Increased tolerance to ischemia exhibited by chronically hypoxic rabbit hearts is associated with increased activation of the KATP channel. This increased KATP activity may be the result of increased intracellular concentrations of lactate.

Electron spin resonance spectroscopy has recently been used by others to detect directly radical species in isolated perfused hearts. Sample processing prior to spectroscopy in this study involved pulverization of tissue, which can artifactually generate radical species. We assessed in isolated perfused hearts the influence of tissue pulverization on the identity of radical species detected by spectroscopy and then, using a processing technique less likely to induce artifacts, whether myocardial ischemia and reperfusion generate radical species. Rat and rabbit hearts (n = 8) were perfused aerobically for 10 min and freeze-clamped to -196C. Frozen tissue was processed at -196°C for spectroscopic analysis by pulverization vs. chopping. Spectra of pulverized tissue consisted of three components: a semiquinone (g = 2.004), a lipid peroxy radical (g11 = 2.04 and gL = 2.006), and a carboncentered radical that is possibly a lipid radical (gl,, = 2.002 and A' 50 G). Chopped tissue consisted of a single component, a semiquinone (g = 2.004). Rat hearts (n = 8 per group) also underwent 10-min global no-flow normothermic ischemia followed by 5-60 sec of either aerobic or anaerobic reperfusion, with frozen tissue chopped prior to spectroscopy. Spectra of ischemic tissue consisted of an iron-sulfur center and a semiquinone. Aerobic reperfusion resulted in a spectrum similar to the control but with increased amplitude that peaked after 10-15 sec of reflow. Anaerobic reperfusion yielded a spectrum identical to that of ischemic tissue. We conclude that pulverization of frozen myocardial tissue artifactually generates radical species. Using a nonpulverization technique for tissue processing, we found that myocardial ischemia and reperfusion produce radical species but that molecular oxygen is necessary for the burst of radical production during reflow.Myocardial ischemia occurs when myocardial oxygen demand exceeds oxygen supply. Unless reversed, this situation results in cell injury. The clinical event is myocardial infarction. Reperfusion of the ischemic myocardium during thrombolysis, coronary artery bypass surgery, or angioplasty can restore oxygen and energy substrates to the ischemic myocardial cell, but this process may create another form of myocardial damage, termed "reperfusion injury." This is characterized by tissue disruption, enzyme leakage, and development of contracture (1). Damage to the myocardial cell induced by a cycle of ischemia and reperfusion has been proposed to be due in part to the generation of toxic oxygen-derived free radicals (2, 3). Until recently, evidence to support the role of free radicals in myocardial cell injury has been of an indirect nature. Their production during ischemia and reperfusion has been implied through the use either of inhibitors of free radical generation or of scavengers of radical production (4-7).Nearly 2 decades ago, Beinert and coworkers (8-10) used low-temperature ESR spectroscopy to study the mechanism of electron transport in the cardiac mitochondrial respirat...

Many infants who require cardiac surgery have cyanotic heart disease. We assessed the relative tolerances to ischemia of hearts from immature normoxemic rabbits versus hearts from immature rabbits subjected to hypoxemia since birth. Normoxemic animals were raised from birth in an environment where the inspired fractional concentration of oxygen (FIO2) was 0.21; for the hypoxemic studies FIO2 was reduced to 0.09. Hearts (n = 6/group) from normoxemic and chronically hypoxemic rabbits at 7-12, 21-28, 35-44, and 51-56 days of age underwent aerobic "working" perfusion with Krebs bicarbonate buffer, and cardiac function was measured. Hearts were then arrested by a 3-min infusion with either cold (14 degrees C) Krebs buffer (hypothermia alone group) or St. Thomas' Hospital II solution (hypothermia plus cardioplegia group) before 6 h of hypothermic (14 degrees C) global ischemia. Hearts were reperfused, and postischemic creatine kinase leakage and recovery of function were measured. For hearts protected with hypothermia alone, recovery of aortic flow was better in hearts hypoxemic from birth compared with normoxemic controls at 7-12 days (78 +/- 7 vs. 60 +/- 6%, P < 0.05) and 21-28 days old (81 +/- 12 vs. 26 +/- 28%, P < 0.05). Protection with hypothermia plus cardioplegia was also better in hearts hypoxemic from birth compared with normoxemic controls at 7-12 days (74 +/- 8 vs. 63 +/- 10%, P < 0.05) and 21-28 days old (84 +/- 3 vs. 71 +/- 5%, P < 0.05). Protection with hypothermia alone and hypothermia plus cardioplegia was no different within chronically hypoxemic age groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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A unique combination of CT findings is reported in a rare case of aortic dissection with intimointimal intussusception. The CT showed a wind sock-like appearance in the contrast column of the aortic arch, which was felt to be characteristic of the intussuceptum. Complementary CT findings, including proximal flap in the dilated root of the aorta, no mid-ascending aortic flap, a descending aortic flap, and pericardial effusion, enabled establishment of the preoperative diagnosis.