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

Direct cardiac and vascular effects of the antikaliuretic diuretic potassium-canrenoate were measured in cardio-surgical patients during extracorporal circulation and immediatly after operations, each time in neuroleptanalgesia. During "steady state" extracorporeal circulation (aorta cross-clamped, constant flow rate of heart-lung-machine, constant hypothermia), in 13 patients no significant influence on peripheral circulation was found after i.v.-injection of 800 mg potassium-canrenoate. Neither arterial perfusion pressure (representing an arterial vascular reaction) nor changes in oxygenator-volume (indicating venous vasodilation or contraction) demonstrated significant differences in comparison to a control group. After cardiac surgery haemodynamic measurements were performed for a period of 60 minutes in 10 patients given 800 mg potassium-canrenoate. In comparison with a control group (n = 6), no significant differences in arterial pressure, heart rate, cardiac index and pulmonary arterial pressure were found. Left ventricular measurements, using a catheter tip manometer, revealed no direct positive inotropic effect of a single i.v.-injection of potassium-canrenoate. In acute myocardial failure during anaesthesia or in "low cardiac ouptut" following open heart surgery no improvement in myocardial contractility is obtained by i.v.-application of potassium-canrenoate; at the present there seems no alternative to other positive inotropic agents such as calcium, glucagon, dopamine, orciprenaline and epinephrine.
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PMID:[Extrarenal effects of potassium-canrenoate. Haemodynamic investigations during neuroleptanalgesia in cardiosurgical patients (author's transl)]. 31 42

In a prospective study, patients who had an ejection fraction of 40% or more and who were undergoing elective coronary artery operation were randomly divided into three groups that differed in the method of anaerobic substrate enhancement during cardiopulmonary bypass. Group 1, the controls (n = 157), received no additional glucose, insulin, and potassium solutions and experienced immediate spontaneous defibrillation (10%), transmural myocardial infarction (10.3%), malignant ventricular arrhythmias (26%), and severe atrial arrhythmias (20%). Group 2 (n = 120) received a bolus of hypertonic glucose, insulin, and potassium in the pump perfusate before aortic cross-clamping. In this group, the rate of spontaneous defibrillation was 41%, of transmural infarction, 8.3%, of malignant ventricular arrhythmias, 31%, and of severe atrial arrhythmias, 19%. Group 3 (n = 114) had the aortic root continuously infused with glucose, insulin, and potassium solution at 4 degrees C during aortic cross-clamping. This group was significantly improved; the rate of spontaneous defibrillation was 60%, there were no transmural myocardial infarctions and the incidence of severe atrial arrhythmias was 6% and that of malignant ventricular arrhythmias, 5%. It is proposed that the superior clinical results in Group 3 resulted from better myocardial preservation achieved by more efficient means of providing continuous anaerobic substrate, coronary washout, and elution of lactic acidosis, uniform global hypothermia, and direct supplemental myocardial potassium in addition to mere cardioplegic effects.
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PMID:Reduction of intraoperative myocardial infarction by means of exogenous anaerobic substrate enhancement: prospective randomized study. 31 65

The hemodynamic and cardiac biochemical effects of global ischemic arrest during cardiopulmonary bypass (CPB) were studied in 54 animals and compared to seven animals without ischemic arrest. Ischemic arrest alone reduced the first derivative of left ventricular force of contraction (LV dF/dt) to 52 percent of control 10 minutes after resuming function and to 64 percent after 1 hour of reperfusion. Cardiac output was depressed to 52 percent of control after 10 minutes of reperfusion, and to 74 percent of control after 60 minutes of reperfusion. In six animals, moderate hypothermia (26 degrees C.) resulted in no protection of cardiac function from ischemic arrest, whereas profound hypothermia to 18 degrees C. resulted in values of LV dF/dt and cardiac output nearly equivalent to the CPB control group (no arrest). A continuous infusion of a hyperkalemic hypothermic solution slightly improved the degree of protection over hypothermia alone. The sarcoplasmic reticulum (SR) isolated from hearts which had undergone 60 minutes of ischemic arrest bound significantly less calcium when the isolation was done after 10 minutes of reperfusion as well as when it was done after 60 minutes of reperfusion. The time to spontaneous release of calcium from the SR also was significantly longer. Moderate hypothermia did not result in improved SR function, whereas deep hypothermia induced by local cooling or by hypothermic potassium infusion retained SR function at normal levels. Oxidative phosphorylation of mitochondria isolated after 60 minutes of reperfusion was also depressed. The mitochondrial respiration rate after normothermic ischemic arrest was 155 natoms of oxygen per minutes versus 237 natoms for the hypothermic hyperkalemic group. Respiratory control index was 5.5 for the normothermic group versus 9.4 for the hypothermic group. It is concluded that hypothermia, whether effected by surface cooling or by hypothermic potassium infusion, allowed full recovery of hemodynamic and biochemical functions within 1 hour of reperfusion.
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PMID:Myocardial depression after elective ischemic arrest. Subcellular biochemistry and prevention. 42 95

