Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since our initial experience on April 28, 1989, a total of nine patients have received treatment for giant cerebral aneurysm using cardiopulmonary bypass with deep hypothermia and circulatory arrest. The following data summarize our findings associated with these patients. The average patient's age was 46 years (range: 16 to 59 years of age). Seven patients were female, two were male. The procedure required approximately eight hours to complete with an average cardiopulmonary bypass time of 104 minutes (range: 60 to 140 minutes). Circulatory arrest time averaged 26 minutes (range, 12 to 45 minutes) with an average of 30 minutes (range: 10 to 62 minutes) required to cool the patient to below 18 degrees C (64 degrees F). An average of 54 minutes (range: 28 to 81 minutes) was required to warm the patient to a bladder temperature of 36 degrees C (96.8 degrees F). During the cooling period, five patients went into asystole spontaneously, four patients required bolus of 20 mEq of potassium chloride, and upon rewarming, spontaneous defibrillation occurred in six patients. Three patients were defibrillated without difficulty with external shock. The average number of blood products administered in each of the nine patients was 3.6 units of packed red blood cells, 3 units of fresh frozen plasma, and 6.5 units of platelets. Six patients recovered postoperatively without complication, and the recovery of three patients was affected by the complex anatomical location of the giant aneurysm. Cardiopulmonary bypass with deep hypothermia and circulatory arrest offers an alternative approach to the treatment of giant cerebral aneurysms considered inoperable by conventional techniques. The effectiveness of each procedure depends on the collaborative efforts of every member of the perioperative nursing team, the neurosurgical team, the cardiac surgical team, the neuroanesthesiology team, and the perfusionists. Careful planning and anticipation at every stage of the surgery can reduce surgical time, cardiopulmonary bypass time, and most importantly, circulatory arrest time.
 ...
PMID:Giant cerebral aneurysm repair. Incorporating cardiopulmonary bypass and neurosurgery. 192 49

The protective effects of hypothermia and potassium-solution cardioplegia on high-energy phosphate levels and intracellular pH were evaluated in the newborn piglet heart by means of in vivo phosphorus nuclear magnetic resonance spectroscopy. All animals underwent cardiopulmonary bypass, cooling to 20 degrees C, 120 minutes of circulatory arrest, rewarming with cardiopulmonary bypass, and 1 hour off extracorporeal support with continuous hemodynamic and nuclear magnetic resonance spectroscopic evaluation. Group I (n = 5) was cooled to 20 degrees C; group II (n = 4) was given a single dose of 20 degrees C cardioplegic solution; group III (n = 7) was given a single dose of 4 degrees C cardioplegic solution; and group IV (n = 4) received 4 degrees C cardioplegic solution every 30 minutes. At end ischemia, adenosine triphosphate, expressed as a percent of control value, was lowest in group I 54% +/- 6.5% but only slightly greater in group II 66% +/- 7.0%. Use of 4 degrees C cardioplegic solution in groups III and IV resulted in a significant decrease in myocardial temperature, 9.9 degrees C versus 17 degrees to 20 degrees C, and significantly higher levels of adenosine triphosphate at end ischemia; with group III levels at 72% +/- 6.0% and group IV levels at 73% +/- 6.0%. Recovery of adenosine triphosphate with reperfusion was not related to the level of adenosine triphosphate at end ischemia and was best in groups I and II, with a recovery level of 95% +/- 4.0%. In group IV, no recovery of adenosine triphosphate occurred with reperfusion, resulting in a significantly lower level of adenosine triphosphate, 74% +/- 6.0%, than in groups I and II. Recovery of ventricular function was good for all groups but was best in hearts receiving a single dose of 4 degrees C cardioplegic solution. In this model, multiple doses of cardioplegic solution were not associated with either improved adenosine triphosphate retention during arrest or improved ventricular function after reperfusion, and in fact resulted in a significantly lower level of adenosine triphosphate with reperfusion. The complete recovery of adenosine triphosphate in groups I and II, despite a nearly 50% adenosine triphosphate loss during ischemia, may result from a decrease in the catabolism of the metabolites of adenosine triphosphate consumption in the newborn heart.
 ...
PMID:Effects of potassium cardioplegia on high-energy phosphate kinetics during circulatory arrest with deep hypothermia in the newborn piglet heart. 199 45

Sixty patients who received massive blood transfusion intraoperatively and/or in the immediate post-operative period were analysed. Six patients had hypokalemia and two had hyperkalemia. The multifactorial changes leading to electrolyte disturbances especially involving potassium are discussed in relation to hypotension, hypothermia, acidosis, pH, and release of catecholamine. Potassium changes in relation to anaesthesia are discussed. The danger of routine administration of calcium during massive blood transfusion is stressed.
 ...
PMID:Potassium and massive blood transfusion. 201 1

