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Query: UMLS:C0020672 (hypothermia)
17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of 6-h hypothermic cardioplegic arrest on myocardial biochemical, morphologic, and functional recovery were investigated in two groups of dogs. Group 1 (n = 6) was subjected to hypothermia of 15 degrees C and group 2 (n = 6) was subjected hypothermia of 5 degrees C. Although the myocardial calcium (Ca) concentration was significantly higher at the end of reperfusion in group 2 compared to group 1, the MB-fraction of creatine kinase, mitochondrial aspartate aminotransferase, recovery of left ventricular systolic function, and mitochondrial morphologic integrity were better in group 2 than in group 1. These findings suggest that hypothermia of 5 degrees C in 6-h cardioplegia is not necessarily coupled with interference in myocardial contractility, despite the Ca overload that occurs during reperfusion.
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PMID:The effects of a temperature below 15 degrees C on the myocardial calcium and ultrastructure in donor heart preservation in a canine model. 786 57

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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PMID:Tolerance of the developing heart to ischemia: impact of hypoxemia from birth. 790 Aug 70

Because many infants who require cardiac operation have cyanotic heart disease, we determined whether the existing calcium content of St. Thomas' II solution (1.2 mmol/L) is optimal to protect the immature rabbit heart hypoxemic from birth during subsequent ischemia. Modified hypothermic St. Thomas' II solutions (calcium content, 0 to 2.4 mmol/L) were compared with hypothermic Krebs bicarbonate buffer in protecting chronically hypoxemic (PaO2 = 34 +/- 11 mmHg, SaO2 = 63% +/- 3%) versus normoxemic (PaO2 = 76 +/- 11 mmHg, SaO2 = 92% +/- 3%) immature hearts (7 to 12 days old) during ischemia. Hearts (n = 6 per group) underwent aerobic 'working' perfusion with Krebs bicarbonate buffer and cardiac function was measured. The hearts were then arrested with a 3 minute infusion of either cold (14 degrees C) Krebs buffer (1.8 mmol calcium/L) as hypothermia alone or modified St. Thomas' II solution before 6 hours of hypothermic (14 degrees C) global ischemia. Hearts were reperfused and postischemic enzyme leakage and recovery of function were measured. A bell-shaped dose-response profile was observed for recovery of postischemic aortic flow but not for postischemic creatine kinase leakage, with improved protection occurring at lower calcium concentrations. Optimal myocardial protection occurred at a calcium content of 0.4 mmol/L, which was significantly better than with hypothermia alone or standard St. Thomas' II solution. We conclude that the existing calcium concentration of St. Thomas' II solution is responsible, in part, for its inadequate protection of immature myocardium hypoxemic from birth during ischemia.
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PMID:Calcium and cardioplegic protection of the ischemic immature heart: impact of hypoxemia from birth. 794 63

The effects of electrical pacing during the early reperfusion following hypothermic global ischemia (60 min, at 25 degrees C) was studied in the isolated working rat heart model. The hearts were divided into three groups. Hearts in Group I (n = 8) were control without hypothermia, ischemia or pacing. Hearts in Group II (n = 16) were paced with ventricular rate at 300 beats/min with 1 mVolt for 10 min during the Langendorff mode after an initial 5 min of reperfusion. Hearts in Group III (n = 14) were not paced. The recovery of aortic flow (both absolute and percent) was significantly better in Group II than in Group III, but was significantly lower in both groups than in control. No significant differences were noted, however, in heart rate, aortic pressure or coronary flow between Group II and III. In contrast, the tissue concentration of adenosine triphosphate (ATP) in Groups II and III decreased significantly by the end of reperfusion relative to Group I, but no difference in ATP existed between Group II and III. Myocardial ATP concentrations did not correlate with percent recovery of aortic flow. The myocardial concentration of calcium in Groups II and III increased by the end of reperfusion as compared with Group I, but no difference in calcium existed between Group II and III. The myocardial concentration of calcium demonstrated a significant correlation with percent recovery of aortic flow (r = 0.71, n = 30, p < 0.005). Our results indicate that an electrical pacing during early reperfusion in the myocardium improves functional recovery of aortic flow.
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PMID:Effects of electrical pacing to the preischemic rate during rewarming after hypothermic ischemia in the rat heart. 794 61

