ejection fraction < 35%). Hemodynamic assessment including the assessment of the pressure-volume relationship was performed 8 weeks after cardiomyoplasty when the latissimus dorsi muscle was fully trained. Instantaneous left ventricular pressure and volume were measured with a catheter-tipped manometer and a conductance catheter during steady-state conditions and after a transient inferior vena cava occlusion. The effect of dynamic cardiac compression on left ventricular systolic function was assessed by comparing pre-assisted and assisted beats and on diastolic function by comparing assisted and post-assisted beats. Result: The slope of the end-systolic pressure-volume relationship decreased by 30.5% +/- 27.8% (p = 0.02) during assisted beats. However, left ventricular pump performance improved by increasing stroke volume and external work by 35.9% +/- 36.0% (p = 0.03) and 9.7% +/- 6.8% (p = 0.03), respectively, resulting in a reduction of the volume intercept. As a result, the end-systolic pressure-volume relationship shifted to the left. The efficiency of energy transfer from the native pressure-volume area to the overall external work improved by 7.6% +/- 8.2% (p = 0.04). Cardiomyoplasty did not affect the time constant of left ventricular isovolumic pressure decline or the maximal rate of pressure decay, which suggested that cardiomyoplasty did not affect left ventricular relaxation. Conclusions: Dynamic cardiac compression in the form of cardiomyoplasty enhanced left ventricular pump performance without interrupting left ventricular filling. The ratio of energy transfer from the native pressure-volume area to the overall external work suggests a myocardial oxygen-sparing effect of cardiomyoplasty. (J Thorac Cardiovasc Surg 1998;115:1358-66)