To investigate whether changes in temperature influence the electrophysiologic effects of the class III antiarrhythmic agent d-sotalol, we studied its effects on propranolol-pretreated guinea pig papillary muscles at temperatures ranging from 37 degrees to 27 degrees C by means of conventional microelectrode techniques. We also examined the rate-dependent effect of d-sotalol at 37 degrees and 27 degrees C. Before the addition of d-sotalol, reducing the temperature from 37 degrees to 27 degrees C increased the action potential duration recorded at 50% repolarization (APD50) from 112 +/- 7 msec to 271 +/- 15 msec and action potential duration recorded at 90% repolarization (APD90) from 136 +/- 7 msec to 325 +/- 10 msec. d-Sotalol (50 mumol/L) lengthened APD50 and APD90 to a greater degree at low temperatures. Thus at 37 degrees C d-sotalol lengthened APD50 and APD90 by 12 +/- 6 msec and 19 +/- 5 msec, and at 27 degrees C by 37 +/- 5 msec and 52 +/- 7 msec, respectively. d-Sotalol produced its greatest effect on APD at long pacing cycle lengths, thus demonstrating reverse dependence. This rate-dependent effect was more marked at 27 degrees C than at 37 degrees C. The greater effect of d-sotalol on APD at long pacing cycle lengths may be explained by the modulated receptor hypothesis, assuming that the drug has a higher affinity for closed potassium channels. Such a mechanism may also explain the accentuated class III antiarrhythmic action of d-sotalol observed during hypothermia.
 ...
PMID:Class III antiarrhythmic action of d-sotalol during hypothermia. 201 75

Hypothermia may contribute to vascular spasm during bypass surgery. The effect of cooling on the reactivity of the human coronary artery (CA), saphenous vein (SV) and internal mammary artery (IMA) was studied in vitro. In CA and IMA cooling diminished the resting tension and the contraction to potassium, noradrenaline and 5-hydroxytryptamine. In contrast, in SV the contraction to noradrenaline and 5-hydroxytryptamine was augmented by cooling. The effect of cold was reversible. These results demonstrate different effects of hypothermia in CA and the graft vessels. Thus, hypothermia augments the receptor-mediated contraction in SV but depresses it in IMA which thereby resembles CA. The difference is most marked in the contractile response to 5-hydroxytryptamine, which may accumulate during surgery. This may contribute to spasm in the saphenous vein grafts and may be involved in the mechanisms responsible for the inferior patency of SV compared to IMA as a graft vessel.
 ...
PMID:Differential effect of hypothermia on the vascular tone and reactivity of the human coronary artery and graft vessels. 205 21

Ventricular dysfunction, then, does indeed occur during liver transplantation, particularly at the time of reperfusion. Pulmonary embolism contributes to right ventricular and right atrial encroachment on left-heart filling, and paradoxical embolism may occur. Pericardial effusions, tricuspid regurgitation, hypothermia, and the release of substances, particularly potassium from the donor liver, may further contribute to compromises in ventricular function. Proper monitoring and appropriate treatment, however, lead to successful operative outcomes in most cases.
 ...
PMID:Ventricular dysfunction does occur during liver transplantation. 206 29

Potassium homeostasis was studied in 30 patients undergoing cardiac surgery by employing cardiopulmonary bypass (CPB) and moderate hypothermia, and using morphine, N2O, relaxant anaesthesia. There was a trend for hypokalemia, and for maintaining a K+ level of 4-4.5 mmol/l, K+ infusion was required during CPB (9.017 mmol/m2 BSA/h). K+ infusion required in the post-operative period was considerably less (1.532 mmol/m2 BSA/h). There was no significant difference in the K+ levels of patients receiving preoperative diuretic therapy, as compared to those not receiving such therapy. Potassium requirement was significantly higher in patients under-going CABG and valvular heart disease, as compared to congenital heart disease. The mean urinary loss of K+ during bypass was found to be 2.95 mmol/m2 BSA/h, which was only 32 per cent of that required to be infused (9.017 mmol/m2 BSA/h). The mean excretion of K+ in the post operative period was significantly higher (4.53 mmol/m2 BSA/h) than K+ required to be infused during this period (1.532 mmol/m2 BSA/h).
 ...
PMID:Potassium homeostasis during & after cardiopulmonary bypass. 207 59