Amino acid enrichment of cardioplegic solutions has been shown to improve both the metabolic and functional recovery of ischemic myocardium. However, because of the marked systemic vasodilatation involved, use of amino acid enrichment is limited to the periods of induction and reperfusion. Fumarate is a Krebs' cycle intermediate whose conversion to succinate is responsible for the generation of adenosone triphosphate and the oxidation of the reduced form of nicotinamide-adenine nucleotide which is the pathway by which aspartate exerts its effect. Fumarate may also function as a free-radical scavenger and is involved in calcium transport. To determine if fumarate-enriched blood cardioplegia would improve the functional recovery of the neonatal heart, 14 neonatal piglet hearts were isolated and placed on a blood-perfused working heart circuit. After the baseline functional and metabolic assessment was done, cold ischemic arrest was initiated with either standard blood cardioplegic solution (group I; N = 7) or fumarate-enriched (13 mmol/L) blood cardioplegic solution (group II; N = 7). Cardioplegic solution was given at a pressure of 40 mm Hg every 20 minutes for 2 hours, and topical hypothermia was used. Sixty minutes after warm whole blood reperfusion, the functional recovery at left atrial pressures of 3, 6, 9, and 12 mm Hg was 70%, 66%, 66%, and 65%, respectively, in group I, versus 102%, 106%, 105%, and 109%, respectively, in group II (p < 0.05). The tissue creatinine phosphate levels after reperfusion were significantly higher in group II hearts (15.0 +/- 1.2 mumol/g dry heart tissue) than in group I hearts (9.2 +/- 1.9 mumol/g dry heart tissue), although the adenosine triphosphate levels were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fumarate-enriched blood cardioplegia results in complete functional recovery of immature myocardium. 801 Aug 14

Hypothermia is believed to improve the tolerance to both ischemia and cardiopulmonary bypass and is commonly used during heart operations, particularly in the neonate. However, hypothermia also causes calcium to accumulate in the myocyte experimentally, and an increase in intracellular calcium during ischemia may worsen the effect of ischemia and impair the postischemic recovery of function. This effect of hypothermia on intracellular calcium has generally not been considered in experiments that attempt to optimize the composition of cardioplegic solutions. We have evaluated the impact of hypothermia before cardioplegic ischemia on the efficacy of two common cardioplegic solutions, one with calcium (St. Thomas' Hospital cardioplegia) and the other without calcium (glucose-potassium cardioplegia), in 37 isolated blood-perfused neonatal lamb hearts. Left ventricular maximal developed pressure, positive maximum of the first derivative of left ventricular pressure, left ventricular stiffness constant at 10 mmHg end-diastolic pressure, coronary blood flow, and myocardial oxygen consumption were measured before and 30 minutes after 2 hours of cold ischemia. After baseline measurements were made, two groups of hearts (ST-C and GK-C) had perfusion-cooling for 10 minutes to 17 degrees C myocardial temperature, and two other groups (ST-NC and GK-NC) had the same period of normothermic perfusion. Then the hearts were arrested with 4 degrees C St. Thomas' cardioplegic in groups ST-C and ST-NC and with glucose-potassium cardioplegia in groups GK-C and GK-NC. In the groups without preischemic cooling, both St. Thomas' (group ST-NC) and glucose-potassium (group GK-NC) cardioplegia resulted in a similar recovery of function compared with baseline levels (group ST-NC: developed pressure = 91.3% +/- 9.2%, dP/dt = 88.1% +/- 8.9%, left ventricular stiffness constant = 96.1% +/- 3.3%; group GK-NC: developed pressure = 89.3% +/- 6.9%, dP/dt = 82.6% +/- 8.8%, left ventricular stiffness constant = 99.4% +/- 2.0%; data are mean plus or minus the standard deviation). However, with preischemic cooling, St. Thomas' cardioplegia (group ST-C) resulted in a significantly reduced recovery of both systolic and diastolic function (developed pressure = 81.6% +/- 6.2%, dP/dt = 75.1% +/- 8.4%, left ventricular stiffness constant = 103.7% +/- 2.7%) compared with that for both glucose-potassium cardioplegia (group GK-C: developed pressure = 92.4% +/- 8.7%, dP/dt = 83.7% +/- 6.0%, left ventricular stiffness constant = 100.5% +/- 2.1%) and St. Thomas' cardioplegia without preischemic cooling (group ST-NC) (p < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Interactions between preischemic hypothermia and cardioplegic solutions in the neonatal lamb heart. 812 11

