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

The effect of pentobarbital and hypothermia on the development of ischemic brain edema was studied in 23 rhesus monkeys undergoing transorbital middle cerebral artery occlusion. Fifteen additional animals served as unclipped controls. Regional cortical cerebral blood flow (rCBF), arteriovenous oxygen content difference (AVDO2), and regional cortical metabolic rate of O2 (rCMRO2) were measured hourly until sacrifie 11 hours postocclusion, at which time ischemic cerebral edema was measured. In 8 animals no treatment followed the occlusion, and these developed edema. In 7 animals pentobarbial 14 mg/kg was administered intravenously 30 min after occlusion and 7 mg/kg every 2 hours thereafter. In this group ischemic brain edema was negligible. In 8 animals, hypothermia to 25.9 +/- 0.5 degrees C was started 30 min after occlusion and maintained until sacrifice; ischemic brain edema was not significantly altered from untreated-clipped animals. On the basis that both pentobarbital and hypothermia produced similar changes in rCBF, AVDO2, and rCMRO2, but only pentobarbital prevented edema, it is postulated that the mode of action of barbiturates in preventing ischemic brain edema is not entirely related to their known effect on blood flow and metabolism.
Stroke
PMID:Ischemic brain edema: comparative effects of barbiturates and hypothermia. 10 24

In a previous study occlusion of a middle cerebral artery (MCA) followed by 48 h of hypothermia (29 degrees) was lethal in 5 of 5 monkeys as compared to only 3 of 9 normothermic animals. The present study extended these observations in monkeys and cats with or without MCA occlusion. In monkeys MCA occlusion plus 48 h of hypothermia was consistently lethal. Without MCA occlusion of 2 of 3 monkeys survived, but were comatose the first 12 h post-hypothermia. In normothermic cats, MCA occlusion was lethal in only one of 5 animals whereas hypothermia was lethal in 20 of 21 cats with or without MCA occlusion. The detrimental effects of hypothermia were not favorably influenced either by hemodilution or by deliberate alterations in PaCO2. The effect of 48 h of hypothermia and rewarming on cerebral blood flow (CBF) and cerebral metabolites was evaluated in 6 normal monkeys. CBF was reduced 60 to 70 percent at 29 degrees C and returned to only a maximum of 50 percent of control with re-warming. Prior to re-warming distribution of CBF was inhomogeneous. Cerebral metabolites were borderline normal prior to re-warming but energy stores decreased while lactate increased with re-warming.
Stroke
PMID:Deterimental effect of prolonged hypothermia in cats and monkeys with and without regional cerebral ischemia. 11 94

A functional classification of hypoxia of the brain has been presented and some of its significant aspects have been discussed. Mechanisms of protection from hypoxia of the brain were reviewed under the headings of prevention, hyperventilation, hypothermia and protection by barbiturates. In prevention of hypoxia of the brain, avoidance of factors producing a fall in cerebral perfusing pressure was emphasized. Hyperventilation is not advised unless one can readily measure regional cerebral blood flow. In the operating room, normocarbia or slight hypocarbia is recommended. Animal studies indicate a protective role of barbiturates in ischaemic hypoxia of the brain. However, it should be emphasized that, at present, hypothermia is the only established means of protection against hypoxia of the brain in man, when it is induced prior to the hypoxic insult. The evidence for protection by barbiturates has been found only in experimental animals. If one can extrapolate the results of studies in animals to man, then potential benefits would be expected in clinical stroke, cardiac arrest, in operations on the carotid artery and in head injury.
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PMID:Protection of the brain from hypoxia: a review. 36 4

The effects of induced hypocapnia, hypothermia, and hypertension were surveyed in a primate model of acute stroke during and following a 48-hour period of intensive care. The results were compared to a group of nine control animals previously studied. Hypocapnia (PaCO2=25 torr) was examined in five animals and did not appear to alter the expected mortality, degree of neurological deficit, or frequency of infarction. There was, however, a suggestion that the size of infarction may be reduced. Hypothermia (29 degrees C) in five animals had a detrimental effect in that no animals survived following the intensive care period and all had infarction with massive edema. We speculate that hypothermia caused a sufficient increase in blood viscosity as to compromise collateral flow, thereby accounting for this detrimental effect. Induced hypertension (to 20% above control levels) was abandoned after three animals because of severe systemic effects (cardiac failure and pulmonary edema) resulting in death during the period of intensive care.
Stroke
PMID:Failure of prolonged hypocapnia, hypothermia, or hypertension to favorably alter acute stroke in primates. 40 43

