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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 temperature on oxygenation and metabolism in perfused rat hindlimb was studied at 35 degrees C and 15 degrees C. Oxygenation of myoglobin and oxidation of cytochrome aa3 in the thigh (quadriceps) muscle were estimated from the difference spectra measured with a rapid-scanning spectrophotometer. Simultaneously, oxygen uptake and release of lactate and pyruvate were measured. (1) In hypothermia, glycolysis played a major role in energy metabolism even though Cyt aa3 was maintained in a more oxidized state than in normothermia. (2) P50 of myoglobin in perfused rat hindlimb was 5.0 mmHg at 35 degrees C, 2.3 mmHg at 25 degrees C and 1.1 mmHg at 15 degrees C. The delta H degree was -13.0 kcal/mol. (3) When about 30% of myoglobin was deoxygenated at both 35 degrees C and 15 degrees C, the oxygen uptake started to decrease and lactate release increased. (4) At 35 degrees C, the oxidation level of cytochrome aa3 was same as the oxygenation level of myoglobin. At 15 degrees C, however, the oxidation level of cytochrome aa3 was clearly higher than the oxygenation level of myoglobin. The oxygen uptake at 15 degrees C was about one third that at 35 degrees C. In conclusion, in order to maintain the aerobic condition of cytochrome aa3 in mitochondria of rat skeletal muscle, a tissue oxygen tension higher than 12 mmHg at 35 degrees C, and higher than 3 mmHg at 15 degrees C is required.
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PMID:Temperature effect on oxygenation and metabolism of perfused rat hindlimb muscle. 196 61

Reduction of the Na concentration in the Ca-free perfusion solution reduces the amount of myoglobin released by the cells when Ca is readmitted if sucrose is used to replace NaCl under mild hypothermia. When salts like cholinechloride or LiCl are used instead of sucrose, no protection is seen at any temperature. The temperature threshold above which myoglobin loss sharply increases is lowered by prolonged Ca depletion or by the addition of EGTA to the Ca-free solution. Protection by sucrose does not occur in the presence of EGTA. An increase of cell Na induced by strophanthidin during the Ca depletion phase has no effect on myoglobin release. The exponential decline in twitch tension in the early phase of Ca deprivation has the same half-live (T1/2) for Ca-free solutions containing 145 mM Na or 35 mM Na (110 mM Li or choline), but its T1/2 is prolonged if sucrose is used to replace NaCl. When 5 mM EGTA is added to the Ca-free solutions, the T1/2 is shortened and is not changed by the replacement of NaCl with sucrose. The rate of washout of Ca within the first 20 s of Ca depletion has a similar time course in a normal Na or in a Li and low Na solution. In a sucrose and low Na solution the rate of the Ca efflux is reduced. The addition of EGTA increases this rate and abolishes the slowing effect of a sucrose and low Na solution. Therefore myoglobin release during the Ca paradox does not depend on the Na gradient across the sarcolemma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of sodium on the calcium paradox in rat hearts. 311 Jul 35

Brief perfusion of heart with calcium-free medium renders myocardial cells calcium-sensitive so that readmission of calcium results in uncontrolled Ca2+ entry and acute massive cell injury (calcium paradox). We investigated the hypothesis that polyamines may be involved in the mediation of abnormal Ca2+ influx and cell damage in the calcium paradox. The isolated perfused rat heart was used for these studies. Calcium-free perfusion promptly (less than 5 min) decreased the levels of polyamines and the activity of their rate-regulating synthetic enzyme, ornithine decarboxylase (ODC), and calcium reperfusion abruptly (less than 15-180 s) increased these components. alpha-Difluoromethylornithine (DFMO), a specific suicide inhibitor of ODC, suppressed the calcium reperfusion-induced increase in polyamines and the concomitant increase in myocardial cellular 45Ca influx, loss of contractility, release of cytosolic enzymes, myoglobin, and protein, and structural lesions. Putrescine, the product of ODC activity, nullified DFMO inhibition and restored the calcium reperfusion-induced increment in polyamines and the full expression of the calcium paradox. Putrescine itself enhanced the reperfusion-evoked release of myoglobin and protein in the absence of DFMO. Hypothermia blocked the changes in heart ODC and polyamines induced by calcium-free perfusion and calcium reperfusion and prevented the calcium paradox. These results indicate that rapid Ca2+-directed changes in ODC activity and polyamine levels are essential for triggering excessive transsarcolemmal transport of Ca2+ and explosive myocardial cell injury in the calcium paradox.
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PMID:Polyamines mediate uncontrolled calcium entry and cell damage in rat heart in the calcium paradox. 311 63

