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

By uni- and multivariate analysis, predictors of surgical mortality and postoperative angina were identified retrospectively in 189 patients having had coronary arterial bypass surgery over the period 1978-1984. After modification of these risk factors, surgical outcome was followed up in another 178 patients undergoing operation from 1985 to 1987. The surgical mortality of 7% in the first series was closely associated with postoperative signs of acute myocardial injury. All deaths occurred in patients having at least 3 out of 5 pre- and peroperative risk factors: triple vessel/left main coronary arterial disease, incomplete revascularization, no propranolol treatment, Bretschneider cardioplegia other than "HTP"-solution with blood preperfusion and perioperative vasopressor support. The procedures of cardiac protection were modified. St Thomas multidose potassium cardioplegia and general hypothermia were introduced, perioperative propranolol treatment increased and bypass time decreased. Improved cardiac protection with this regime was seen in the patients operated in 1985-1987 when compared with the first series with regard to perioperative vasopressor support (8 vs 33%, P less than 0.001), spontaneous operative defibrillation (72 vs 52%, P less than 0.001), postoperative arrhythmias (20 vs 43%, P less than 0.001), peak levels of serum enzymes (P less than 0.001), myocardial infarction (7 vs 19%, P less than 0.001) and hospital mortality (2 vs 7%, P less than 0.05). The incidence of freedom from symptoms at 3 months was also increased in the patients undergoing operation from 1985 to 1987 (72 vs 61%, P less than 0.05). Even small centers can improve their surgical outcome by carefully analysing their own results and modifying the identified risk factors.
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PMID:Improved outcome of coronary arterial bypass surgery in a small center after identification and modification of peroperative risk factors. 229 14

Intramyocardial voltage and myocardial oxygen consumption were measured in the fibrillating heart between the temperatures of 37 degrees C and 25 degrees C and in the arrested heart after infusion of potassium cardioplegic solution in 10 adult mongrel dogs. Electrical activity from the myocardium was recorded using specially designed plunge electrodes, and intramyocardial voltage was monitored by an in-line voltmeter. Myocardial oxygen consumption gradually decreased from 5.8 +/- 0.6 ml O2/min at 37 degrees C to 2.3 +/- 0.5 ml O2/min at 25 degrees C. In contrast, hypothermia did not cause a similar decrease in intramyocardial voltage which remained within a range of 1.8 +/- 0.5 mV to 2.4 +/- 0.5 mV between the temperatures of 37 degrees C and 25 degrees C. The infusion of potassium cardioplegic solution resulted in a dramatic decrease in voltage to 43 +/- 5 microV, and myocardial oxygen consumption fell to 0.5 +/- 0.3 ml O2/min. Our data demonstrated that the mean voltage of the fibrillating heart remains constant between the temperatures 37 degrees C and 25 degrees C and myocardial oxygen consumption decreases with hypothermia, which suggests that voltage does not correlate with the level of myocardial oxygen consumption. Myocardial oxygen consumption and intramyocardial voltage, however, decrease dramatically when cardioplegia is instituted.
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PMID:Effect of hypothermia and cardioplegia on intramyocardial voltage and myocardial oxygen consumption. 230 99

The myocardial protective effect of intravenous (i.v.) lidoflazine with potassium cardioplegia and hypothermia (28 degrees C) was investigated in 21 greyhounds. Animals were injected a single dose of cardioplegia (30 ml/kg body weight) and subjected to 120 minutes of ischaemia and 60 minutes of reperfusion. Ten dogs served as controls (Group C) and 11 dogs received i.v. lidoflazine (1.25 mg/kg b.w.) (Group L). Myocardial drill biopsies for the adenosine triphosphate (ATP) and the creatine phosphate (CP) levels were obtained. Hemodynamic measurements were made at intervals. In Group C, no dog could be weaned from bypass, whereas all 11 dogs in Group L came off bypass and maintained their circulation for 15 minutes. After a 120 minute ischemic period, the ATP and CP contents diminished significantly in both groups. Following reperfusion, the ATP level was 28% of the control level in Group C (p less than 0.005) and 38% in Group L (p less than 0.01). The CP levels showed an overshoot in both groups. There was no significant difference between the groups. In Group L animals, cardiac output (CO) and mean aortic pressure (MAP) were significantly reduced after bypass; from 5 +/- 1/min to 3.2 +/- 1, from 156 +/- 26 mmHg to 82 +/- 11 mmHg respectively (p less than 0.005). Left ventricular minute work (LVMW) also deteriorated markedly from 9.7 +/- 2 kg-m to 3.2 +/- 1 (p less than 0.005). The use of lidoflazine achieved considerable protection in terms of survival, but did not prevent the severe loss of high-energy phosphates in this experimental model.
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PMID:Myocardial protective effects of lidoflazine during ischemia and reperfusion. 230 23

