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)

The first 100 liver transplantations at the Mayo Clinic were performed in 83 patients, who required a total of 917 patient days in the intensive-care unit (ICU). The mean duration of stay in the ICU was 5.91 days after liver transplantation and 6.15 days for patients who subsequently required readmission to the ICU. During the immediate postoperative period, hypothermia and hyperglycemia invariably occurred. Later during the initial admission or on readmission to the ICU, there arose the possibility of infections and renal insufficiency. Prompt diagnosis and treatment are necessary for hypertension, hypokalemia, severe metabolic alkalosis, fever, altered mental status, oliguria, and signs of graft failure in liver transplant patients. In our patient series, selective bowel decontamination minimized the occurrence of gram-negative and fungal sepsis, and use of antihypertensive agents and correction of coagulopathies may have decreased the risk of intracranial bleeding in patients with hypertension and clotting defects. Anticipation of potential conditions postoperatively and early implementation of treatment are key factors in the successful ICU management of patients who have undergone liver transplantation.
 ...
PMID:Intensive-care unit experience in the Mayo liver transplantation program: the first 100 cases. 265

Anesthesia, surgery, and hypothermia are conventionally considered the major stress factors in the metabolic and hormonal responses to cardiac surgery. We compared these responses in 14 nondiabetics during and for 24 h after coronary artery bypass surgery; 8 received cardioplegic solutions (C+), and 6 did not (C-). The mean intraoperative glucose load in C+ was 106 g compared to 32 g in C-; postoperatively both groups received 50 g. Marked hyperglycemia (31.8 +/- 4.8 mmol/L) occurred during hypothermia in C+, but dropped to 18.9 mmol/L before surgery ended and to 11.2 +/- 1.1 mmol/L by 2 h postop. In contrast, C- showed constant mild hyperglycemia of 8.3-9.8 mmol/L throughout, significantly less than C+ until 1 h postop. Insulin was suppressed by 55% only during hypothermia, peaking with rewarming in C+ at 2,849 +/- 911 vs. 639 +/- 251 pmol/L in C- (P less than 0.05); as with glycemia, values were comparable after 2 h postop. The pancreatic beta-cell thus responded to hyperglycemia during restoration of normothermia, resulting in a rapid decline in glycemia. This occurred despite elevations in antiinsulin factors in both groups; GH was 14 +/- 4 micrograms/L, cortisol was 607 +/- 38.6 nmol/L, norepinephrine was 11.5 +/- 3.7 nmol/L, epinephrine was 13,863 +/- 3,875 pmol/L, and FFA were 0.36 +/- 0.05 g/L. Early postop, a secondary rise in stress hormones occurred in both groups. Maximal cortisol values were at 4 h (1,186 +/- 140 nmol/L) and peaks of norepinephrine (6.50 +/- 1.66 nmol/L), epinephrine (7,969 +/- 3,602 pmol/L), and FFA (0.27 +/- 0.03 g/L) occurred. The only significant glucagon elevation was at 24 h (C+, 464 +/- 53 ng/L; C-, 350 +/- 241 ng/L; P less than 0.02), Thus, 1) many metabolic responses during coronary artery bypass surgery are influenced by the glucose-containing cardioplegic solution; 2) hypothermia suppresses insulin secretion, but it responds thereafter despite marked elevations of catecholamines, and is associated with decreasing glycemia despite elevated antiinsulin factors; 3) a lesser but highly significant stress response corresponds to awakening from anesthesia; and 4) glucagon plays a minor role in intraoperative hyperglycemia; the rise at 24 h is unexplained.
 ...
PMID:Hormonal and metabolic responses during coronary artery bypass surgery: role of infused glucose. 267 36

