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

The livers of 20 pigs were preserved for up to 16 hours, applying hypothermia (4 degrees C) and hyperbaric oxygenation (3 ata). As a preparation solvent we used in one group the solution by Lie (17) which is rich in potassium and glucose, and in the other group the cryoprecipitated serum by Belzer (5). After 8 and 16 hours of preservation, the fine structure was examined light- and electronmicroscopically. After 8 hours of preservation, there were only little reversible changes in both groups. After 16 hours, both groups showed distinct changes of the endoplasmatic reticulum e. g. desorganisation, vesicular dilatation, and dissociation of the mural ribosomes. In addition, there were swellings of mitochondriae and Kupffer's cells. These changes were particularly distinct after preservation in cryoprecipitated serum. In this group a cellular depletion of glucogen was noticeable.
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PMID:[Swine liver ultrastructure following hypothermia and hyperbaric oxygenation preservation]. 70 10

The measurement of lactate dehydrogenase (LDH) release into perfusates after hypothermic storage was found to be a reliable index of ischemic injury of rabbit kidneys. Kidneys were exposed to warm and cold ischemia for varying periods. Each kidney was perfused before and after storage at simple hypothermia with 25 ml of a modified Collins solution. The venous effuent was collected in 5 ml fractions. Total LDH activity was measured in the first fraction after storage and used as a measure of ischemic tissue damage. It was confirmed that increasing the period of cold ischemia result in significant increases in LDH activity. The release of LDH into perfusates was then used to compare kidney damage after preservation with various fluids. With this method, it was not possible to demonstrate any difference in the extent of tissue damage after preservation with sodium-rich vs. potassium-rich perfusion fluid. Addition of steroids, vitamins and essential amino acids did not prevent or reduce tissue damage, estimated in this way. The effects of adding cryoprotectants to the perfusion fluid varied; LDH release following addition of 5% DMSO was significantly greater, and after addition of 5% glycerol smaller than the release after perfusion with a modified Collins solution alone. Stepwise addition of DMSO up to 20% resulted in serious tissue damage with a large LDH release into the perfusate.
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PMID:LDH release into perfusates of preserved kidneys. 78 32

1 The effect of altering the ionic balance of the cerebrospinal fluid (CSF) on cloacal temperature of unanesthetized pigeons kept at room temperature (20-25 degrees C) was examined by injection or infusion of solutions of different ionic composition into a cannulated lateral cerebral ventricle. 2 An increase in the concentration of calcium ions caused a fall in temperature and behavioural sedation. The effects were the same whether the calcium was present as calcium chloride or as the calcium disodium salt of ethylenediamine tetra-acetic acid (CaNa2EDTA). 3 When the concentration of sodium ions in the CSF perfusate was increased by addition of NaCl or that of calcium ions was decreased by addition of Na2EDTA a rise in temperature was often produced but this was not consistent. NaCl sometimes had either no effect or lowered the temperature. Na2EDTA while producing a rise when first injected failed to do so when repeated a few hours, 24 h and often 72 h later. Prolonged infusion of either agent caused intense behavioural excitement leading to death. 4 Potassium ions, like sodium ions, caused a rise in temperature but only when infused continuously. Behavioural excitement was only rarely observed. 5 Magnesium produced a fall in temperature. The concentration required was much higher than that of calcium but the hypothermia was more prolonged suggesting a slower elimination of the magnesium ions from the CSF. Magnesium ions caused tremors, nystagmus and ataxia as opposed to sedation caused by calcium. 6 All these were central effects as they were not obtained when the substances were injected intravenously. 7 Since changes in body temperature of the pigeon produced by injection of calcium or sodium ions into the CSF were similar to those seen in various species of mammal, it is concluded that the relative concentration of these ions within the brain plays an important role in establishing the temperature setpoint in both birds and mammals.
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PMID:Sodium and calcium ions in the control of temperature set-point in the pigeon. 81 41

Isolated rat liver was studied before, during, and after hypothermic perfusion at 5 C for 24, 48, or 72 hr with an acellular perfusate consisting of 7% bovine serum albumin in Kreb-Ringer buffer containing glucose, penicillin, and streptomycin. Bile production ceased at 5 C but resumed when the temperature was raised to 35 C. The rate of flow and the total amount produced was unaffected by 24 hr of hypothermia but decreased when the cooling period was extended to 48 and 72 hr. The data of other workers was used to show a correlation between bile flow and oxygen consumption by the liver. Cooling also caused the release of potassium into the perfusate but it was quickly reaccumulated after rewarming; however, the extent and rate of reaccumulation decreased as the cooling period increased, as did the ability of the livers to retain the ion. Urea synthesis did not cease after cooling and after rewarming, the rate of synthesis increased as the period of hypothermia was lengthened. The maximum concentration of urea in the perfusate was found when rewarmed livers had produced 200 mumol of urea but at this point, control livers had produced 280 mumol. The concentration of glucose in the perfusate of livers maintained at 35 C showed peaks at 2 and 9 to 10 hr after the start of perfusion. After cooling for 24 hr these peaks arose at 2 and 7 hr after rewarming, but with 48 hr of hypothermia, these peaks were higher and appeared at 2 and 4 hr. When the cooling period was extended to 72 hr, only a single peak was seen 2 hr after rewarming. These results suggest that rat liver can be cooled to 5 C for 24 hr with little effect on its functional characteristics but a marked decline becomes apparent when the cooling period is extended beyond 24 hr. None of the livers studied was transplanted after perfusion and it remains to be seen how the functional tests conducted in vitro correlate with the ability of the livers to support life.
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PMID:Maintenance of the functional state of isolated rat liver by hypothermic perfusion with an erythrocyte-free medium. 83 68