We determined the influence of perfusate composition and reinfusion during ischemia upon myocardial protection in the immature rabbit heart. Isolated "working" hearts (n = 6 per group) from 7-10-day-old New Zealand White rabbits were perfused with Krebs bicarbonate buffer and function measured. Hearts were then arrested with 3 minutes cold (14 degrees C) perfusion with bicarbonate buffer (as hypothermia-alone group) or St. Thomas' II cardioplegic solution (as hypothermia-plus-cardioplegia group). Hearts were then subjected to hypothermic (14 degrees C) global ischemia for 2 or 6 hours, with and without multiple reinfusion of the coronary vasculature. Following 2 hours ischemia impaired recovery of aortic flow occurred after multiple reinfusion in comparison with a single infusion with the cardioplegic solution (64 +/- 3% versus 72 +/- 4%) but not with bicarbonate buffer (79 +/- 3% versus 83 +/- 4%). However after 6 hours ischemia impaired recovery of function occurred after multiple reinfusion in comparison with single infusion both with the cardioplegic solution (60 +/- 3% versus 68 +/- 3%) and with bicarbonate buffer (57 +/- 4% versus 75 +/- 5%). There were no differences in post-ischemic creatine kinase leakage or myocardial water content between groups. These results suggest (i) that reinfusion itself, regardless of the composition of the perfusate, caused decreased recovery of function after an extended period of ischemia, and (ii) protection of the ischemic immature heart with St. Thomas' II solution remains inadequate and requires improvement.
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PMID:Protection of the ischemic immature heart--effect of perfusate reinfusion and composition. 830 94

Profound hypothermic circulatory arrest is frequently used to facilitate the surgical repair of congenital heart defects in neonates. Deep hypothermia is achieved by a period of core systemic cooling during cardiopulmonary bypass before cardioplegic arrest. There have been conflicting reports with respect to the consequence of perfusing a nonarrested newborn heart under hypothermic conditions. This in vitro study was designed to prolong the clinically simulated hypothermic perfusion sequence into an extreme condition and to test the hypothesis that prolonged cold perfusion of the nonarrested newborn myocardium could, in fact, be detrimental. Twenty-four newborn piglets (5 to 7 days old) were randomly assigned to four groups and studied in a crystalloid perfused Langendorff heart model. The first two groups of hearts (n = 6 per group) were subjected to either 30 minutes (group I) or 90 minutes (group II) of cold perfusion at 15 degrees C, followed by 90 minutes of ischemia and then 30 minutes of normothermic reperfusion. In a second experiment, group III hearts subjected to 30 minutes of cold perfusion were compared with group IV (90 minutes of cold perfusion) without ischemic insult in either case. Postischemic recovery of isovolumetric developed pressure was significantly impaired in group II (16.1% +/- 7.4% [II] versus 65.5% +/- 4.8% [I], p < 0.05), and 50% of the hearts had no spontaneous cardiac activity on reperfusion. End-diastolic pressure showed significant contracture with prolonged cold perfusion: group II 57.3 +/- 13.9 mm Hg versus group I 14.8 +/- 1.8 mm Hg, p < 0.05. In the absence of ischemia, a similar relationship was observed between groups IV and III (left ventricular developed pressure 68.5% +/- 3.6% versus 82.4% +/- 4.2%, p < 0.05, and left ventricular end-diastolic pressure 23.5 +/- 6.2 mm Hg versus 13.3 +/- 2.6 mm Hg, p = not significant. Ultrastructural examination revealed severe damage to the myocardial cells and contraction band necrosis in group II (prolonged cooling and ischemia). These results suggest that prolonged cold perfusion of the nonarrested newborn heart impairs functional recovery and is therefore detrimental. When followed by a period of ischemic arrest, it further potentiates the myocardial injury and induces severe contracture. This preceding adverse effect of prolonged myocardial cold perfusion before cardiac arrest may, in part, explain the suboptimal protective effect of cardioplegia in neonates.
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PMID:Contracture of the newborn myocardium after prolonged prearrest cooling. 841 58

