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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 pentobarbital on survival times of mice exposed to oxygen, 5 per cent, were studied over a large dosage range in normal mice and in mice made tolerant to the effect of barbiturates. Tolerance was induced by pretreatment with phenobarbital, 210 mg/kg, for three days, which increased the median anesthetic dose (AD50) for pentobarbital from 34 to 53 mg/kg. In nontolerant mice there was a dose-related increase in mean survival times for doses between 35 and 60 mg/kg, with a maximum increase to 303 per cent above control. At doses of more than 60 mg/kg survival times progressively decreased toward control. For tolerant mice survival time as a function of pentobarbital dosage was shifted to the right, i.e., protection necessitated higher doses. This shift was not explained by lower brain concentrations of pentobarbital in tolerant animals, but rather parallelled the increased tolerance to the anesthetic effect of the barbiturate. The authors conclude that in this model the protective effect of barbiturate is a function of the anesthetic effect rather than the barbiturate concentration in brain per se. Hypothermia (29 C) resulted in an increase in mean survival time comparable to that in barbiturate-treated animals. This supports the hypothesis that protection is ultimately a function of decreased cerebral metabolism, whether produced by anesthesia or by hypothermia. This model measures only the effect on spontaneous respiration during hypoxia. It is possible that other mechanisms are involved if barbiturates protect in other situations, such as during or after periods of complete ischemia.
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PMID:Barbiturate protection in tolerant and nontolerant hypoxic mice: comparison with hypothermic protection. 45 57

Fortyone of 187 infants undergoing corrective surgery for their congenital cardiac lesions using profound hypothermic circulatory arrest were randomly selected for metabolic studies. Deep hypothermia of 21 to 22 degrees C core temperature was reached by two different techniques: 1. Perfusion cooling by extracorporeal circulation (ECC-C) 2. Surface cooling with ice bags combined with perfusion cooling (SC + ECC-C) After circulatory arrest (34.2 min. ECC-C v.s. 46.7 min. SC + ECC-C) bypass rewarming was used in both groups. The metabolic reaction to these interventions are described. No significant differences in acid base status in oxygen consumption, lactate concentration, serum electrolytes (K+, Na+, Ca++,Cl-) and serum enzyme activity (CPK, alpha-HBDH, LDH, SGOT, SGPT) could be demonstrated between the two groups of patients during the entire course of cooling, circulatory arrest and rewarming. The glucose concentration was significantly lower in the ECC-C group during the entire period of operation. Total cooling time was significantly shorter in the group without surface cooling. (ECC-C: 12 min, v.s. SC + ECC-C: 64 min). Since no favourable effects of the SC + ECC-C method on systemic metabolism could be demonstrated and operative results were similar we now prefer the time-saving ECC-C technique.
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PMID:The effects of deep hypothermia and circulatory arrest on systemic metabolic state of infants undergoing corrective open heart surgery: a comparison of two methods. 46 66

Hypothermia remains the primary adjunct employed to lower cellular metabolism during various cardiac procedures. In these experiments, left ventricular myocardial oxygen consumption (MVO2) and transmural blood flow (TBF) were measured during cardiopulmonary bypass with the range of temperatures used clinically. Determinations were made in empty beating normothermic hearts and after potassium cardioplegia at 37, 32, 28, 22, 18, and 15 degrees (K+ = 15--37 meq/L: Hct 25 volumes %). Oxygen content of the total coronary sinus collection was compared with a large volume arterial sample using a Lex-O2-Con-TL analyzer (vs Van Slyke, R = 0.98). Transmural blood flow was measured at each temperature using microspheres (8 microns), and perfusion was maintained at 80 mmHg. Asystole (37 degrees) alone decreased MVO2 from 5.18 +/- 0.55 to 1.85 +/- 0.20 ml O2/min/100 g of left ventricle or approximately 65% (p less than 0.001). With progressive cooling to 15 degrees an additional 82% decrement in oxygen uptake occurred during asystole (p less than 0.001). During asystole at 37 degrees the decrease in MVO2 was reflected mainly by a large decrement (p less than 0.01) in TBF (1.27 +/- 0.19 to 0.74 +/- 0.17 ml/min/g of mean left ventricular flow). However, with cooling below 32 degrees, the arteriovenous oxygen difference narrowed progressively (p less than 0.001) while TBF paradoxically returned to control levels. Endocardial/epicardial flow ratios were not altered by cooling. These data not only confirm earlier reports describing a sequential drop in MVO2 with incremental myocardial cooling, but also establish MVO2 levels for perfused hearts arrested by potassium at lower temperatures (18--15 degrees). Moreover, as transmural blood flow becomes independent of metabolic necessity during hypothermia, coronary autoregulation appears to be impaired, possibly affecting detrimental tissue over perfusion.
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PMID:The effects of hypothermia on myocardial oxygen consumption and transmural coronary blood flow in the potassium-arrested heart. 46 72

The effects of a dopamine antagonist (pimozide) and an alpha-adrenergic receptor blocking agent (phenoxybenzamine) on caffeine-induced changes in oxygen consumption. body temperature, blood glucose and non-esterified fatty acids (NEFA) were studied in mice. Both drugs had no effect on the increase of the oxygen consumption produced by caffeine. The decline of the body temperature induced by caffeine was not significantly influenced by pimozide, while phenoxybenzamine accentuated the hypothermic effect of caffeine. The results indicate that alpha-adrenergic and dopamine receptors do not play an essential role in the caffeine-induced stimulation of overall metabolism and hypothermia.
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PMID:Failure of phenoxybenzamine and pimozide to diminish changes in oxygen consumption and body temperature produced by caffeine. 48 30

