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

Clinical application of hypothermic pharmacologic cardioplegia in pediatric cardiac surgery is less than satisfactory, despite its well known benefits in adults. Protection of the ischemic immature rabbit heart with hypothermia alone is better than with hypothermic St. Thomas' II cardioplegic solution. Control of cellular calcium is a critical component of cardioplegic protection. We determined whether the existing calcium content of St. Thomas' II solution (1.2 mmol/L) is responsible for suboptimal protection of the ischemic immature rabbit heart. Modified hypothermic St. Thomas' II solutions (calcium content, 0 to 2.4 mmol/L) were compared with hypothermic Krebs bicarbonate buffer in protecting ischemic immature (7- to 10-day-old) hearts. Hearts (n = 6 per group) underwent aerobic "working" perfusion with Krebs buffer, and cardiac function was measured. The hearts were then arrested with a 3-minute infusion of either cold (14 degrees C) Krebs buffer (1.8 mmol calcium/L) as hypothermia alone or cold St. Thomas' II solution before 6 hours of hypothermic (14 degrees C) global ischemia. Hearts were reperfused, and postischemic enzyme leakage and recovery of function were measured. A bell-shaped dose-response profile for calcium was observed for recovery of aortic flow but not for creatine kinase leakage, with improved protection at lower calcium concentrations. Optimal myocardial protection occurred at a calcium content of 0.3 mmol/L, which was better than with hypothermia alone and standard St. Thomas' II solution. We conclude that the existing calcium content of St. Thomas' II solution is responsible, in part, for its damaging effect on the ischemic immature rabbit heart.
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PMID:Calcium content of St. Thomas' II cardioplegic solution damages ischemic immature myocardium. 192 65

Hypothermic perfusion before cardioplegic ischemic arrest is commonly used in neonatal cardiac surgery. However, perfusion cooling of the heart in the nonarrested state results in an inotropic response and may induce myocardial contracture secondary to a sustained elevation of intracellular calcium levels. The effect of prearrest cardiac cooling was examined in two groups of isolated parabiotic, blood-perfused neonatal rabbit hearts. Group C (cooling group, n = 12) was exposed to 15 minutes of cold perfusion to 12 degrees C before 1 hour of cardioplegic arrest. Group N (normothermia group, n = 11) underwent identical arrest conditions but without prearrest cold perfusion. Developed pressure at constant volume in group C fell from 109 +/- 8.7 mm Hg at baseline to 55.2 +/- 5.5 mm Hg after 30 minutes of reperfusion versus no significant change in group N. Diastolic compliance showed significant deterioration in group C, with marked elevation of diastolic pressure from 9.8 +/- 0.4 mm Hg at baseline to 22.0 +/- 4.4 mm Hg after ischemia and reperfusion. This experimental data demonstrates that profound hypothermic perfusion of the myocardium in the nonarrested state may induce a rise in resting myocardial tension and that cardioplegic ischemic arrest in the presence of cooling contracture may result in important myocardial injury.
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PMID:Effect of rapid cooling contracture on ischemic tolerance in immature myocardium. 193 35

The intracerebroventricular (i.c.v.) administration of pertussis toxin (0.5 microgram) to rats significantly reduced the hypothermic and behavioural effects (episodic bizarre postures characterized by limb rigidity and followed by barrel rolling) induced by i.c.v. dynorphin A (10 micrograms). These central effects of dynorphin A thus appear to be initiated at a receptor site that interacts with G proteins substrates sensitive to pertussis toxin. Dynorphin A-induced hypothermia was also significantly reduced by i.c.v. pretreatment with the Ca2+ antagonist, verapamil (10 micrograms), although verapamil per se did not modify the behavioural effects elicited by the peptide.
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PMID:Gi proteins and calcium in dynorphin-induced hypothermia and behaviour. 197 19

The synthesis and biological properties of a novel series of selective calcium-independent phosphodiesterase inhibitors are described. These compounds also inhibit the specific binding of [3H]rolipram to rat brain membranes and exhibit efficacy in preclinical models of antidepressant activity in mice, such as reducing immobility in the forced-swim test and reversing reserpine-induced hypothermia. Imidazolidinones 4 and 16 were found to be the most potent compounds studied.
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PMID:Calcium-independent phosphodiesterase inhibitors as putative antidepressants: [3-(bicycloalkyloxy)-4-methoxyphenyl]-2-imidazolidinones. 199 29

