Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Creatine kinase BB isoenzyme (CK-BB) was detected intraoperatively in 22 of 25 patients undergoing aortocoronary bypass surgery, both in the coronary sinus and in the mixed venous blood. In a group of 10 patients in whom selective intracavitary profound hypothermic arrest was used, CK-BB values were lower than in another group of 10 patients, in whom controlled ventricular fibrillation with moderate total body hypothermia was instituted. This latter group also had higher levels of CK-MB. Patients who developed acute myocardial infarction immediately prior to or during the surgical intervention had the highest CK-BB values. This enzyme appeared as early as 15 minutes after the institution of cardiopulmonary bypass and disappeared within 6 hours. It is considered that part of the BB isoenzyme in serum of patients undergoing heart surgery is of myocardial origin.
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PMID:Detection of creatine kinase BB isoenzyme in sera of patients undergoing aortocoronary bypass surgery. 30 Jun 59

Six patients with severe medical disorders and profound hypothermia are presented who had elevated total serum creatine phosphokinase (CPK) and CPK-MB isoenzyme activity without clinical or postmortem evidence of acute myocardial infarction. Experiments in dogs indicate that hypothermia reduces total CPK activity in both striated and myocardial muscle resulting in increased serum enzyme activity. These data suggest that profound hypothermia may result in diffuse striated and cardiac muscle cellular injury without evidence of discrete infarction with consequent release of CPK-MB isoenzyme into serum.
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PMID:Creatine phosphokinase MB isoenzyme in hypothermia: case reports and experimental studies. 62 78

This study examined the pathophysiology of the myocaridal damage produced by direct current shock over a dose range of 10 to 90 watt-seconds, applied directly to the heart in 26 dosgs. The extent of injury produced was assessed with creatine kinase depletion and light and electron microscopy, and was correlated with in vivo imaging and tissue distributions of the isotopes technetium-99m pyrophosphate and thallium-201. Changes in intramyocardial temperature and regional myocardial blood flow were also measured. Uptake of technetium-99m pyrophosphate occurred exponentially with graded increases in shocks, and this agent was more sensitive than thallium-201 in detecting injury both on imaging and at tissue level. The threshold for significant injury was approximately 30 watt-seconds, and on electron microscopy a characteristic feature was marked dehiscence of the intercalated disks between the damaged myocytes. The use of different-size paddles did not appear to affect the total number of cells damaged. However, with large paddles the injury was more superficial and spread over a wider area. With short time intervals between successive shocks, a greater amount of injury occurred, in part because of a compounding of the thermal component of the damage. Hypothermia can reduce the degree of injury.
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PMID:Cardiac damage produced by direct current countershock applied to the heart. 76 Apr 77

It has been proposed that a single preoperative dose of a corticosteroid may protect the myocardium from ischemic injury during open heart surgery. To test this hypothesis, a prospective, randomized, double blind study was carried out in ninety-five patients undergoing coronary bypass surgery using intermittent ischemic arrest with systemic and local hypothermia. Half the patients received 2 gm (approximately 30 mg/kg) of methylprednisolone 2 hours prior to the initiation of cardiopulmonary bypass and the other half received a placebo. Postoperative electrocardiograms and blood levels of serum creatine phosphokinase (CPK), lactic dehydrogenase (LDH), and serum glutamic oxalacetic transaminase (SGOT) were compared in the two groups. No apparent difference was noted in the number of patients with significantly elevated levels of CPK, LDH, or SGOT or in the number with positive isoenzyme patterns of CPK and LDH. Moreover, there was no significant difference in the mean values of CPK, LDH, or SGOT between the two groups. The number of patients with electrocardiographic evidence of myocardial injury (10 per cent) was the same in both groups and no difference was noted in (1) the ease with which patients could be weaned from cardiopulmonary bypass, (2) postoperative arrhythmias, (3) postoperative bleeding, (4) postoperative respiratory insufficiency, and (5) length of hospital stay. It is concluded that a single preoperative dose of 2 gm of methylprednisolone offers no demonstrable protection to the myocardium from the effects of ischemia during coronary artery bypass surgery.
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PMID:Effect of methylprednisolone on myocardial preservation during coronary artery surgery. 77 98

