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

Lowering temperature from 37 degrees C to 22, 18, and 14 degrees C triggered automaticity of smooth longitudinal muscle of guinea pig isolated ileum. The amplitude of the hypothermia-induced automaticity was dependent on the degree of temperature drop: the greater the temperature drop, the greater the amplitude. However, when the preparation was initially prepared and maintained at 14 degrees C and then the temperature was raised at a similar rate to 18, 22, and 37 degrees C, the automaticity was not observed. This series of observations suggests that cooling rate may be the trigger and/or part of the triggering mechanism for the observed automaticity. Mepenzolate (1.0 x 10(-6) M), a specific muscarinic receptor antagonist, blocked the automaticity suggesting the involvement of muscarinic receptors in the pathogenesis and/or the manifestation of the automaticity. Verapamil (1.0 x 10(-7) M), a calcium channel blocker which inhibits the transmembrane Ca2+ influx into smooth muscle cells during excitation, blocked the automaticity suggesting that transmembrane Ca2+ influx plays a significant role in the pathogenesis and/or manifestation of the automaticity. A specific cytoplasmic calcium channel blocker, 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate hydrochloride (1.0 x 10(-6) M) blocked the automaticity, suggesting that cytoplasmic calcium also plays a significant role in the pathogenesis and/or manifestation of the automaticity. In order to characterize the temperature-induced changes in the muscarinic receptors, an attempt was made to use the classic method of Furchgott and Burstyn to determine the dissociation constants of acetylcholine at muscarinic receptors at different temperatures. However, the alkylation of muscarinic receptors with phenoxybenzamine at lower temperatures was erratic and the recovery from the occlusion was too rapid to apply the method of Furchgott and Burstyn. We concluded that the lack of reversibility of the effects of phenoxybenzamine at 37 degrees C is due to the predominance of covalent bonding of phenoxybenzamine with the receptors, whereas at lower temperatures like 24 degrees C, the blockade of the muscarinic receptors by phenoxybenzamine is mainly due to simple occlusion.
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PMID:Low temperature and muscarinic receptor activities. 279 13

Hypothermia has previously been demonstrated to induce supersensitivity (defined as a decrease in the ED50) of guinea pig left atria to the negative inotropic effect of carbachol. In the present investigation, the dissociation constant (pKA or -log KA) for carbachol, determined using benzilylcholine mustard, was found to be significantly increased at 25 degrees C compared to 37 degrees C. However, the increase in pD2 (-log ED50) for carbachol at 25 degrees C was much less than would be predicted from the increase in pKA. Increasing the extracellular Ca2+ concentration or the frequency of stimulation, both of which, like hypothermia, are believed to increase Ca2+ influx into cardiac cells, resulted in a decrease in sensitivity to carbachol. Carbachol had no significant effect on cAMP or cGMP levels at either 37 degrees C or at 25 degrees C. These results suggest that the hypothermia-induced increase in sensitivity of left atria to carbachol can be explained by an increase in the affinity of the muscarinic receptor for this agonist. However, the expression of this increased affinity appears to be limited. This may be due to a concurrent decrease in the efficacy of the carbachol muscarinic receptor complex.
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PMID:The mechanism of hypothermia-induced supersensitivity of guinea pig left atria to carbachol. 285 62

1. Hens received ICV injections of Ca2+ (1.98 g/100 ml) or Na+ (7.25 g/100 ml) at 28 degrees C and, following acclimation, at 37 or 20 degrees C, respectively. 2. At 28 degrees C (thermoneutrality), rectal temperature rose (P less than 0.05) following Na+ and fell (P less than 0.05) following Ca2+, similar to mammals and broiler chickens. 3. At 37 degrees C, Ca2+-induced hypothermia did not occur; nor did the Na+-associated hyperthermia at 20 degrees C. 4. Acclimation to a high or low temperature may produce an endogenous shift in CSF ion levels that make additional ion administration ineffective in affecting body temperature.
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PMID:Thermoregulatory responses of laying hens under cyclic environmental temperature to intraventricular calcium and sodium. 289 77

Calcium pantothenate (CaP), calcium 4'-phosphopantothenate (CaPP), pantethine, panthenol, sulfopantetheine and CoA decrease acute toxicity of acetaldehyde in mice. All studied compounds diminish duration of the narcotic action of ethanol--ET (3.5 g/kg intraperitoneally) in mice and rats. In the latter this effect is realized at the expense of "long sleeping" and "middle sleeping" animals. CaP (150 mg/kg subcutaneously) and CaPP (100 mg/kg subcutaneously) prevent hypothermia and a decrease of oxygen consumption in rats induced by ET administration. Combined administration of ET, CaP and CaPP leads to a characteristic increase of acid-soluble CoA fractions in the rat liver and a relative decrease of acetyl CoA synthetase and N-acetyltransferase reactions. The antitoxic effect of preparations of pantothenic acid is not mediated by CoA-dependent reactions of detoxication, but most probably is due to intensification of ET oxidation and perhaps to its elimination from the organism.
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PMID:[The protective effect of pantothenic acid derivatives and changes in the system of acetyl CoA metabolism in acute ethanol poisoning]. 290 77