Although standard blood cardioplegia provides good myocardial protection for cardiac operations in adults, protection of the cyanotic, immature myocardium remains suboptimal. Calcium, which has been implicated in reperfusion injury and in the development of "stone heart" in mature myocardium, is routinely lowered in standard cardioplegic solutions. Immature, neonatal myocardium has lower intracellular calcium stores and is more reliant on extracellular calcium for contraction. To determine if normocalcemic cardioplegia would result in improved cardiac function in the neonatal heart, we conducted a series of experiments using an isolated, blood-perfused working heart model. Thirty-two neonatal piglet hearts (24 to 48 hours) were excised without intervening ischemia and were placed directly on a blood-perfused circuit. Baseline stroke work index was assessed. Hearts were then arrested with cold cardioplegic solution delivered at 45 mm Hg for 2 minutes: group I, low-calcium blood cardioplegic solution (Ca = 0.6 mmol/L); group II, normal-calcium blood cardioplegic solution (Ca = 1.1 mmol/L); group III, University of Wisconsin solution; and group IV, University of Wisconsin solution with added calcium (Ca = 1.0 mmol/L). Cardioplegic solution was administered every 20 minutes for 2 hours and topical hypothermia was used. Hearts were then reperfused with warm whole blood. Functional recovery, expressed as a percentage of control stroke work index, was determined minutes after reperfusion. Hearts preserved with normocalcemic cardioplegic solution (groups II and IV) had complete functional recovery at 60 minutes, whereas hearts preserved with low-calcium cardioplegic solution (groups I and III) achieved functional recoveries of only 80% and 65%, respectively, at a left atrial pressure of 9 mm Hg. Electron micrographs taken 1 hour after reperfusion showed minimal edema and only mild myofibrillar changes. They were identical in both the low-calcium and normocalcemic groups. Complete functional recovery is possible in immature myocardium when calcium is added to either blood or an intracellular crystalloid cardioplegic solution. The addition of calcium does not result in ultrastructural damage and does result in good functional recovery.
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PMID:Normocalcemic blood or crystalloid cardioplegia provides better neonatal myocardial protection than does low-calcium cardioplegia. 841 79

Hypothermia has been reported to increase intracellular ionized calcium, which may aggravate injury resulting from ischemia and reperfusion. The effects of plasma ionized calcium concentration ([Ca2+]) during hypothermic perfusion on recovery after 2 hours of cold cardioplegic ischemia were evaluated in 32 isolated, blood-perfused neonatal lamb hearts. Three groups of hearts (B, C, and D) were perfusion-cooled for 10 minutes to a myocardial temperature of 17 degrees C and then arrested with St. Thomas' Hospital cardioplegic solution. Group A had 10 minutes of normothermic perfusion before cardioplegia. Group B had cooling with normal [Ca2+]. Group C had citrate added as cooling was started to lower [Ca2+] (0.26 mmol/L), and it was not normalized until 15 minutes into reperfusion. Group D received citrate plus Ca2+ to give normal [Ca2+] during cooling. Groups B and D showed a significantly reduced recovery (p < 0.05) in left ventricular systolic function (developed pressure and the rate of pressure rise) and diastolic function (stiffness constant) than groups A and C. During preischemic cooling, oxygen consumption per beat and coronary vascular resistance increased significantly in groups B and D, but both oxygen consumption and coronary vascular resistance were significantly lower in group C than in groups B and D so long as [Ca2+] was low. The data show that preischemic hypothermia results in reduced postischemic recovery of function compared with simultaneous induction of cardioplegia and hypothermia. Low [Ca2+] during preischemic hypothermia and early reperfusion offsets this deleterious effect of hypothermia.
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PMID:Effect of calcium and preischemic hypothermia on recovery of myocardial function after cardioplegic ischemia in neonatal lambs. 842 46

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