Intraoperative myocardial protection was evaluated in two groups of patients undergoing coronary surgery in whom different techniques for cardiac arrest were utilized. In group A, profound selective myocardial hypothermic (15 to 18 C) arrest was achieved by perfusing a coolant (7 to 10 C) into the left ventricular cavity and the coronary circulation. The average anoxic arrest time was 82.5 +/- 27 minutes. In group B, ventricular fibrillation and moderate hypothermia were used. Group A patients showed rapid physiologic recovery, low average myocardial creatinine phosphokinase (MB-CK) isoenzyme levels (7.8 IU) , and a well-preserved myocardial ultrastructure. In group B, three patients showed abnormal physiologic recovery; six patients needed postoperative inotropic support; and in seven patients, electron-microscopy revealed irreversible focal changes. The average MB-CK isoenzyme level was 85.6 IU. Analysis of our data demonstrates that when myocardial protection during coronary bypass grafting is achieved by selective profound intracavitary and coronary cooling, there is physiological, ultrastructural, and biochemical evidence of less intraoperative myocardial damage than when ventricular fibrillation is applied.
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PMID:Selective intracavitary and coronary hypothermic cardioplegia for myocardial preservation.Clinical, physiologic, and ultrastructural evaluation. 98 67

The relative efficacy of potassium-induced ischemic arrest using buffered, isosmotic potassium (25 mEq/liter) was compared with hypothermic arrest in an experimental protocol employing an intact canine heart preparation. Myocardial function (LVSW, dp/dt max), serum creatine phosphokinase levels, myocardial perfusion, and light and electron microscopical examination of the heart were assessed in five groups of 5 dogs each. There was one control group (90 minutes of bypass, no anoxia) and four experimental groups, each subjected to 1 hour of ischemic arrest and 30 minutes of reperfusion, comparing normothermic ischemic arrest (NIA), hypothermic ischemic arrest (myocardial temperature less than 25 degrees C) (HIA), normothermic potassium arrest (NKA), and hypothermic potassium arrest (HKA). Myocardial function decreased significantly following NIA and NKA but remained essentially equal in the control, HIA and HKA groups. Serum creatine phosphokinase analysis documented a significant increase in each group of animals: 2,250 mU after NIA, 1,778 mU after NKA, 1,388 mU after HIA, 1,220 mU after HKA, and 838 mU after control bypass. Left ventricular myocardial perfusion was unmeasurably low after NIA, reduced to 111 m/100 gm of tissue/min after NKA, and increased to 165 to 188 ml/100 gm/min in the control, HIA and HKA groups. Electron microscopical studies showed a range of myocardial changes, from probably irreversible damage after NIA to similar but less diffuse changes after NKA, and to potentially reversible changes after HKA and HIA with the least alteration from control after HIA. The results indicate that potassium arrest alone is not as effective as hypothermia in preventing ischemic injury, and the combination of hypothermia with a single 150 cc administration of potassium (25 mEq/liter) does not appear to provide significant additional protection.
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PMID:Myocardial injury associated with potassium arrest. 99 81

The following abnormalities were observed during the first 24 hours of admission for 162 drug overdosage (OD) episodes in 152 patients: abnormal chest x-ray films; increased A-aO2 gradient; elevated white blood cell (WBC) counts; elevated serum enzyme levels; gross myoglobinuria; skin lesions suggestive of pressure necrosis; and abnormal electrocardiograms. Many sputum cultures were positive for single or multiple potentially pathogenic organisms. These correlations existed: all patients with OD duration of less than 12 hours were hyperthermic; as temperatures increased so did WBC counts; hyperthermic patients had higher creatine phosphokinase (CPK) values than those with hypothermia or normothermia; patients with skin lesions had higher temperatures and CPK values and longer OD duration; serum enzme levels increased with increasing OD duration; patients with CPK levels greater than 10,000 mU/ml had myoglobinuria; and patients with the most abnormal chest x-ray films had higher temperatures and larger A-aO2 gradients. Incidence of pneumonitis is low, even with abnormal chest radiograms, leukocytosis, hyperthermia, and positive sputum cultures. Abnormal temperatures and leukocytosis are probably secondary to stress, hypoxemia, acidosis, and specific drug ingestion rather than infection.
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PMID:Physiologic and biochemical abnormalities in self-induced drug overdosage. 119 Sep 31

The objective of this study was to assess the influence of temperature on the coupling among energy failure, depolarization, and ionic fluxes during anoxia. To that end, we induced anoxia by cardiac arrest in anesthetized rats maintained at a body temperature of either 34 degrees C or 40 degrees C, measured extracellular K+ concentration (K+e), and froze the neocortex through the exposed dura for measurements of phosphocreatine (PCr), creatine (Cr), ATP, ADP, and AMP, glucose, glycogen, pyruvate and lactate content after ischemic intervals of maximally 130 s. Free ADP (ADPf) concentrations were derived from the creatine kinase equilibrium. Hypothermia reduced the initial rate of rise in K+e, and delayed the terminal depolarization; however, both hypo- and hyperthermic animals showed massive loss of ion homeostasis at a K+e of 10-15 mM. The initial rate of rise in K+e did not correlate to changes in ATP, or ATP/ADPf ratio, suggesting that temperature changes per se may control the degree of activation of K+ conductances. The results clearly showed that, in both hyper- and hypothermic subjects, energy failure preceded the sudden activation of membrane conductances for ions. The results indicate that temperature primarily influences membrane permeability to ions like K+e (and Na+), and that cerebral energy state is secondarily affected. It is proposed that the higher rate of rise of K+e at high temperatures accelerates ATP hydrolysis primarily by enhancing metabolic rate in glial cells.
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PMID:Changes of labile metabolites during anoxia in moderately hypo- and hyperthermic rats: correlation to membrane fluxes of K+. 142 48