Canine kidneys were subjected to continuous nonpulsatile perfusion using 200 ml of a perfusate containing 50 g/l albumin. When optimal oxygenation was achieved, perfusate K+ contents were unchanged for 24 h, indicating adequate membrane function but tended to increase thereafter. Lowered oxygen pressures resulted in significant cellular K+ loss during the first hours of perfusion. During oxygenated perfusion, glucose and free fatty acids (FFA) were oxidized in considerable amounts with a preferential consumption of octanoate. A capacity for long-chain FFA oxidation became obvious when the octanoate had been used up, but the amount of these FFA in the perfusate depended preferentially on FFA being liberated from tissue lipids during the 1st day of perfusion. Glucose consumption rates were highest during the first 2 days of perfusion but the subsequent reduction of the metabolic rate was not accompanied by an accumulation of lactate. Thus medium-chain FFA and glucose should be supplied to the continuously perfused kidney in hypothermia and optimal oxygenation of the perfusate should be guaranteed. However, it seems to be unnecessary to supply exogenous long-chain FFA.
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PMID:Free fatty acid and glucose metabolism during hypothermic perfusion of canine kidneys. 48 47

Myocardial performance was evaluated intraoperatively in 20 patients undergoing myocardial revascularization when hypothermic potassium cardioplegic arrest was used. High concentrations of potassium (20 mEq/L) were compared to normal concentrations of potassium (5 mEq/L) in hypothermic cardioplegic solutions. The cardioplegic arrest period averaged 53 +/- 3 minutes in the high potassium group and 54 +/- 4 minutes in the low potassium group, Intraoperative calculation of ejection fraction and end-diastolic volume was accomplished by the technique of radiocardiography. All data were grouped according to end-diastolic volume index (EDVI) for both high (HK) and low (LK) potassium comparisons. Comparisons between high and low potassium groups demonstrated no significant differences in ejection fraction (HK = 66%, LK = 61%), cardiac index (HK = 2.74 L/min/m2, LK = 3.0 L/min/m2), stroke work (HK = 36 gm.m/m2, LK = 30 gm.m/m2), oxygen consumption as measured by left heart double product (HK = 9,438; LK = 9,209), and myocardial compliance (HK = 2.8 cc/torr, LK = 4.2 cc/torr at the post-cardioplegic arrest period). The role potassium plays in producing a rapid cardiac arrest is well accepted. Its protective effect on the preservation of high-energy phosphate stores is postulated, but its addition to perfusion hypothermia does not appear to enhance the protective effect observed with perfusion hypothermia alone.
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PMID:Protection of myocardial function not enhanced by high concentrations of potassium during cardioplegic arrest. 49 23

Potassium (34 mEq/L) cardioplegia was induced with cold blood (CBK) in three groups of six dogs undergoing 60 minutes of myocardial ischemia at a systemic temperature of 27 degrees +/- 2 degrees and a myocardial temperature of 7 degrees +/- 2 degrees C (crushed ice). Group 1 (CBK) animals were reperfused initially with 400 ml cold blood over 8 to 10 minutes at increasing pressures of up to 75 mm Hg. Group II (CBK-K) dogs were reperfused in the same manner as Group I with the addition of potassium chloride, 30 mEq/L. In Group III (CBKG-KG) glutathione, 30 mg/100 ml, was added to both the pre- and postischemic perfusions with CBK. After 30 minutes of reperfusion control studies were repeated. Heart rate, peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of contractile element, pressure-volume curves, coronary flow distribution, muscle stiffness, and heart water were not significantly different from control values. Total coronary flow and myocardial uptake of oxygen, lactate, and pyruvate did not serve to separate the three groups; the same was true for right ventricular creatine phosphate, adenosine triphosphate, and adenosine diphosphate during ischemia and recovery. Ultrastructural myofibrillar lesions were noted in all groups. thus, postischemic cardioplegia and use of a physiological reducing agent do not enhance CBK cardioplegia with topical and systemic hypothermia.
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PMID:Cold-blood potassium cardioplegia: evaluation of glutathione and postischemic cardioplegia. 50 72

The heart and diaphragm efficiency seems to be an actively regulated variable. It alters in prolonged adaptation (raises in adaptation to hypoxia; diminishes in cold adaptation which means an increase in heat production per unit of muscle's contractile activity). Enhancement of noradrenaline calorigenic effect on skeletal muscles during cold adaptation is corroborated in an isolated diaphragm. Diminishing of the heart and diaphragm efficiency in thyrotoxicosis suggests participation of thyroid hormones in formation of adaptive decrease of muscular contraction efficiency in cold adaptation. The heart efficiency raises in hypothermia and, probably, in limitation of the myocardium oxygen supply. Possible mechanisms of changes of muscular contraction efficiency are discussed.
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PMID:[Changes in the efficiency coefficient of the heart and diaphragm during cold adaptation]. 51 Jun 17

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

A technique of myocardial protection using a perfusion circuit in deep hypothermia via the ascending aorta or by selective cannulation of the coronaries has been used over a period of 2 years in almost 200 patients undergoing surgery requiring prolonged aortic clamping. It ensures rapid and homogeneous cooling of the myocardium (10-12 degrees C) and meets its reduced oxygen needs. It may be completed by cardioplegia (infusion of potassium chloride or lidocaine using an automatic syringe at a determined level). This simple technique permits a rapid spontaneous return of normal effective cardiac action. No low cardiac output syndromes have been seen since it has been used. Laboratory, histological, biochemical and haemodynamic studies carried out have confirmed its harmless nature.
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PMID:[Myocardial protection by perfusion in deep hypothermia (10 degrees C) with or without cardioplegia (author's transl)]. 53 Aug 27


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