A 23-year-old male was admitted to hospital with severe dehydration and hypokalemic myopathy due to secondary aldosteronism. On admission serum sodium and chloride were markedly elevated to 198 mEq/l and 169 mEq/l, respectively, and serum potassium was down to 2.3 mEq/l. Serum electrolytes were normalized by transfusion therapy, but subsequently rhabdomyolysis grew worse due to metabolic abnormalities such as dehydration, hypothermia, oppressive ischemia and metabolic acidosis, at the same time transient polyuria and the elevation of serum myoglobin and enzymes originating in muscle tissue were observed. Serum CPK went up to 26,532 IU/l on the sixth day and other enzymes reached a peak following CPK. Dexamethasone was administered when the increase in enzyme levels caused the patient to fall into a stupor. He rapidly regained consciousness from the 15th day after admission, and he was able to stand up on the 29th day. Serum enzymes originating in muscle tissue decreased gradually to the normal range by the 30th day and no renal failure occurred.
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PMID:A case of severe dehydration with marked rhabdomyolysis. 402 Dec 12

Serum time-activity curves for myoglobin, creatine-kinase (CK) and its isoenzyme MB were determined during and after coronary bypass surgery and aortic valve replacement. Hypothermic potassium cardioplegia was the method employed to initiate cardiac arrest. Cardiac myoglobin and CK-MB release rates were maximal 0.5 to 1.0 h post aortic cross-clamp release (PACR) with maximal concentrations at 1 and 4 h PACR respectively. The cardiac release ceased within 5 h PACR but was followed by a noncardiac release with maximal concentrations from 10 to 35 h PACR. The cardiac myoglobin release was significantly lower in the coronary bypass group, whereas no significant intergroup difference was observed for CK-MB. The cumulative CK-MB release corresponded roughly to about 5 g of myocardium.
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PMID:Myocardial and non-myocardial release of myoglobin and creatine-kinase MB following cardiac operations with hypothermic potassium cardioplegia. 697 88

Temperature-induced metabolic change was studied with isolated rat hindlimb muscle to elucidate how tissue viability is maintained under hypothermia. The hindlimb was perfused with Krebs-bicarbonate buffer containing 4% (w/v) polyvinylpyrrolidone (PVP-40T) in a flowthrough mode at 35-8 degrees C. When the temperature was lowered, the following results were observed: (i) Vascular resistance (defined as perfusion pressure divided by flow rate) increased proportionally with elevation of the viscosity of the perfused medium, suggesting that the capillary bed in the perfused muscle is maintained under a similar condition under these temperatures; (ii) the Arrhenius plot of the O2 uptake rate showed a break at ca. 20 degrees C; (iii) the rates of O2 uptake and lactate release decreased, but the lactate/pyruvate ratio increased even under aerobic conditions; (iv) oxygenation of myoglobin and oxidation of cytochromes increased, suggesting a reduced electron-transfer rate in spite of improved or sufficient oxygenation of the tissue. Based on these results, we concluded that oxidative phosphorylation is more affected by temperature than glycolysis, and thus under hypothermia, the role of glycolysis in energy production increases in rat skeletal muscle, especially below 20 degrees C.
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PMID:Effect of hypothermia on skeletal muscle metabolism in perfused rat hindlimb. 868 91

The level of glutathione and the activity of its exchange enzymes (glutathione reductase, glutathione-S-transferase, glutathione peroxidase), the content of malonic dialdehyde were studied in the red blood levels of 70 patients operated on under hypothermal perfusion for correction of acquired cardiac diseases. The plasma concentrations of myoglobin were also measured. There was a relationship of the time course of changes in the parameters in question to the depth of the body's cooling during surgical interventions. Shallow hypothermia (30-34 degrees C) caused a compensatory increase in the activity of glutathione peroxidase (by more than 30%) and in the concentration of glutathione (by more than 60%) at the cooling stage. Moderate hypothermia (26-29 degrees C) produced no impact on the level of glutathione and the activity of its exchange enzymes while deeper hypothermia (25 degrees C or below) induced decreases in the levels of glutathione (by more than 30 degrees C) and suppressed the activity of all the tested enzymes of its exchange. At the same time there are elevated concentrations of malonic dialdehyde at the warming-up stage and during early postperfusion. Myoglobin washing into plasma occurs under all temperature conditions of perfusion at the warming-up stages and in the early postperfusion period, but it is most profound in deeper hypothermia, which is caused by the toxic effect of oxygen whose plasma solubility increases with lowered temperatures.
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PMID:[Effect of various perfusion temperature regimens in heart surgery with extracorporeal circulation on glutathione levels and activity of enzymes of glutathione metabolism in erythrocytes]. 915 86