Nifedipine, a slow-channel calcium blocker, is thought to provide useful myocardial protection during prolonged total ischemia and reperfusion. An isolated, isovolumic, feline heart model was used to asses the effectiveness of nifedipine in both cardioplegic (100 microgram/10 ml) and noncardioplegic (10 microgram/10 ml) doses for providing myocardial preservation during 90 minutes of hypothermic ischemic arrest and 45 minutes of normothermic reperfusion. Use of nifedipine was compared to hypothermia (27 degrees C) alone and to hypothermia with potassium cardioplegia. Ventricular function was assessed by recovery of isovolumic left ventricular developed pressure and dP/dt. Myocardial carbon dioxide tension (PCO2) and myocardial oxygen tension (PO2) were measured by mass spectrometry. Potassium cardioplegia and the higher dose of nifedipine resulted in immediate asystole. The rates of rise of PCO were greatest in the group receiving 10 microgram nifedipine and in the control group. The rates of rise in the two cardioplegic groups were significantly lower. Recovery of ventricular function was significantly lower with low-dose nifedipine than with potassium cardioplegia. Higher dose nifedipine resulted in a return of function, which was no different than with potassium cardioplegia. Morphologic protection was better with higher dose nifedipine and potassium cardioplegia than with either low-dose cardioplegia or hypothermia alone. These results demonstrate that nifedipine in a cardioplegic dose results in preservation of myocardial structure and function that is similar to that obtained with potassium cardioplegia. In lower noncardioplegic dose, nifedipine does not appear to offer additional protection compared to hypothermia alone. Whether persistent depression of ventricular contractility will limit nifedipine's clinical usefulness as a myocardial protection agent will require further study.
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PMID:Comparison of myocardial protection with nifedipine and potassium. 44 71

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

1 The effect of the antidysrhythmic aminosteroid, ORG 6001, on hypothermia-induced ventricular fibrillation was investigated in cats anaesthetized with pentobarbitone. 2 ORG 6001 (total dose, 10 mg/kg, by intravenous injection) reduced both the incidence of fibrillation and the temperature at which it occurred. The number of animals that survived to 16 degrees C was increased. 3 This protective effect of ORG 6001 could not be explained by changes in respiratory acidosis, plasma concentrations of sodium and potassium, or by changes in the action potential of excised hypothermic ventricular muscle. The hypothermia-induced elevation of blood lactate was less in cats treated with the aminosteroid. 4 Over a limited temperature range, ORG 6001 prolonged the P wave and QRS duration and shortened the QTc interval. ST segment elevation was slightly reduced in the drug-treated group. J deflections were observed but were not correlated with the development of fibrillation. 5 The onset of fibrillation was not considered to be due to temperature differences between the myocardium and arterial blood or between localized areas of the left ventricular wall.
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PMID:The effect of aminosteroid, ORG 6001, on hypothermia induced ventricular fibrillation in the cat. 46 98

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

Rats with dietary potassium (K) depletion have an altered breathing pattern compared to age matched control rats. The K depleted rats also have a decreased body weight gain, basal metabolic rate and body temperature. In this study, age matched controls are underfed (UFC) to match for body weight gain and metabolic rate and controls are exposed to different ambient temperatures to alter metabolism and body temperature. Compared to UFC rats with the same body weight and basal metabolic rate the K depleted rats breathe slower and with a larger tidal volume in the basal state and in response to hypercapnia and hypoxia. With heat stress body temperature is increased in K depleted rats as is metabolic rate. While frequency is increased it is still slower than in controls at the same ambient and body temperatures. We conclude that the low metabolic rate and body temperature of K depleted rats is not the cause of the altered breathing pattern. In addition, it is shown that the hypothermia of K depletion is present only at ambient temperatures below the thermoneutral zone and that is is apparently due to an inability of the K depleted rat to increase metabolic heat production with cold stress.
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PMID:Breathing in the potassium depleted rat: the role of metabolic rate and body temperature. 50 31

Our entire experience (33 patients) of combined aortic and mitral valve replacement was reviewed. In 20 patients, coronary perfusion with moderate hypothermia (28-32 degrees C) was used with 7 operative deaths (35% mortality). Catecholamines were used in 14 patients (70%). Potassium cardioplegia was used in 13 patients with no mortality (P less than 0.02) and use of catecholamines in only 4 (P less than 0.05). These data suggest that potassium cardioplegia is the method of preference for myocardial preservation for combined aortic and mitral valve replacement.
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PMID:Improving results in combined aortic and mitral valve replacement using cold potassium cardioplegia. 51 7


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