The effects of carbamazepine (CBZ) on brain 5-hydroxytryptamine (5-HT) function were investigated in rodents pretreated with CBZ acutely or for 14 days. In behavioural experiments, mice pretreated with 14 days CBZ showed increased 5-HT2-mediated head twitch behaviour after injection of carbidopa (25 mg/kg) followed by 5-hydroxytryptophan (5-HTP, 100 mg/kg). However, no change in head twitches after 5-methoxy,N,N,-dimethyltryptamine (5MeODMT 5.0 mg/kg), a direct agonist, was observed. Chronic CBZ administration to rats did not alter either the behavioural syndrome induced by 8-hydroxy-2-dipropylaminotetralin (8-OH-DPAT, 1.0 mg/kg), an index of postsynaptic 5-HT1A responses, or hypothermia after 8-OH-DPAT (0.5 mg/kg) which is thought to reflect presynaptic 5-HT1A activity. Both hyperactivity and the behavioural syndrome seen after tranylcypromine (20 mg/kg) followed by L-tryptophan (100 mg/kg) were decreased by prior treatment with CBZ (14 days). Accumulation of 5-HTP after administration of the amino acid decarboxylase inhibitor NSD1015 (100 mg/kg) was decreased after acute CBZ (50 mg/kg) in hippocampus. However, after 14 days oral treatment no change in this measure of 5-HT synthesis was seen, in either hippocampus or frontal cortex. CBZ (50 microM) added to superfused brain slices did not affect potassium-stimulated [3H]-5-HT release. However, hippocampal slices from rats pretreated with CBZ (14 days) showed increased potassium-stimulated [3H]-5-HT release. CBZ (14 days) did not alter 5-HT2 binding in rat frontal cortex.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of carbamazepine on 5-hydroxytryptamine function in rodents. 213 52

Isolated rat hearts were used to examine whether reperfusion-induced arrhythmias may be caused by washout of substances accumulating during ischemia. This was achieved by subjecting hearts to 10 min of regional ischemia and rendering them transiently inexcitable during the first 1.5 min of reperfusion. Transient inexcitability was induced by switching to cold solution (4 degrees C) shortly before reperfusion (-1.5 min). In controls (no hypothermia), the incidences of ventricular tachycardia (VT) and ventricular fibrillation (VF) were 83% and 92%, respectively, during the first 1.5 min of reperfusion. Transient hypothermia caused inexcitability and asystole, impaired recovery of coronary flow and abolished VT and VF (all P less than 0.05). On subsequent rewarming to 37 degrees C, coronary flow and sinus rate recovered in all hearts. However, VT and VF occurred in only 58% and 25%, respectively (P less than 0.05). These values were similar to those of new episodes of VT and VF occurring in controls during the equivalent period. Therefore arrhythmias had been abolished during transient hypothermia, not merely delayed. The relative contributions of transient impairment of recovery of coronary flow and transient asystole to the antiarrhythmic effects were examined in a further 10 groups of hearts (n = 12/group) in which reperfusion conditions were transiently manipulated. We utilized combinations of hypothermia, ventricular pacing, acetylcholine (ACh) 55 microM (to cause asystole and impairment of recovery of coronary flow), and right atrial excision and left atrial pacing (to permit bradycardia to be transiently induced during reperfusion by temporarily switching off the pacemaker). The results indicated that transient hypothermia was antiarrhythmic as a result of a reduction of excitability, not because of bradycardia or impairment of recovery of flow. The data support the hypothesis that reperfusion unmasks (disinhibits) latent arrhythmogenic components of ischemia (particularly during the first 1.5 min of reperfusion) and that, by inducing inexcitability, transient hypothermia allows these substances to be washed out without their arrhythmogenic effects being manifested. The identities of the arrhythmogenic and antiarrhythmic substances remain to be determined; we suggest that cyclic AMP and potassium, respectively, are likely candidates.
 ...
PMID:Are reperfusion-induced arrhythmias caused by disinhibition of an arrhythmogenic component of ischemia? 223 48

The aftereffects of renal function were studied in rats exposed to profound hypothermia and 5 min of cardiac arrest. All experimental rats were reanimated and survived at least 1 week. It was observed that the water intake and the basal renal excretion of urine, potassium and urea were decreased 24 hr after cooling, but did return to normal within 1 week. The renal handling of a large volume of infused saline was retarded 4 hr but recovered by the end of 24 hr after hypothermia. At both 4 and 24 hr after deep cooling, clearance of inulin and p-aminohippuric acid showed there were no change in glomerular filtration rate and effective renal plasma flow. It was concluded that the renal function was altered shortly after deep cooling and 5 min of cardiac arrest, however, this alteration could be completely recovered thereafter.
 ...
PMID:The renal functions following a profound hypothermia in rats. 226 26


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>