Authors examined levels of glucose, insulin, and C-peptide in the plasma of 6 infants and small children with the isolated transposition of the great arteries (3 pts) and ventricular septal defect (3 pts) in the course of open-heart surgery in deep hypothermia. The mean age of the patients was 7.2 months (6 to 15) and weight 5.6 kg (5.2-7.5). Exogenous intake of glucose during the operation was excluded. Methods of anaesthesia, operation technique, and conduction of extracorporeal circulation (ECC) were constant in all patients. Fresh ACD blood diluted with Hartman solution approximately 1:1 was used for the prime of ECC circuit (content 800 ml) to get the hematocrit 0.27 +/- 0.2 after mixing the prime with the patient's blood volume. Glycemia was determined by Beckman ERA 2001 analyzor, and levels of insulin and C-peptide by radioimmunoassay kits MJ-96 (Poland) and Novo (Denmark). Significant hyperglycemia was found in all patients during the period of hypothermia, and was overlasting to the rewarming period until the end of the operation and 1 hour postoperatively. Then level of glycemia was decreasing to the normal values which were found in the last sample (17 hours post-op). The raise of glycemia was not a stimulus to the proportional increase of insulin and C-peptide levels in plasma. It proved transitional suppress of insulin secretion in the beta cells of the pancreas in the cooling period. Levels of insulin and C-peptide significantly and concordantly increased after 20 min. of rewarming (r = 0.83). However, hyperglycemia overlasted during the course of rewarming, too.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[The effect of heart surgery during extracorporeal circulation and deep hypothermia on glucose metabolism in infants and young children]. 269 56

Blood glucose and rectal temperatures were monitored in two strains of genetically obese mice (C57 BL/6J ob/ob) prior to and following intragastric ethanol administration in an attempt to relate the hypothermic response to ethanol to extracellular glucose concentration. In contrast to expectation, ethanol administration was typically associated with a hyperglycemia and a hypothermic response. In the ob/ob genotype, the hypothermic response was associated with pronounced hyperglycemia which was more emphatic in older animals. The data support the conclusion that ethanol-induced hypothermia is independent of blood glucose levels. In light of the known sensitivity of ob/ob mice to insulin, it is suggested further that the observed hypothermic response was not a function of the animals' ability to transport glucose into peripheral cells. The observed hyperglycemia of the obese animals was most likely stress-related.
 ...
PMID:Ethanol-induced hypothermia and hyperglycemia in genetically obese mice. 271 75

A retrospective chart review was conducted of 26 organ donors to determine hemodynamic and metabolic derangements encountered and nursing requirements for donor organ maintenance. There were 15 boys and 11 girls with a mean age 6.57 +/- 5.46 years. Mean donor maintenance time was 10.5 +/- 6.7 hours. Cardiorespiratory derangements included hypotension in 16, hypertension in 6, arrhythmias in 17 (premature ventricular contraction in 4, bradycardia in 8, paroxysmal atrial tachycardia in 3, and ventricular tachycardia in 2), asystolic events in 5, pulmonary insufficiency in 6, anemia in 8, and thrombocytopenia in 8. Metabolic and hormonal derangements included hyperglycemia in 18, hypokalemia in 20, hyperkalemia in 4, hyponatremia in 3, hypernatremia in 17, metabolic acidosis in 10, and diabetes insipidus in 15. Hypothermia (temperature 33.3 degrees +/- 0.4 degrees C, mean +/- SD) occurred in 14 donors. The mean physiologic Stability Index score was 22.2 +/- 4.7 and mean Therapeutic Intervention Score was 46.7 +/- 5.8. Total number of nursing hours spent in donor maintenance was 424.5 hours. Therapies offered included diuretics in 10, sodium bicarbonate in 8, antibiotics in 6, insulin in 12, pitressin in 13, verapamil in 3, isoproterenol in 3, dopamine in 17, and intravenous potassium boluses in 14. Of the potential 26 donors, 46 kidneys, 8 hearts, 14 livers, 3 pancreas, and 9 corneas were retrieved in transplantable condition. With appropriate donor maintenance, organs suitable for transplantation can be retrieved despite significant pathophysiologic derangements. Physicians intending to provide donor support should be comfortable with invasive monitoring and cardiorespiratory support and be prepared to provide a nurse to patient ratio of 2:1 at the bedside.
 ...
PMID:Pediatric organ donor maintenance: pathophysiologic derangements and nursing requirements. 278 Jan 31

