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

Although a role for free radicals in myocardial damage during cardiopulmonary bypass for open heart surgery has been postulated, direct evidence of free radical production as well as consumption of tissue antioxidants such as vitamin E is still lacking. Twenty patients (age 26-66 yr, mean 48) undergoing elective open heart surgery with moderate hypothermia, and cold crystalloid cardioplegia, were studied. Cardiopulmonary bypass time was 61.4 +/- 31.2 min. The specimens of atrial tissue collection before and after cardiopulmonary bypass, were immediately frozen in liquid nitrogen. Mean vitamin E atrial content, measured by reverse phase HPLC, was 355 +/- 249 pmol/mg of dry weight basally, 135 +/- 85 pmol/mg (p < 0.05) at the end of the ischemic period and 405 +/- 288 pmol/mg after the reperfusion period (p < 0.01). Microscopic examination of right atrial biopsies ruled out differences in fibrosis or cellular damage as the cause of vitamin E changes. Although a great basal variability in atrial vitamin E content was observed, which was independent of age, sex and clinical status, a reproducible and substantial decrease in atrial vitamin E content after cardiopulmonary bypass occurred (mean reduction 45 +/- 17% and 55 +/- 22%, respectively, after ischemia and after reperfusion). This was directly related to the aorta cross-clamping duration and partially to the minimum temperature achieved. In conclusion, apart from the great variability observed in basal vitamin E tissue content, vitamin E was always reduced during cardiopulmonary bypass, suggesting an oxidative stress on the myocardium during open heart surgery.
Int J Cardiol 1992 Dec
PMID:Myocardial vitamin E is consumed during cardiopulmonary bypass: indirect evidence of free radical generation in human ischemic heart. 146 17

The natural course of post myocardial infarction ventricular septal defect is towards cardiogenic shock and death. 50% in the first week, over 90% a year latter. Between 1973-1989, 28 patients where operated on. Before surgery 14 patients (53%) where in Killip IV, 5 patients (19%) in III, 5 patients (19%) in II and 2 patients in I. The repair was accomplished under hypothermia and cardioplegia, with the insertion of a Teflon patch to close the defect in 20 patients (70%). Complementary procedures (CABG, Pacemaker, repair of dissections) were performed in 12 patients (47%). Three patients (10%) could not be weaned from the pump; another 10 (36%) died before discharge: 2 with multisystem failure and sepsis, the other 8 with cardiogenic shock (4 with residual VSD). The only independent predictor of operative mortality, by univariate analysis, was preoperatory cardiogenic shock. All 15 survivors (100%) where followed between 5 months and 14.5 years (mean 104.5 months). Two patients died at 4 years, one at 10, another at 10.5 years. The actuarial probability of being alive after discharge was 100% at 4 years, 75% at 5, and 50% at 10 years. At last follow up only 2 patients had mild dyspnea, the remaining where asymptomatic. Surgical treatment provides an opportunity to improve this otherwise dismal survival and offers a surprising good long term result. An early diagnosis and efficient repair, before the onset of cardiogenic shock, should provide better results.
Rev Esp Cardiol 1992 Oct
PMID:[Interventricular rupture following myocardial infarction. Surgical treatment and long-term follow-up]. 147 Jul 42

A significant reduction in the extent of cell necrosis or the incidence of reperfusion-induced arrhythmias can be achieved with ischaemic preconditioning. If preconditioning was also found to be effective in protecting against global ischaemia, then this may have significant implications for the preservation of the heart during cardiac surgery. We therefore investigated this phenomenon in relation to recovery of contractile function after global ischaemia in the isolated rat heart. Isolated working rat hearts (n = 6 per group) were perfused aerobically at 37 degrees C for 20 min and contractile function recorded. This was followed by 10 min of aerobic Langendorff perfusion (control hearts) or 5 min global ischaemia (37 degrees C) + 5 min Langendorff reperfusion (preconditioned hearts). The hearts were then subjected to 10, 15, 20 or 25 min of global ischaemia (37 degrees C) and reperfusion (15 min Langendorff + 20 min working) after which function was again assessed. Preconditioning improved functional recovery after all durations of ischaemia. Thus aortic flow after 10, 15, 20 and 25 min of ischaemia and 35 min of reperfusion recovered to 84, 58, 16 and 5%, respectively, in controls and 88, 74, 55 and 20%, respectively, in the preconditioned groups. To assess whether preconditioning was effective in a surgically relevant model of hypothermic ischaemia, the experiments were repeated with longer periods (45, 70, 90, 115, 135 and 160 min) of ischaemia at 20 degrees C. Under these conditions, normothermic preconditioning increase the post-ischaemic recovery of aortic flow after 115, 135 and 160 min of ischaemic (from 36, 20 and 10%, respectively, in controls to 57, 39 and 26%, respectively, in preconditioned hearts). There was no consistent correlation between tissue high energy phosphate content and enhanced post-ischaemic recovery. Thus, we have demonstrated that ischaemic preconditioning can improve contractile function after global ischaemia in the isolated rat heart, we have defined the duration of ischaemia for which it is operative, and we have shown that this protection is additive to that of hypothermia-induced protection during ischaemia. This may have clinical implications for cardiac surgery.
J Mol Cell Cardiol 1992 Oct
PMID:Ischaemic preconditioning and contractile function: studies with normothermic and hypothermic global ischaemia. 147 13