Release of myoglobin (Mg) into the plasma and increase of its concentration during perfusion are a result of muscle cell injury during artificial circulation. High values of oxygen tension and hypothermia during cardiosurgery are sources of active oxygen forms damaging the biomembranes. We investigated release of Mg into the blood and relationship of this parameter with oxygen tension and depth of cooling. 95 patients were tested during open-heart surgery and operations on the main vessels: 25 perfusions at 30-32 degrees C, 41 at 26-29 degrees C, and 20 at 12-14 degrees C. The patients were divided into subgroups depending on arterial blood oxygen pressure. Myoglobin release into the blood was minimum under mild hypothermia and moderate PaO2. The degree of myoglobinemia increased with elevation in PaO2. As body temperature decreased, the concentration of Mg increased and differences between the groups with different PaO2 leveled. Critical myoglobinemia (30-fold vs. the initial value) was observed in the group with the deepest hypothermia (14 degrees C). Since the myocardium contains high amounts of Mg, it is clear that loss of this heme-containing protein impairs the feeding of the myocardium and, hence, decreases its contractility.
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PMID:[Causes of myoglobinemia in surgery with artificial circulation]. 1122 Sep 41

Disorders of skeletal muscle and peripheral nervous system are collectively called neuromuscular disorders (NMD). Important for anesthesia is that these disorders show various symptoms and have a high risk during general anesthesia. Especially administration of succinylcholine and volatile anaesthetics may cause problems. Under special circumstances opioids, nondepolarising muscle relaxants and intravenous anaesthetics can interfere with this kind of disorder, too. Complications during and after anaesthesia may result in malignant hyperthermia, malignant hyperthermia-like reactions and primary or secondary changes relating to the underlying NMD. These include cardiac and respiratory problems, dysautonomia as well as hypothermia or hyperthermia. Thus the perioperative management must be determined individually to assure the best possible safety for each patient. Preoperative examination such as ECG, echocardiography, respiratory function test including arterial blood-gas analysis, x-ray of the thorax, neurological status, and extended serum chemistry (such as CK and myoglobin) needs to be done. For premedication no drugs suppressing respiratory function should be administered. Regional anesthesia should be used whenever possible, especially in patients with respiratory and cardiac problems. The dosage of all recommended drugs should be as low as possible. Volatile anaesthetics should not be administered in the majority of NMD and succinylcholine is contraindicated, with the exception of myasthenia gravis. Additionally to the usual intraoperative monitoring, the invasive measurement of blood pressure allows frequent blood-gas analysis. It is obligate to monitor neuromuscular function and body temperature. During recovery special attention should be paid to maintain normal body temperature and electrolytes and acid-base status. The discharge of the patient from the recovery area to the normal ward should be performed only after respiratory function is normalized.
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PMID:[Anesthesia in neuromuscular disorders. Part 1: introduction]. 1186 84

Ninety six patients were examined during operations on the open heart and great vessels: 25 perfusions were performed at a temperature of 30-32 degrees C; 41 perfusions at 26-29 degrees C; 10 at 23-26 degrees C; 20 at 12-14 degrees C. It was found that with superficial hypothermia and moderate PaO2, blood myoglobin (MG) release was minimal and the count and activity of platelets were optimal. The degree of myoglobinemia increased as PaO2 rose. As the body's temperature lowered, the blood concentrations of MG, its differences smoothed in the subgroups with different PaO2 values. Critical myoglobinemia (over 30 times higher than the baseline values) was noted in a group with superdeep cooling to a temperature of 14 degrees C. By taking into account the fact that the myocardium contains large quantities of MG, loss of this heme-containing protein involves myocardial blood supply disorders and hence decreased myocardial contractility. A considerable platelet loss entails higher postoperative hemorrhagic diathesis and requires efforts in correcting coagulopathies.
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PMID:[Hypothermal perfusion: protection or damage?]. 1209 46


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