During open-heart operations, periods occur during which the blood supply to the heart is stopped. Myocardial damage can be limited by cooling and induction of electromechanical arrest (cardioplegia). Many animal studies and some clinical trials provide strong evidence for the use of calcium antagonists, such as nifedipine, verapamil hydrochloride, diltiazem hydrochloride, and lidoflazine, as adjuncts to cardioplegia to optimize the protection. Salutary effects of calcium antagonists are discussed in regard to possible mechanism of action, application time, and efficacy during hypothermia. A major conclusion is that virtually no negative effects on cardiac protection have as yet been described in experimental or clinical studies, apart from short-term negative inotropic responses, while there is an increasing body of positive evidence for their efficacy. A new development is the use of these drugs for regional cardioplegia during dilation of coronary arteries (transluminal angioplasty).
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PMID:Cardioplegia and calcium antagonists: a review. 294 69

Calcium channel blockers have an important role in the pharmacotherapy of cardiovascular disorders. These agents act by inhibiting the slow inward current into excitable cells, exert direct negative inotropic, chronotropic, and dromotropic activity, and are potent vasodilators. These direct effects are modified by reflex autonomic stimulation and by pathologic states. Serious adverse effects of the calcium channel blockers are most frequently observed in patients with ventricular dysfunction, conduction system disease, or concomitant beta blockade. Calcium channel blockers are indicated in the treatment of angina pectoris, supraventricular arrhythmias, and hypertension. The use of these agents in patients with hypertrophic cardiomyopathy, congestive heart failure, and pulmonary hypertension is investigational. The calcium channel blockers are gaining increased importance in the management of patients undergoing cardiac surgery. Verapamil is indicated for the treatment of post-cardiac-surgical atrial flutter and fibrillation; however, the calcium antagonists are not effective as prophylaxis against postoperative supraventricular arrhythmias. Laboratory studies have shown that drug interactions exist between calcium channel blockers and inhalational anesthetics and nondepolarizing neuromuscular blocking agents; clinical studies have demonstrated that these interactions are rarely significant. Perioperative coronary spasm can be effectively treated with the calcium channel blockers. The timing of calcium antagonist withdrawal prior to surgery is controversial, but continuation of therapy until surgery is usually safe. The clinical significance of platelet function inhibition by the calcium antagonists is unknown. Protection of ischemic myocardium by calcium channel blockers has been demonstrated. Important interactions between the calcium antagonists, hypothermia, and the ionic constituents of cardioplegia require further study before the role of these agents as adjuncts to clinical cardioplegia is defined. Expanded indications and the introduction of new calcium channel blockers will result in increased use of these agents in the future.
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PMID:Calcium channel blockers and cardiac surgery. 297 80

The effect of the opiate antagonists naloxone and MR2266 on ethanol-induced hypothermia and changes in Ca2+-stimulated Mg2+-ATPase activity in brain regions were investigated in the present study. Administration of different doses of ethanol (0.5-2 g/kg, IP) produced a dose-dependent hypothermia. Ca2+/Mg2+-ATPase activity in the hypothalamus was stimulated at 30 min and 2 hr after ethanol (2 g/kg, IP) treatment. In cortex, enzyme activity was inhibited by ethanol at 30 min with no change seen at 2 hr. Naloxone (7.5 mg/kg, SC) at a dose which did not affect body temperature or enzyme activity, partially inhibited ethanol-induced hypothermia and enzyme activity at the earliest time (30 min) but not at 2 hours. The opiate Kappa antagonist MR2266 (5 mg/kg, SC), however, significantly protected against ethanol hypothermia and enzyme activation measured at 30-120 min. This evidence suggests that ethanol-induced hypothermia and subsequent activation changes of Ca2+/Mg2+-ATPase in the hypothalamus may be regulated by opiate Kappa receptors, and that Ca2+ ions play an important role in mediating the effects of ethanol.
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PMID:Ethanol-induced hypothermia in rats: possible involvement of opiate kappa receptors. 301 66