The combined action of phosphatidylcholine preferring phospholipase C (PC-PLC) and intracellular lipases has recently been shown to cause glycerol output in energy deprived rat cardiomyocytes. In the present study we examined the effect of hypothermia and rewarming on PC-PLC evoked glycerol output in freshly isolated, calcium-tolerant myocytes. The cells were preincubated for 60 min at hypothermic (5 degrees C) or normothermic (37 degrees C) conditions in Krebs-Henseleit bicarbonate buffer (pH 7.4) supplemented with 1 mM DL-carnitine, 1% B.S.A. and 5 mM glucose. Addition of PC-PLC resulted in a significantly higher (P less than 0.05) output of glycerol in myocytes undergoing rewarming than in myocytes kept constantly at 5 degrees C or 37 degrees C. The values obtained for PC-PLC induced glycerol output (difference in glycerol output between incubations with and without PC-PLC) were 6.77 +/- 2.6 (37 degrees C), 4.54 +/- 1.7 (5 degrees C) and 22.85 +/- 5.9 (5-37 degrees C) nmol/10(6) cells.h. Rewarming in addition caused a significantly higher (P less than 0.05) leakage of lactate dehydrogenase (LDH) from the rewarmed cells as compared to cells at constant temperatures (5 degrees C or 37 degrees C). However, there was no additional effect of PC-PLC on LDH leakage. The elevated PC-PLC induced glycerol output in rewarmed myocytes was not related to a fall in the percentage of rod-shaped cells or a reduced cellular content of ATP, since no differences could be detected between the various myocyte preparations with respect to these parameters.(ABSTRACT TRUNCATED AT 250 WORDS)
J Mol Cell Cardiol 1992 May
PMID:Effects of hypothermia and rewarming on phospholipase C-evoked glycerol output in rat myocardial cells. 163 71

During cardiac surgery, the heart is infused with cold crystalloid cardioplegic solutions such as St. Thomas' Hospital (StT) solution, which contains high concentrations of K+ and Mg2+. The high K+ and Mg2+ block impulse conduction and inhibit Ca2+ influx, thereby arresting the heart and reducing cardiac oxygen consumption. Nevertheless, myocardial edema and post-operative abnormalities have been noted after cardioplegia and attributed to ischemia and reflow or to hypothermia. We found, however, that cold StT (9 degrees C) was hypotonic and induced cell swelling in the absence of ischemic injury. Cell swelling in cold StT was not due to hypothermia alone, but rather was caused by KCl influx and was prevented by partially replacing Cl- with an impermeant anion. After exposure to cold StT, cells transiently shrank to less than control volume on rewarming in physiological saline (Tyrode's solution, 37 degrees C). The transient shrinkage was blocked by ouabain suggesting that Na+ loading of depolarized hypothermic cells and Na(+)-K+ pump activation on rewarming were responsible. Hypothermic ventricular cells seem to follow Donnan equilibrium, and the product of [K+] x [Cl-] in cardioplegic solutions affects cell volume in the absence of ischemic injury.
J Mol Cell Cardiol 1991 Nov
PMID:Prevention of myocardial intracellular edema induced by St. Thomas' Hospital cardioplegic solution. 166 12

The purpose of this investigation was to determine the effect of body temperature on the pharmacodynamics (convulsant activity) of pentylenetetrazol (PTZ). Rats received an iv infusion of PTZ until the onset of maximal seizures, at which time samples of cerebrospinal fluid (CSF), brain, and blood (for serum) were obtained for subsequent determination of PTZ concentrations by HPLC. The PTZ infusion caused a decrease in body temperature of approximately 4 degrees C within 20 min and onset of seizures in approximately 40 min. Compared with animals whose temperature was maintained in the normal range by heating pads, the hypothermic rats required significantly larger doses and higher serum, brain, and CSF concentrations of PTZ to produce seizures. Other rats received an injection of brewer's yeast to produce fever. Then, PTZ was infused 6, 12, or 24 h later when body temperature was elevated by an average of 1.3, 1.1, or 0.4 degrees C, respectively. Compared with control rats, whose temperature was maintained in the normal range by heating pads, moderate hyperthermia had no significant effect on the dose and concentrations of PTZ required to produce maximum seizures. Pentylenetetrazol exemplifies a drug that can produce hypothermia which, in turn, reduces the sensitivity of rats to its pharmacologic action. Unlike the central nervous system (CNS) depressants phenobarbital and ethanol, whose pharmacologic activity in rats is enhanced at elevated body temperature, the activity of the CNS stimulant PTZ is apparently not altered by fever.
 ...
PMID:Kinetics of drug action in disease states. XXXVIII: Effect of body temperature on the convulsant activity of pentylenetetrazol in rats. 178