This retrospective analysis tests the hypothesis that topical cardiac hypothermia is an unnecessary adjunct to intraoperative myocardial protection and an avoidable cause of pulmonary morbidity in patients with coronary disease receiving blood cardioplegia. The hospital records of 150 nonrandomized consecutive patients undergoing elective and emergency isolated coronary revascularization were reviewed. All patients received multidose cold blood cardioplegia followed by warm blood cardioplegic reperfusion distributed through grafts. Fifty patients received iced slush, 50 received topical 4 degrees C saline, and no topical cooling was used in 50 others. Patients groups were comparable in number of grafts (3.7 versus 3.5 versus 3.5) and crossclamp time (61 versus 62 versus 61 minutes). More emergency operations were performed in the patients receiving no topical hypothermia (12/50 versus 8/50 versus 7/50). Postoperative x-ray films were reviewed by a radiologist who did not know of patient grouping. Postoperative results were comparable in hemodynamics, inotropic requirements (10/50 ice versus 8/50 saline versus 5/50 no cooling), myocardial infarction (1/50 versus 2/50 versus 2/50), and enzymes (aspartate aminotransferase myocardial band creatine kinase). No patient died. Ice topical hypothermia (versus no topical cooling) was associated with more left pleural effusions (25/50 versus 9/50; p less than 0.05), atelectasis (33/50 versus 18/50; p less than 0.05), elevated left hemidiaphragms (13/50 versus 0/50; p less than 0.05), and longer postoperative hospitalization (11.2 versus 8.5 days; p less than 0.05). Topical 4 degrees C saline reduced diaphragmatic elevation and pleural effusion (versus topical ice) but was associated with more atelectasis (34/50 versus 18/50; p less than 0.05) than no topical cooling. These data suggest that routine topical hypothermia is an unnecessary adjunct to blood cardioplegic protection in patients with coronary disease, since supplemental topical cooling does not improve postoperative hemodynamics or reduce inotropic requirements, enzyme release, or prevalence of postoperative myocardial infarction, and it increases pulmonary morbidity, which can be reduced by its avoidance.
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PMID:Topical cardiac hypothermia in patients with coronary disease. An unnecessary adjunct to cardioplegic protection and cause of pulmonary morbidity. 151 52

Thyroid storm is a rapid decompensation of severe hyperthyroidism which can best be described by the three criteria of hyperthermia, tachycardia and altered mental state with severe agitation. There has to be a precipitating factor such as infection, iodine contamination, surgery or even I-131 treatment. Severe hyperthyroidism not fulfilling the criteria of thyroid storm can also be an indication for emergency treatment, particularly in the elderly with heart disease. Suppressed serum TSH and elevated free T4 levels are essential to confirm the diagnosis. When rapidly available, radioiodine uptake of the thyroid can be useful. Therapy aims at rapidly reducing the active circulating hormone pool, hypermetabolic state, tachycardia, and finally hormone synthesis. Thyroid secretion can be blocked by ioipanoic acid or ipodate while hypermetabolic state can be reduced with beta-blockers or calcium channel-blockers. Treatment of hyperthyroidism in patients with iodine contamination is a real therapeutic challenge. Myxoedema coma, a complication of severe hypothyroidism, is defined by hypothermia (rectal temperature less than 36 degrees C), bradycardia, slow mentation, precipitating factor such as infection or drug overdose, and increased serum creatine phosphokinase levels. Diagnosis of severe hypothyroidism should be confirmed by serum measurements of TSH and free T4. Treatment consists of general supporting measures including rewarming, correction of serum electrolyte disturbances, and adequate alimentation. Thyroid hormone treatment should initially be aggressive using either 300-400 micrograms of T4 or 20-40 micrograms of T3 intravenously. Cortisone therapy may be added. Patients should be under close monitoring as arrhythmias and myocardial infarction are frequent complications of myxoedema coma and/or its treatment with thyroid hormones.
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PMID:Thyroid emergencies. 173 98


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