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

Cold blood with potassium, 34 mEq/L, was compared with cold blood and with a cardioplegic solution. Three groups of 6 dogs had 2 hours of aortic cross-clamp while on total bypass at 28 degrees C with the left ventricle vented. An initial 5-minute coronary perfusion was followed by 2 minutes of perfusion every 15 minutes for the cardioplegic solution (8 degrees C) and every 30 minutes for 3 minutes with cold blood or cold blood with potassium (8 degrees C). Hearts receiving cold blood or cold blood with potassium had topical cardiac hypothermia with crushed ice. Peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of the contractile element, pressure volume curves, coronary flow, coronary flow distribution, and myocardial uptake of oxygen, lactate, and pyruvate were measured prior to ischemia and 30 minutes after restoration of coronary flow. Myocardial creatine phosphate (CP), adenosine triphosphate (ATP), and adenosine diphosphate (ADP) were determined at the end of ischemia and after recovery. Changes in coronary flow, coronary flow distribution, and myocardial uptake of oxygen and pyruvate were not significant. Peak systolic pressure and lactate uptake declined significantly for hearts perfused with cold blood but not those with cold blood with potassium. ATP and ADP were lowest in hearts perfused with cardioplegic solution, and CP and ATP did not return to control in any group. Heart water increased with the use of cold blood and cardioplegic solution. Myocardial protection with cold blood with potassium and topical hypothermia has some advantages over cold blood and cardioplegic solution.
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PMID:Cold blood as the vehicle for potassium cardioplegia. 51 80

We evaluated the effects of methylprednisolone sodium succinate (MPSS) on 60 minutes of myocardial ischemia during profound (5 degrees C) topical cardiac hypothermia (ice chips) in a canine right heart bypass preparation. The ventricular function curve shifted to the right and downward, but not significantly, after ischemia, and stroke work declined significantly for both control and treated dogs. Contractility (rate of rise of left ventricular pressure and maximum velocity of the contractile element) declined for both groups but not significantly. Total coronary flow, oxygen consumption, and metabolism of lactate and pyruvate were not different for control and treated dogs. Ultrastructure of the outer and inner myocardium did not demonstrate benefit from MPSS. Intracellular and extracellular edema of moderate severity was slightly worse in the subendocardium, and reversible mitochondrial injury of a mild to moderate degreee was symmetrically present. Ice-related injury was not noted. We were unable to deomonstrate that pretreatment with MPSS favorably alters cardiodynamics or ultrastructure after 60 minutes of profound topical cardiac hypothermia.
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PMID:Topical cardiac hypothermia: the effect of methylprednisolone sodium succinate. 65 47

The extent of myocardial protection afforded by a procaine cardioplegic solution during cardiac ischemia has been evaluated and compared with the protection seen using a potassium cardioplegic solution. An isolated cat heart model was employed, and ventricular function parameters, intramyocardial gas tensions, and postischemic myocardial edema were measured and compared following 60 minutes of induced ischemia at 37 degrees C. and 27 degrees C. There was no significant improvement in recovery of postarrest ventricular function when procaine cardioplegia was used during normothermic ischemia. When used at 27 degrees C., however, both cardioplegic solutions were associated with significantly better recovery of postarrest ventricular function, although there was less myocardial edema formation in the potassium-treated hearts. Results of this study indicate that procaine-induced cardioplegia provides myocardial protection during anoxic cardiac arrest which is additive to that afforded by hypothermia alone. In addition, procaine cardioplegia results in postarrest functional recovery which is similar to that seen with potassium cardioplegia.
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PMID:Effects of procaine-induced cardioplegia on myocardial ischemia, myocardial edema, and postarrest ventricular function. A comparison with potassium-induced cardioplegia and hypothermia. 66 57

Forty-two operations were done on patients suffering from extensive nephrolithiasis. The procedure was performed in the complete absence of blood, using a special clamp. No hypothermia was applied. The special clamp was placed at the renal hilum. The meantime of ischemia amounted to 17.8 min. The technique of this operative procedure is described. Complications, postoperative urograms, late follow-ups, and the results of differential isotope clearances are discussed.
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PMID:[Kidney operations in ischemia (author's transl)]. 68 88