Experiments to assess left ventricular function in dogs during and after 2 hours of hypothermic cardioplegia are reported. During the experiment myocardial temperature was maintained between 15 degrees C and 18 degrees C by controlling the rate of flow of a cool cardioplegic solution into the coronary vessels. Before and after the period of hypothermia the left atrial pressure was gradually changed and the aortic flows and pressures that changed in response were recorded. The left ventricular stroke work (gm) was then calculated using the relationship: LVSM = (formula: see text) where: SV = stroke volume (ml), AP = arterial pressure (mmHg), LAP = left atrial pressure (mmHg). Comparison of the calculated values indicated that this method of maintaining cardiac hypothermia reduced cardiac function only slightly.
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PMID:Coronary perfusion under general and selective cardiac hypothermia. 42 58

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

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

To evaluate the importance of time, temperature, and cardioplegia on the ability of the canine myocardium to maintain functional and ultrastructural integrity following induced arrest, we studied 220 dogs by varying myocardial temperature (34 degrees, 24 degrees, and 11 degrees C.), arrest time (0 to 120 minutes), and cardioplegic agents. Change in left ventricular function (LVF) was defined as the arithmetic difference in the center of mass between prearrest and postarrest LVF curves and was expressed as percent recovery of left ventricular stroke work. Left ventricular biopsies were obtained for semiquantitative electron microscopic analysis. After 90 minutes of cross-clamping, only hearts protected with combined hypothermia (H) and potassium-induced cardioplegia (K) significantly recovered prearrest function (24 degrees C.--80 percent, 11 degrees C.--99 percent). Hypothermia (H) alone for 90 minutes was less protective (24 degrees C.--49 percent, 11 degrees C.--59 percent). H preserved 84 percent of function after 60 minutes and 91 percent after 45 minutes. Normothermic arrest resulted in only 39 percent return of function at 45 minutes but could be extended with potassium-induced cardioplegia(K) to 78 percent at 60 minutes and 54 percent at 90 minutes. The addition of procaine plus HK improved protection over HK alone (95 percent versus 80 percent) but by itself was not effective. Neither hydrocortisone nor pretreatment with glucose-insulin-potassium, branched chain amino acids, or propranolol increased the protective effect of HK plus procaine. Inadequately protected groups (normothermia or H without K) showed more myocytic and capillary endothelial damage than the HK groups. No technique of myocardial protection studied completely preserved LVF, but the combination of HK plus procaine resulted in maximal recovery of LVF following cross-clamping for up to 120 minutes.
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PMID:Effect of cross-clamp time, temperature, and cardioplegic agents on myocardial function after induced arrest. 70 64

Acute myocardial infarction with shock (AMI/S) was produced in 46 anesthetized "closed-chest" dogs by catheter injection of metallic mercury into the circumflex coronary artery. Twenty-four dogs were kept normothermic and 22 were maintained at 32 degrees C. Nine of the latter were rewarmed to 37 degrees C. and the experiments then were terminated, so that true survival time was arbitrarily shortened. Including these dogs, the survival time was three times longer than in the normothermic series (p less than 0.001). Hypothermia reduced heart rate (HR) by 34 percent, oxygen consumption by 38 percent, and myocardial oxygen consumption by an estimated 30 to 40 percent, while cardiac output (CO), stroke volume, and stroke work were unchanged. Left ventricular end-diastolic pressure (LVEDP) was reduced by 40 percent during hypothermia (p less than 0.05) and increased by 60 percent on rewarming. HR during rewarming increased substantially more than CO and thereby significantly reduced stroke volume.
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PMID:Induced hypothermia in dogs with acute myocardial infarction and shock. 88 82

The authors examined in 25 patients, of which 15 were normo- and 10 in hypothermic, the cardiovascular effects of 1 mg atropine i.v. In normothermia the heart rate increased significantly from 100 to 110 beats/min after atropine. At the same time the stroke index and stroke work decreased significantly. The mean arterial pressure, the heart index, the left ventricular minute- and stroke work and the total peripheral resistance did not change. In two patients with an arteriovenous fistula and hypervolaemia, the atropine injection caused an increased of heart- and stroke index. Arrhythmias did not occur after atropine. In hypothermia on the other hand atropine was shown to have no effect on heart frequency and all other examined parameters. In one patient in which the P-R interval was shortened, the atropine injection was followed by an total atrio-ventricular block. The authors cannot recommend atropine therapy in cases of hypothermic bradycardia, because of its lack of effect on the heart rate in hypothermia.
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PMID:[Cardiovascular changes caused by atropine in normo- and hypothermic methoxyflurane anaesthesia (author's transl)]. 97 May 97


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