The ability of the putative ethanol antagonist RO 15-4513 to antagonize ethanol - induced hypoactivity, hypothermia and hyperglycemia was investigated in rats. Although RO 15-4513 produced hypoactivity by itself, it attenuated ethanol - induced hypoactivity. This antagonism suggests that ethanol - induced hypoactivity is mediated by the GABA-benzodiazepine receptor complex which is thought to be the site of action of RO 15-4513. In contrast, although RO 15-4513 produced hypothermia by itself, it had no significant effect on ethanol - induced hypothermia. This suggests that the hypothermic effect of ethanol is not mediated by the GABA-benzodiazepine receptor complex. The fact that RO 15-4513, ethanol and the vehicle all produced hyperglycemia suggests a common stress effect and does not permit any firm conclusions to be drawn as to the interaction between ethanol and RO 15-4513 in modulating glycemic responses. These data indicate that the ethanol antagonism of RO 15-4513 is primarily confined to ethanol's behavioural effects and that ethanol's behavioural and physiological effects are mediated by neurochemically distinct mechanisms.
 ...
PMID:The intrinsic and interactive effects of RO 15-4513 and ethanol on locomotor activity, body temperature, and blood glucose concentration. 281 3

LS/Ibg (LS) and SS/Ibg (SS) mice differ in ethanol-induced duration of loss of righting response or sleep time, hypothermia, hyperglycemia, and blood ethanol concentrations at regaining righting response. These differences in response to ethanol are a result of differences in central nervous system sensitivity and are mediated by polygenic systems. Studies have indicated that catecholaminergic systems may be involved in the differential effects of ethanol in LS and SS lines of mice (Masserano JM, Weiner N: Investigations into the neurochemical mechanisms mediating differences in ethanol sensitivity in two lines of mice. J Pharmacol Exp Ther 221:404-408, 1982). In this study the neurotoxin, 6-hydroxydopamine (6-OHDA), intracerebroventricular, was used to test this hypothesis. Administration of 6-OHDA markedly altered thermoregulation in LS mice but produced little effect in SS mice, and ethanol-induced hyperglycemia was attenuated in both LS and SS mice by 6-OHDA. Ethanol-induced sleep time was increased in SS mice pretreated with 100 micrograms of 6-OHDA, intracerebroventricular, whereas this response in LS mice was unaffected by 6-OHDA administration. Changes in sleep time were not related to changes in blood ethanol concentrations, indicating that 6-OHDA alters ethanol-induced sleep time by mechanisms other than brain sensitivity. Levels of norepinephrine and dopamine were determined in three brain regions, and the altered capacities for thermoregulation and glucoregulation were associated with changes in hypothalamic catecholamine levels.
 ...
PMID:Effects of 6-hydroxydopamine on brain catecholamines and on acute actions of ethanol in LS/Ibg and SS/Ibg mice. 309 Sep 1