The concentration of calcium (1.2 mmol/L) in clinical St. Thomas' Hospital cardioplegic solution was chosen several years ago after dose-response studies in the normothermic isolated heart. However, recent studies with creatine phosphate in St. Thomas' Hospital solution demonstrated that additional myocardial protection during hypothermia resulted principally from its calcium-lowering effect in the solution. The isolated working rat heart model was therefore used to establish the optimal calcium concentration in St. Thomas' Hospital solution during lengthy hypothermic ischemia (20 degrees C, 300 minutes). The calcium content of standard St. Thomas' Hospital solution was varied from 0.0 to 1.5 mmol/L in eight treatment groups (n = 6 for each group). During ischemia, hearts were exposed to multidose cardioplegia (3 minutes every 30 minutes). Postischemic recovery of function was expressed as a percentage of preischemic control values. Release of creatine kinase and the time to return of sinus rhythm during the reperfusion period were also measured. These dose-response studies during hypothermic ischemia revealed a broad range of acceptable calcium concentrations (0.3 to 0.9 mmol/L), which appear optimal in St. Thomas' Hospital solution at 0.6 mmol/L. This concentration improved the postischemic recovery of aortic flow from 22.0% +/- 5.9% with control St. Thomas' Hospital solution (calcium concentration 1.2 mmol/L) to 86.0% +/- 4.0% (p less than 0.001). Other indices of functional recovery showed similar dramatic results. Creatine kinase release was reduced 84% (p less than 0.01) in the optimal calcium group. Postischemic reperfusion arrhythmias were diminished with the loser calcium concentration, with a significant decrease in the time between initial reperfusion until the return of sinus rhythm. In contrast, acalcemic St. Thomas' Hospital solution precipitated the calcium paradox with massive enzyme release and no functional recovery. Unlike prior published calcium dose-response studies at normothermia, these results demonstrate that the optimal calcium concentration during clinically relevant hypothermic ischemia is considerably lower than that of normal serum ionized calcium (1.2 mmol/L) and appears ideal at 0.6 mmol/L to realize even greater cardioprotective and antiarrhythmic effects with St. Thomas' Hospital solution.
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PMID:Lowering the calcium concentration in St. Thomas' Hospital cardioplegic solution improves protection during hypothermic ischemia. 199 42

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.
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PMID:Potassium and massive blood transfusion. 201 1

Idiopathic hypoparathyroidism was diagnosed in five young to middle-aged cats of mixed breeding. Three of the cats were male and two were female. Historic signs included lethargy (n = 5), anorexia (n = 5), muscle tremors (n = 4), weakness (n = 4), generalized seizures (n = 3), ataxia (n = 3), mental dullness or disorientation (n = 3), panting (n = 2), pruritus (n = 1), ptyalism (n = 1) and dysphagia (n = 1). Weakness (n = 4), dehydration (n = 2), cataracts (n = 2), hypothermia (n = 1), and bradycardia (n = 1) were found on physical examination. Results of electrocardiography revealed a prolonged Q-T interval in two cats. Results of initial laboratory tests revealed profound hypocalcemia and severe hyperphosphatemia with normal renal function. The diagnosis of hypoparathyroidism was made on the basis of the history, clinical signs, and results serum biochemical testing (i.e., severe hypocalcemia and hyperphosphatemia); in two cats, the diagnosis was also confirmed by histologic examination of parathyroid glands. Initial treatment included intravenous administration of 10% calcium gluconate and oral administration of large loading doses of calcium and vitamin D (dihydrotachysterol). Successful long-term management with dihydrotachysterol and calcium was achieved in all cats. The final dosage of dihydrotachysterol required to maintain normocalcemia in the five cats ranged from 0.004 to 0.04 mg/kg/day (mean = 0.015 mg/kg/day). Long-term calcium supplementation was given to three of the cats in dosages ranging from 29 to 53 mg/kg/day (mean = 42 mg/kg/day) of elemental calcium. One cat died after 28 months of therapy from widely metastatic hemangiosarcoma; the other three cats are still alive and well after 5 to 37 months of treatment.
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PMID:Idiopathic hypoparathyroidism in five cats. 202 14