The effect of verapamil administered before aortic cross-clamping was assessed in 40 patients undergoing elective coronary artery bypass grafting. Myocardial protection consisted of cold blood potassium cardioplegia, topical ice slush, and moderate (28 degrees C) systemic hypothermia. Patients were randomly divided into two groups: group 1 (18 patients) received verapamil (0.1 mg/kg up to 10 mg) intravenously three to five minutes before aortic cross-clamping; group 2 (22 patients) did not (control). Myocardial injury was assessed by cumulative release of the cardiac-specific isoenzyme of creatine kinase (CK-MB) after release of the aortic cross-clamp. Release of CK-MB was significantly lower in the verapamil group (44.9 +/- 6.2 versus 72.2 +/- 9.0 IU at 24.5 hours, p = 0.005). Calculated total infarct size was also lower in the verapamil group (6.0 +/- 0.9 versus 8.9 +/- 1.0 g-Eq, p = 0.035). Individual CK-MB release curves showed either one or two peaks. The two-peak pattern was more frequent in control patients (18 of 21 control patients versus 6 of 18 verapamil patients, p = 0.001) and was associated with a larger infarct size. Atrioventricular pacing was not required in any verapamil patient, but was needed in 1 control patient. We conclude that verapamil administered before aortic cross-clamping protects against myocardial injury during coronary artery bypass grafting with no increase in the incidence of atrioventricular block.
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PMID:Reduction of myocardial injury with verapamil before aortic cross-clamping. 231 Feb 48

The cellular response to hypotonic stimulation was studied with videometric methods in 266 proximal renal tubules dissected from Carassius auratus (goldfish). In hypotonic solutions (low NaCl), cells underwent rapid swelling followed by gradual shrinking toward isotonic volume (volume-regulatory decrease phase, VRD). Hypothermia (8 degrees C), increased extracellular potassium (15, 25, and 40 mM), quinine (0.1 mM), barium (0.5 mM), 4,4'-diisothio-cyanostilbene-2,2'-disulfonic acid (DIDS; 0.02 mM), acetazolamide (0.1 mM), decrements in extracellular bicarbonate, and increases in extracellular chloride impaired VRD. Ouabain (1.0 mM), furosemide (0.1 mM), and the chloride channel blocker 5-nitro-2-(3-phenylpropylalanine) benzoate (NPPB; 0.001 mM) had no effect. While VRD occurred in the absence of extracellular calcium influx, addition of the calcium ionophore A23187 (0.01 mM) in the presence of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA; 2.0 mM) impaired this process both in acidic and alkaline media. Trifluoroperazine (0.01 mM) reversibly inhibited VRD. The effect of this calmodulin inhibitor could not be overridden with the cationic ionophore gramicidin (0.5 microM). The data suggest that Carassius proximal renal tubular cells volume regulate in hypotonic solutions by the loss of KCl and osmotically obligated water. We postulate that the main efflux of potassium is through a calcium-gated potassium channel with its counter ion extruded through a calmodulin-regulated Cl(-)-HCO3- exchanger.
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PMID:Possible role of basolateral cell membrane in proximal renal tubule osmoregulation. 233 Oct 23

The effectiveness of various methods of myocardial protection were evaluated retrospectively in 59 infants less than 12 months of age who underwent open heart surgery for ventricular septal defect with severe pulmonary hypertension. Intermittent aortic clamping and electrically induced ventricular fibrillation (EF) were employed in 13 infants (Group I), and potassium induced cold cardioplegia and topical cardiac cooling (TC) were used in 14 infants (Group II). Six infants in Group II had additional EF after declamping of the aorta (Group II-A) but the rest of Group II infants did not have any EF (Group II-B). Profound hypothermia and circulatory arrest were utilized in 17 infants (Group III). Cold blood cardioplegia with TC were used in 15 infants (Group IV). Moderate hypothermia were used during cardiopulmonary bypass in Group I, II and IV. The operative mortality for Group I was 15% and was 0% for Group II, III and IV. The incidence of spontaneous resumption of cardiac beat following declamping of the aorta were 33.3, 0, 100, 94.1, 93.3% for Group I, II-A, II-B, III and IV respectively. The urinary output obtained in the postoperative 72 hours was significantly lower in Group I than in Group II, III and IV (Group I less than II less than IV less than III).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical evaluation of various methods of myocardial protections during open heart surgery in infants with ventricular septal defect and severe pulmonary hypertension]. 239 43