Administration of the opiate U-50,488H (3-20 mg/kg s.c.), a selective kappa receptor agonist, produced a dose-dependent decrease of rectal temperature in rats. This hypothermic effect of U-50,488H was accompanied by an enhanced activity of Ca2+/Mg2+ ATPase in crude synaptosomal (P2) fractions obtained from hypothalamus but not from cortex or cerebellum. Mg2+ ATPase activity in these regions was not altered by U-50,488H (15 mg/kg s.c.). Naloxone (5 mg/kg) partially and MR2266 (5 mg/kg) completely reversed the temperature and enzyme changes. Pretreatment with the calcium channel blockers nimodipine (1 mg/kg s.c.), diltiazem (10 mg/kg s.c.) and verapamil (2.5 mg/kg s.c.) potentiated the hypothermic effect of U-50,488H as well as the stimulation of Ca2+/Mg2+ ATPase in hypothalamus. These observations suggest that kappa agonists may produce opiate receptor mediated hypothermia through changes in intracellular Ca2+ levels in the hypothalamus.
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PMID:Interaction of kappa receptor agonists with Ca2+ channel antagonists in the modulation of hypothermia. 302 38

Preserved stored blood undergoes metabolic changes depending on the duration of storage. These metabolic changes include a deprivation of 2,3-diphosphoglycerate (2,3-DPG), acidosis and hyperkalemia. The preservative contains citrate as an anticoagulant which binds the ionised serum calcium. 2,3-DPG depleted erythrocytes show a clearly elevated oxygen affinity. Following massive transfusion, these changes can also occur in the recipient. Under these conditions, patients with coronary artery disease show impaired heart function. Prejudicial changes concerning other vital systems have not yet been definitely proved. Acidosis, hypocalcemia and hyperkalemia can take place under massive transfusion. Normally the body's own compensatory mechanisms ensure sufficient recompensation; however, under hypothermia or shock these mechanisms can be impaired. Disturbances of the electrolyte and acid base system are safely detected by ECG and regularly performed acid base analysis.
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PMID:[Metabolic disorders caused by blood transfusions]. 306 47

Oxygenation of crystalloid cardioplegic solutions is beneficial, yet bicarbonate-containing solutions equilibrated with 100% oxygen become highly alkaline as carbon dioxide is released. In the isolated perfused rat heart fitted with an intraventricular balloon, we recently observed a sustained contraction related to infusion of cardioplegic solution. In the same model, to record these contractions, we studied myocardial preservation by multidose bicarbonate-containing cardioplegic solutions in which first the calcium content and then the pH was varied. An acalcemic cardioplegic solution (Group 1) and the same solution with calcium provided by adding calcium chloride (Group 2) or blood (Group 3) were equilibrated with 100% oxygen. Ionized calcium concentrations were 0, 0.10 +/- 0.06, and 0.11 +/- 0.07 mmol/L and pH values were 8.74 +/- 0.07, 8.54 +/- 0.08, and 8.40 +/- 0.07, all highly alkaline. Hearts were arrested for 2 hours at 8 degrees +/- 2.5 degrees C and reperfused for 1 hour at 37 degrees C. At end-arrest, myocardial adenosine triphosphate was depleted in all three groups, significantly in Groups 2 and 3. In Group 1 the calcium paradox developed upon reperfusion, with contracture (left ventricular end-diastolic pressure = 60 +/- 7 mm Hg), creatine kinase release up to 620 +/- 134 U/L, a profound further decrease in adenosine triphosphate to 1.9 +/- 1.7 nmol/mg dry weight, and either greatly impaired or no functional recovery (17% +/- 10% of prearrest developed pressure). Three hearts in this group released creatine kinase during arrest and did not resume beating during reperfusion. In Groups 2 and 3, the calcium paradox did not occur; functional recovery was 61% +/- 4% and 71% +/- 9% at 5 minutes of reperfusion. In two additional groups (4 and 5), the pH of the acalcemic cardioplegic solution was decreased by equilibration with 2% and 5% carbon dioxide in oxygen to 7.53 +/- 0.03 and 7.11 +/- 0.02. Contractions during arrest were smaller than in Groups 1, 2, and 3; adenosine triphosphate was maintained during arrest; functional recovery was 101% +/- 3% and 96% +/- 4% at 5 minutes of reperfusion. We conclude that acalcemic solutions with carbon dioxide are superior to highly alkaline calcium-containing solutions. If oxygenation of cardioplegic solutions, of proved value, causes severe alkalinity, then calcium paradox may result even with hypothermia. This hazard is prevented by adding calcium or blood to the solution or carbon dioxide to the oxygen used for equilibration.
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PMID:Oxygenation of cardioplegic solutions. Potential for the calcium paradox. 311 49


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