The effects of hypothermic ischemia and reperfusion on sarcolemma and sarcoplasmic reticulum Ca2+ transport were studied in vesicles isolated from rabbit hearts. Hypothermic global ischemia was produced by immersing hearts in saline at 4 degrees C for 3 h. Following hypothermic ischemia, reperfusion was carried out for 40 min using a Langendorff perfusion system for the working heart. Na+,K(+)-ATPase activity of sarcolemmal vesicles (SL), was not depressed by hypothermic ischemia nor by ischemia and reperfusion. The initial rate of Na(+)-Ca2+ exchange in SL vesicles was not depressed, but the maximum amount of Ca2+ uptake was increased both after hypothermic ischemia and after reperfusion. Ca2+ uptake activity of sarcoplasmic reticulum vesicles (SR) isolated from hearts subjected to hypothermic ischemia was slightly lower than that of control, and was further reduced following reperfusion. Ca(2+)-ATPase activity of SR was unaffected by hypothermic ischemia, while it was markedly lowered after reperfusion. Although the phosphoenzyme level in SR vesicles was slightly decreased, the turnover rate was reduced after reperfusion. Reperfusion injury thus took place mainly in SR while SL appeared to be tolerant to ischemia and reperfusion.
J Mol Cell Cardiol 1991 May
PMID:Effect of hypothermic ischemia and reperfusion on calcium transport by myocardial sarcolemma and sarcoplasmic reticulum. 183 91

Between January 1979 and July 1989, 15 children of Jehovah's Witnesses underwent corrective open surgery for congenital heart disease (CHD) on cardiopulmonary bypass (CPB). Ages ranged from 1.5-17 years and body weight from 9.1-63 kg, with five patients weighing less than 15 kg. Eight children were cyanotic, and two of them had had previous thoracic operations. All operations were performed in moderate to deep hypothermia using a modified version of isovolemic hemodilution with bloodless priming technique of extracorporeal circulation. Mean hematocrit levels decreased from 47.3% (36.9-70%) to 34.6% (27.2-49.1%) after hemodilution, and then to 17.9% (10.5-25.6%) during bypass. They increased again to 34.1% (24.4-50%) at the end of the operation and to 33.4% (25.1-40%) on day 12. All intra- and postoperative hematocrit levels were significantly lower (p less than 0.001). There was one postoperative death, not related to the technique. Our results demonstrate that bloodless cardiac surgery on bypass is feasible in children as shown in this special group of children of Jehovah's Witnesses. Knowing the risks of homologous blood transfusion this technique should be used more extensively in the future.
Pediatr Cardiol 1991 Jul
PMID:Open heart surgery in children of Jehovah's Witnesses: extreme hemodilution on cardiopulmonary bypass. 187 16

Chorea is a rare complication of major cardiac surgery, which has been related to profound hypothermia and circulatory arrest. We describe a case of choreic syndrome in a child which followed normothermic cardiac bypass and only became apparent clinically when the child was treated with captopril.
Int J Cardiol 1991 Feb
PMID:Chorea after cardiopulmonary bypass: exacerbation by captopril. 201 Feb 50

A 14-year-old male presented with a one week history of weakness, lightheadedness and vomiting. Bilateral pleural effusions were evident on chest radiography; electrocardiogram revealed decreased voltages. Echocardiogram, abdominal ultrasound and magnetic resonance imaging revealed a mass in an hepatic vein and the inferior vena cava extending up to and filling the right atrium. Under deep hypothermia and extracorporeal circulation the mass was removed en bloc. It originated from the hepatic vein. Pathology revealed a smooth muscle tumour intermediate between benign and malignant (atypical leiomyoma). This is the first reported pediatric primary leiomyoma of the hepatic vein. It caused the Budd-Chiari syndrome, a rare pediatric entity.
Can J Cardiol 1990 Apr
PMID:Atypical hepatic vein leiomyoma extending into the right atrium: an unusual cause of the Budd-Chiari syndrome. 218 75


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