A total of 204 patients, ages 3 months to 84 years, underwent open-heart surgery with the aid of cardiopulmonary bypass with moderate hypothermia. For protection of the myocardium, cardioplegia was induced by washing out the coronary arteries with an iced, buffered, isoosmolar, potassium-based infusate. After aortic cross-clamping, the aortic root or individual coronary arteries were perfused with 500 to 2,000 c.c. of an aqueous solution (at zero to 4 degrees C.) containing 20 mEq. of potassium. Periods of ischemic arrest as long as 208 minutes have been well tolerated, with only two of the eleven hospital deaths considered heart related. Defibrillation occurred spontaneously in 41 per cent and after one shock in 47 per cent of patient, without apparent correlation between duration of ischemia and restoration of effective rhythm.
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PMID:Myocardial protection with cold, ischemic, potassium-induced cardioplegia. 83 26

Extracellular potassium activity, [K+]0, was continuously measured using potassium specific microelectrodes in the cerebral cortex of cats before and after hypoxic or anoxic insults. Two patterns of [K+]0 increase were seen. A slow, linear rise occurred during hypoxia and hypothermia and was correlated with changes in mean blood pressure (B/P). A fast, complex, exponential rise resembling spreading depression occurred during anoxia and was unassociated with B/P changes. The fall of [K+]0 after reversal of the insult was described by a single exponential function with rate constants from 0.009 to 0.0194 sec-1. It is suggested that the linear rise is primarily a result of sodium pump inhibition and that the exponential rise is due to a superimposed sudden increase in cell membrane permeability perhaps secondary to transmitter release. The kinetics of the fall of [K+[0 is consistent with the normalization of the sodium and potassium gradients across the cell membranes secondary to Na+-K+ATPase activity.
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PMID:The kinetics of extracellular potassium changes during hypoxia and anoxia in the cat cerebral cortex. 84 9

Urethral obstruction induced in adult male cats caused clinical signs identical with those observed in naturally occurring disease. Central nervous system depression, anorexia, dehydration, vomiting, muscle weakness, and hypothermia occurred. Weight loss (due to water loss and catabolism), metabolic acidosis, mild hyponatremia, hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia, hyperglycemia, azotemia, and hyperproteinemia were also observed. Serum amylase, alkaline phosphatase, and alanine aminotransferase activities were normal. Ten of 13 cats (group 1), with 72 hours' induced obstruction but not treated with parenteral fluids, died either before the obstruction was relieved or within 8 days afterward. Eight cats (group 2) with induced obstruction for 49 to 98 hours developed severe clinical and biochemical alterations. Treatment with a multiple-electrolyte solution, in addition to relief of urethral obstruction, resulted in favorable clinical and biochemical responses. These cats survived and were clinically healthy at 9 to 10 days after relief of obstruction. It was concluded that use of a multiple-electrolyte solution to correct acidosis, restore circulatory volume, and enhance renal excretion of potassium was effective supportive therapy after urethral obstruction was removed.
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PMID:Characterization and treatment of water, electrolyte, and acid-base imbalances of induced urethral obstruction in the cat. 87 80

An isolated perfused working rat heart model was used to investigate the extent to which various protective agents, used either singly or in combination, were able to increase the resistance of the heart to periods of transient ischemia. The aim of the studies was to develop a solution which, if infused into the coronary vessels just prior to the onset of ischemia, would rapidly induce arrest and would also counteract several of the deleterious cellular changes known to occur during myocardial ischemia. Agents with induce cardiac arrest, modify cellular ion loss, affect substrate utilization, energy production and energy stores, affect coronary vessel diameter and cell swelling, prevent dysrhythmias, and affect metabolic rate were investigated. The additive effects of these agents were evaluated. An aqueous solution was formulated which contained high concentrations of potassium and magnesium, in combination with adenosine triphosphate, creatine phosphate and procaine. This solution increased the recovery of the ischemic (37 degrees C for 30 min) rat heart from 0% to 93%. The safe period of ischemia could be further increased by the use of hypothermia.
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PMID:Cellular protection during myocardial ischemia: the development and characterization of a procedure for the induction of reversible ischemic arrest. 93 20

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

Hypothermic arrest, potassium arrest, and ischemic arrest, either singly or in combination, with or without coronary perfusion were studied in an isolated perfused rat heart preparation. Procedures that permitted the maintenance of high cellular levels of adenosine triphosphate (ATP) and creatine phosphate during arrest, e.g., coronary perfusion with hypothermic solutions or solutions containing 16.0 mM potassium, produced a fully reversible arrest with complete cardiac recovery. Cardiac arrest and coronary flow were related to the degree of hypothermia and the concentration of potassium in the coronary perfusate, and the minimum conditions required to induce complete cardiac arrest were ascertained. The effects of hypothermia and potassium were additive; total cardiac arrest could be obtained by combining small evaluations of potassium with moderate hypothermia. Under these conditions, cellular high-energy phosphates were maintained, and complete recovery was possible. Under conditions in which arrest was obtained without maintaing coronary perfusion, e.g., ischemic arrest, cellular high-energy phosphates declined rapidly, and the hearts exhibited poor recoveries. Some protection could be afforded to the ischemic myocardium by topical hypothermia or by combining the ischemia with potassium arrest. In both instances, ATP and creatine phosphate were maintained at higher levels, and improved recoveries were observed.
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PMID:Hypothermic arrest and potassium arrest: metabolic and myocardial protection during elective cardiac arrest. 111 43


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