In the open-chested dog, coronary flow reduction results in a decrese of regional myocardial temperature (T). We assessed the contribution of T decrease to changes in refractoriness and conduction delay attributed to ischemia. The independent effect of regional hypothermia on effective refractory period (ERP) was a linear function of the temperature (ERP = -b T +a) with a -r = 0.97 0.02 in 11 dogs. The effect on conduction time of a ventricular premature beat was a linear function of the dog T at both endocardium (-r = 0.95 +/- 0.02) and epicardium (-r = 0.96 +/- 0.01). A 75% reduction in coronary flow resulted in a mean T decrease of 1.0 +/- 0.3 degrees C. The T decrease was sufficient to mask the effects of ischemia on shortening of the ERP. Furthermore, the conduction delay of ventricular premature beats during 75% coronary flow reduction could be accounted for by the decrease in T alone in five of seven dogs. We conclude that changes in refractoriness and conduction during acute coronary flow reduction in the open-chested dog are due to the composite effects of ischemia and the decrease in regional temperature. The open-chested model may have important limitations in understanding the electrophysiologic effects of acute coronary insufficiency. However, it may have important applications in defining the electrophysiologic environment at the time of coronary artery surgery.
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PMID:Electrophysiologic effects of partial coronary flow reduction in the exposed canine heart. Effects of ischemia and ischemic-induced regional hypothermia on refractoriness and conduction delay. 68 78

A new colloid hyperosmolar solution with high concentrations of proteins, potassium, and glucose has been favorably compared with a crystalloid, intracellular, and hyperosmolar solution (Sacks II) for 24-hr hypothermic storage of ischemic and nonischemic canine kidneys. Sixty minutes of warm ischemia was overcome by all kidneys flushed with the colloid hyperosmolar solution. In four of six ischemic kidneys flushed with Sacks' solution the function returned to normal limits. Hypothermic storage (24 hr) without warm ischemia did not cause any deleterious effects on either one of the flushed group of kidneys. Thirty minutes of warm ischemia followed by 24-hr hypothermic storage was tolerated by most of the kidneys (83%) flushed with the colloid hyperosmolar solution and one-half of the kidneys flushed with the crystalloid hyperosmolar solution. Sixty minutes of warm ischemia and 24-hr hypothermic storage was detrimental to 50% of the kidneys flushed with the colloid hyperosmolar solution.
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PMID:Comparison of sacks and a new colloid hyperosmolar solution for hypothermic renal storage. 70 72

In order to determine the incidence of subendocardial ischemia after open heart surgery, subendocardial blood flow was monitored in 171 patients subjected to mitral and/or aortic valve replacement or coronary revascularization by on-line calculation of Diastolic (DPTI) and Systolic Pressure Time Index (TTI). Body hypothermia with an esophageal temperature of 25 degrees C and magnesium-aspartate-procaine cardioplegia were applied for myocardial protection. Ten patients developed low cardiac output state with two early deaths. In the two patients with fatal low cardiac output DPTI/TTI remained below 0.8. In the remaining 8 patients DPTI/TTI rose to 1.4 after a mean recovery time of 36 hours. In 161 patients (94%) no low cardiac output state evolved and DPTI/TTI rose to 1.3 within 60 min. after termination of cardiopulmonary bypass. Our results indicate that body hypothermia of 25 degrees C combined with magnesium-aspartate-procaine cardioplegia can reduce the incidence of subendocardial ischemia, but does not prevent this complication completely after anoxic times beyond 60-70 minutes.
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PMID:[Monitoring myocardial performance after open heart surgery by calculation of diastolic and systolic pressure time index (author's transl)]. 71 54

In 53 patients with mitral- or aortic-mitral valve disease, the content of ATP and lactate of the papillary muscles resected at the time of valve replacement was investigated at the beginning of ischemic arrest and at the time of reperfusion. Profound body hypothermia (25 degrees C) and injection cardioplegia using magnesium-aspartate-procaine were applied for myocardial protection. In hypertrophic papillary muscles the myocardial ATP content decreased at a slower rate (ATP decay 12% of the initial value after 60 minutes of ischemia) than in normal papillary muscles obtained from patients with isolated mitral stenosis (ATP decay 33% of the initial value after 40 minutes of ischemia). 20% of the patients required temporary inotropic circulatory support postoperatively for 12 to 88 hours. The ATP content of the papillary muscles of these patients differed only little from those, in who no myocardial failure occurred. However the myocardial lactate levels were higher in patients in whom a low cardiac output state evolved.
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PMID:[Behaviour of ATP and lactate in human papillary muscle during profound hypothermia and injection cardioplegia with magnesium-asparatate-procaine (author's transl)]. 75 Dec 88

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

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


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