The rat appears to be unable to utilize glucose during hypothermia. The objective of this study was to examine carbohydrate homeostasis during induction, hypothermia, and rewarming phases. Groups of normothermic animals were euthanized to serve as time controls for comparison. Hypothermia (15 degrees C) was produced by exposure to helox (80% helium:20% oxygen) at 0 +/- 1 degree C. Hyperglycemia was noted during the induction process (169 +/- 8 in control vs 326 +/- 49 mg/dl). Serum glucose increased further during 4 hr of hypothermia, but following rewarming (Tre of 33 +/- 1 degrees C) was reduced (153 +/- 16 mg/dl) significantly (P less than 0.05). Serum insulin was depressed during hypothermic induction (from 48 +/- 4 in controls to 19 +/- 3 microU/ml in hypothermic rats) and increased only slightly during the arousal process, remaining significantly lower than in normothermic subjects. Initial hepatic, skeletal muscle, and cardiac glycogen concentrations were reduced 34, 68, and 75%, respectively, during hypothermic induction. While liver glycogen decreased further during 4 hr of hypothermia, skeletal and cardiac stores increased markedly. During rewarming, hepatic glycogen was markedly decreased, while skeletal and cardiac stores were maintained. These data suggest that hyperglycemia in the hypothermic rat can be accounted for by glycogenolysis and hypoinsulinemia. In addition, this study indicates repletion of skeletal and cardiac muscle glycogen during maintained hypothermia and sparing of muscle glycogen during rewarming.
 ...
PMID:Glucose, glycogen, and insulin responses in the hypothermic rat. 328 25

The resistance of the brain to ischemia depends not only on the duration and severity of flow reduction but also on a number of pre- and post-ischemic metabolic and hemodynamic factors which are able to improve or impair the post-ischemic recovery process. Among pre-ischemic protective factors, the suppression of metabolic rate by drugs or hypothermia, the increase of brain tissue energy reserves and the inhibition of membrane permeability of cations are of particular importance. In contrast, increase of metabolic rate and increase of tissue acidosis induced by hyperglycemia or residual blood flow, reduce the ischemic tolerance of the brain. As long as cell membranes do not depolarize during ischemia, restitution of blood flow results in spontaneous recovery. After depolarization of membranes, however, numerous post-ischemic complications evolve, such as the no-reflow phenomenon, post-ischemic hypoperfusion, post-ischemic brain edema, disturbances of the coupling between metabolic activity and blood flow, etc. These complications require therapeutic intervention in order to prevent irreversible injury. By optimizing this therapy in a model of 1 hour complete normothermic brain ischemia in cat and monkeys, post-ischemic recovery of energy metabolism, protein synthesis, spontaneous and evoked electrocortical activity and even integrative neurological performance were observed. The resistance of the brain to ischemia, in consequence, is much higher than previously assumed and can be substantially improved by adequate post-ischemic treatment.
 ...
PMID:[Experimental principles of tolerance of the brain to ischemia]. 332 66

The high-dose effects of chlorocitrate [(-)-threo-chlorocitric acid] were compared in vivo to another halogenated citrate analog, and a well-known inhibitor of the tricarboxylic acid (TCA) cycle, fluorocitrate. The compounds were given iv to two dogs per sex per group, and a control group received an equimolar amount of citric acid. Chlorocitrate (100 mg/kg) showed TCA cycle inhibition as did fluorocitrate (8 mg/kg) in that both caused depletion of ATP and accumulation of citrate in the liver. Chlorocitrate was a significantly weaker inhibitor of citrate metabolism than fluorocitrate as evidenced by a substantially lower accumulation of serum citrate despite a much higher dose. Both halocitrates produced a similar diabetes-like syndrome (hyperglycemia, glycosuria) mediated by a significant hyperglucagonemia and slight hypoinsulinemia. Chlorocitrate was more potent in this effect and a much greater buildup of plasma lactate ensued (18- versus 3.7-fold increase), enough to explain lethality observed in earlier studies. In contrast, fluorocitrate produced a severe life-threatening hypocalcemia (-30%), and hypercalcuria was observed. This effect on calcium distribution was only minimal with chlorocitrate. Both halocitrates had a similar depressive effect on circulation as evidenced by hypothermia, bradycardia, and elongation of the QT-interval. These changes were considered to be the result of lactic acidosis and the ongoing ion imbalance since heart ATP levels were not depleted.
 ...
PMID:Comparative acute toxicity of chlorocitrate and fluorocitrate in dogs. 359 Jan 93


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