When hypothermic patients appear to be dead, the decision to resuscitate may be difficult due to lack of reliable criteria of death. To discover useful prognostic indicators, we reviewed the hospital charts of nine hypothermic victims of snow avalanches (group A: median value of rectal temperature, 29.6 degrees C; range, less than 12 degrees C to 34 degrees C) and of 15 patients with hypothermia following acute drug intoxication and/or cold exposure (group B: 28.8 degrees C; range, 25.5 degrees C to 32 degrees C. In group A, plasma potassium level on admission was extremely high (14.5 mmol/L; range, 6.8 to 24.5 mmol/L) compared with that obtained in group B (3.5 mmol/L; range, 2.7 to 5.3 mmol/L). All patients in group A were in cardiorespiratory arrest. None could be successfully resuscitated despite effective rewarming by cardiopulmonary bypass or peritoneal lavage. In contrast, all of the patients in group B recovered from hypothermia, including two in cardiorespiratory arrest. Thus, extreme hyperkalemia during acute hypothermia appears to be a reliable marker of death. It might be used to select those patients in whom heroic resuscitation efforts can be useful.
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PMID:Hyperkalemia. A prognostic factor during acute severe hypothermia. 240 46

The possible myocardial protective effect of oral propranolol in combination with potassium cardioplegia and hypothermia was investigated in 30 greyhounds, divided into 2 sub-groups, by determining the changes in myocardial ATP and CP levels, ultrastructural changes and the changes in hemodynamics after a 2-hour period of myocardial ischemia. In group 1, in animals with multiple doses of cardioplegia during the 2-hour ischemic period, preoperative treatment with propranolol did not have a significant myocardial protective effect. In group 2, in animals with a single dose of cardioplegia, during the 2-hour ischemic period, propranolol resulted in a trend of improved survival, although the myocardial ATP and CP levels were the same in both sub-groups. In addition, the multiple doses of cardioplegia in group 1 caused increased subcellular edema in the myocardium. This study suggests that oral propranolol treatment may provide additional myocardial protection during ischemic periods when used with potassium cardioplegia and hypothermia. The mechanism of this effect is not established, but could relate to reduced transmembrane calcium influx.
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PMID:Oral beta-blockade with hypothermic potassium cardioplegia in cardiac surgery: is there an additive protective effect? 242 43

The effect of variation in temperature (37-32 and 27 degrees C) on electrical and mechanical activity of depolarized and isoprenaline- or barium-reactivated guinea pig ventricular strips was studied. Lowering the temperature brings a marked prolongation of isoprenaline-induced slow action potentials. In addition the maximal rate of depolarization was strongly reduced at lower temperatures. These effects were observed at an extracellular Ca2+ concentration of either 0.9 or 2.5 mM. The accompanying mechanical activities was significantly increased by reduction in temperature. Barium-induced slow action potentials were similarly affected by temperature variations. These observations suggest that hypothermia exert a sort of calcium antagonistic action probably coupled to a reduction of repolarizing outward potassium currents.
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PMID:Effect of temperature on isoprenaline- and barium-induced slow action potentials in guinea-pig ventricular strips. 243 Aug 55

Developmental differences in ischemic and potassium cardioplegic arrest were evaluated in newborn (birth to 7 day old) and adult (6 to 12 month old) New Zealand white rabbit hearts isolated and perfused by Langendorff's method. An extracellular space washout technique was used to measure intracellular sodium and calcium in the two age groups after ischemia alone, after normothermic and hypothermic cardioplegia, and after cardioplegia with reperfusion. Although the intracellular ionic contents of nonreperfused adult hearts after 30 and 40 minutes of ischemia were identical, there was a twofold elevation in intracellular sodium level after 40 minutes of ischemia in the newborn hearts. Adult hearts arrested by normothermic potassium cardioplegia demonstrated no alteration in the intracellular ionic content, whereas in the newborn hearts, potassium cardioplegia produced excess intracellular calcium loading before reperfusion, which was greater than that occurring with ischemia alone. When hypothermia (12 degrees C) was combined with cardioplegic arrest, a prereperfusion influx of sodium and calcium was not observed in the newborn hearts, and ionic reperfusion injury was blunted in both newborn and adult hearts. These studies demonstrate that the newborn heart is more susceptible than the adult to both ischemia and cardioplegia. This may be due to age-dependent differences in transmembrane passive diffusion, sodium/calcium exchange, or calcium slow channel properties and suggests alternative myocardial protective strategies for the newborn infant.
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PMID:Developmental changes in reperfusion injury. Comparison of intracellular ion accumulation in ischemic and cardioplegic arrest. 245 61


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