The role of the anesthesiologist in myocardial protection is to optimize myocardial oxygen balance during the perioperative period. Nonpharmacological steps that can be taken to achieve this revolve around maintaining a satisfactory hemoglobin concentration and oxyhemoglobin saturation through maximizing ventilation. In addition, alkalosis and hypothermia should be prevented since they cause a left shift of the oxyhemoglobin dissociation curve, thus interfering with tissue oxygen delivery. Hypocarbia increases coronary vascular resistance. Blood volume must be adequate with an optimal hemoglobin concentration. Pharmacological measures should also be used, and it is important to continue through the perioperative period any previously administered cardioactive drugs. Furthermore, in the prebypass period, tachycardia may not be controlled by anesthetics; unless the tachycardia is paroxysmal, beta blockers are the drugs of choice. Depending on the cause, diastolic hypotension also needs to be treated either with volume, vasoconstrictors, or inotropes. Likewise, major hypertension can produce increased demand and, again depending on the cause, either anesthetics, vasodilators, beta blockers, or calcium blockers may be useful. Finally, myocardial ischemia without obvious cause probably should be treated with nitroglycerin or calcium blockers. During surgery, the effect of the anesthetic drugs on myocardial oxygen balance is important.
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PMID:Myocardial protection: what the anesthesiologist does. 213 51

An accumulation of experimental data suggests that N-methyl-D-aspartate (NMDA) receptor antagonists will prevent ischemic neuronal injury following transient global ischemia and reduce infarct volumes following focal ischemic insults. The excitotoxic hypothesis states that the excitatory amino acid neurotransmitter L-glutamate has neurotoxic properties that can be attenuated by antagonism of the NMDA receptor. In vitro work has shown that a variety of NMDA antagonists will prevent the death of neurons grown in culture and subsequently exposed to either brief periods of hypoxia or glutamate exposure. In vivo it has been shown that glutamate is released following ischemia, that the NMDA receptors remain functional both during and following ischemia, and that the concentration of NMDA receptors is highest in those regions that are most sensitive to ischemic neuronal injury. Once stimulated, these receptors mediate a lethal influx of calcium. Experiments with global ischemia have reported a cytoprotective effect by either prior removal of glutamate afferents or pretreatment with either competitive or noncompetitive receptor antagonists. Some of these data have been challenged and one suggestion that has been made is that the observed pharmacoprotection may be the result of coincidental drug-induced hypothermia. Numerous studies using a variety of models of focal ischemia have shown that the volume of a cortical infarct can be reduced with NMDA antagonists given either before or after an ischemic insult. These data are more consistent than those achieved for models of global ischemia and have led to proposals for clinical trials. Novel compounds that antagonize the NMDA receptor are now the subject of phase I clinical studies that are envisaged as a prelude to randomized acute stroke trials. The hypothesis that blockade of excitatory amino acid receptors will prevent neuronal death presages a new era in acute stroke treatment.
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PMID:Do NMDA antagonists protect against cerebral ischemia: are clinical trials warranted? 214 95

Adenosine exerts numerous effects in the central and autonomic nervous systems, most of which seem to be receptor mediated. Several studies have revealed two distinct receptors, based upon effects of adenosine on adenylate cyclase activity, designed A1 or A2 according to whether the cyclase is inhibited or activated. However, since not all adenosine receptors are linked to adenylate cyclase some authors base their classification on the rank orders of potencies of adenosine analogues in eliciting responses. The purine seems to function as a modulatory substance in the heart, blood, ileum, vas deferens, and adipose tissue. In addition, important responses to exogenously added adenosine are also induced in the bronchi, urinary bladder, taenia coli, parietal cells of the stomach and renin secretion. Adenosine and its analogues elicit anticonvulsant responses, sedation and hypothermia through their actions in the central nervous system. The mechanisms by which adenosine elicits its responses have not been clearly established. The activation of A1 receptors depresses the release of neurotransmitters and inhibit the influx of Ca into nerve terminals. Whether this effect is induced by interaction with Ca channels or by impairment of Ca dependent processes associated with neurotransmitter release is unknown. In the rat heart adenosine inhibits adenylate cyclase and subsequently the phosphorylation of L-type Ca channels, resulting in a decrease of calcium influx in the muscle cell. The responses to activation of A2 receptors in smooth muscle consist in relaxation presumptively by an increase of K current which would hyperpolarize the cell.
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PMID:[Adenosine: physiological and pharmacological actions]. 215 91


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