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

Hypothermia during calcium-free perfusion of hearts protects them from injury caused by subsequent calcium repletion at 37 C (calcium paradox). Injury to calcium-free hearts is also associated with contracture caused by anoxia, 2,4-dinitrophenol (DNP), or caffeine. This study was done for the purpose of determining whether hypothermia during calcium-free perfusions protects hearts from contracture-associated injury. Langendorff-perfused rat hearts were studied in four experimental groups: I) Anoxia: Thirty minutes of anoxic perfusion at 37 C was followed by thirty minutes of anoxic calcium-free perfusion at 37-18 C. II) Calcium paradox: Five minutes of calcium-free perfusion at 37-18 C was followed by calcium repletion at 37 C. III, IVa) Caffeine or DNP: Five minutes of calcium-free perfusion at 37-18 C was followed by addition of 10 mM caffeine or 1 mM DNP in calcium-free medium at 37 C or, IVb) 1 mM DNP in calcium-free medium at 22 C. Injury was assessed by measurement of serial releases of creatine kinase (CK) in effluents and by cellular morphology. The results show that progressive hypothermia to 22 C during calcium-free perfusion periods produced a progressive reduction of CK release and morphologic evidence of injury due to anoxia, caffeine, or DNP, which closely paralleled protection of hearts from the calcium paradox. Protection from injury in all experimental groups was associated with preservation of sarcolemmal membrane integrity and prevention of cell separations at intercalated disk junctions. It is proposed that weakening of intercalated disks occurs during calcium-free perfusions and may be a cause of mechanical fragility of the sarcolemma. Hypothermia may protect hearts from contracture-associated injury by preserving the integrity of intercalated disk junctions during periods of extracellular calcium depletion.
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PMID:Parallel temperature dependence of contracture-associated enzyme release due to anoxia, 2,4-dinitrophenol (DNP), or caffeine and the calcium paradox. 674 11

Acute administrations (IP) of caffeine produced dose-dependent changes in the body temperature of rats. Low doses (12.5 and 25 mg/kg) induced hyperthermia soon after drug administration, while high doses (50 and 100 mg/kg) produced maximal hypothermia approximately 2 hr later. The acute effects of caffeine were also dependent on ambient temperature. The hyperthermic and hypothermic responses were attenuated and blocked, respectively, in rats maintained at 32 degrees C. At 4 degrees C, the hypothermic response was exacerbated, and the hyperthermic response was absent. Tolerance rapidly developed to the hypothermic actions of caffeine when rats were administered the drug over 28 days. Following the emergence of tolerance, hyperthermia was observed in rats given 50 mg/kg of caffeine. The hyperthermic responses to the low doses of caffeine were not altered by the frequency of drug administration. Both the acute and chronic effects of caffeine on thermoregulation are not unlike those found for morphine. Possible mechanisms of action underlying the thermoregulatory effects of caffeine are discussed.
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PMID:Temperature responses in rats after acute and chronic administrations of caffeine. 688 19

Administered intracisternally, adenosine (ADO), 2-chloroadenosine (CADO), adenosine-5'-cyclopropylcarboxamide (ACC) and adenosine-5'-ethylcarboxamide (AEC) caused dose-related increases in hot plate reaction times in mice. The rank order of potency was AEC=ACC greater than CADO greater than ADO and ACC exerted demonstrable effects with doses as low as 10 ng/mouse. ADO itself was more potent than AMP, ADP, ATP and several other related compounds of interest. Theophylline, caffeine and 8-phenyltheophylline antagonized the antinocisponsive effect of CADO or ACC. Papaverine (an adenosine uptake blocker) and erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA: an adenosine deaminase inhibitor) potentiated the effect of ADO. EHNA did not potentiate the action of CADO in this procedure. The antinocisponsive effect of CADO was not antagonized by a host of neurally active agents including naloxone, clonidine and RO 20-1724. Time course studies indicated that the antinocisponsive effect of ADO was transient with the peak effect occurring 5 min after injection and disappearing by 60 min, whereas the effect of CADO persisted for at least 90 min. Intracisternally administered CADO also caused a pronounced hypothermia, loss of muscle tone and was active in the mouse writhing test. Taken together, these data demonstrate that purine exert potent in vivo behavioral effects and are consonant with the existence of a central purinergic P1-receptor which is amenable to selective pharmacological manipulation.
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PMID:In vivo behavioral assessment of central nervous system purinergic receptors. 689 75

Cytosolic Ca2+ concentration of rat ventricular cells was measured under varying experimental conditions by using a fluorescent Ca2+ indicator, Fura-2. Resting [Ca2+]i of rat myocyte was 150 +/- 30 nM (n = 39), and this value was compatible with others. The Perfusion of cardioplegic solution significantly increased [Ca2+]i, and this effect was further augmented by hypothermia (p < 0.05). Application of nifedipine (5 x 10(-7) M) to the perfusate or pretreatment of caffeine (10 mM) had no apparent effect on this cardioplegia-induced [Ca2+]i change. But Ni2+ (5 mM), an antagonist of Na+/Ca2+ exchange mechanism, prevented the [Ca2+]i change during cardioplegia (p < 0.05). Magnitude of cardioplegia-induced [Ca2+]i increase was also dependent on the Ca2+ concentration of cardioplegic solution. These results suggest that Na+/Ca2+ exchange may play an important role in cardioplegia-induced [Ca2+]i change. To rule out the possibility whether the protective effect of hypothermic cardioplegia is due to the preservation of high-energy phosphate store or decreasing the transmembrane ionic fluxes by phase transition, we exhausted a energy store of cardiac cell by application of 2,4 dinitrophenol to the bath and measured its effect on [Ca2+]i change during cardioplegia. Hypothermic cardioplegia delayed the onset of [Ca2+]i increase and decreased its amplitude compared to those of normothermic cardioplegia. From the above results, hypothermic cardioplegia may protect the cardiac cells from ischemic insult by preserving a high-energy phosphate store. Application of Ni2+ to the cardioplegic solution or reduction of external Ca2+ concentration also had some protective effect, since it prevented [Ca2+]i increase during cardioplegia.
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PMID:Effect of hypothermic cardioplegia on cardiac protection--I. Effect of hypothermic cardioplegia on the cytosolic Ca2+ concentration in rat ventricular myocytes. 809 93

The case reported here concerns a 40-year-old woman who has suffered from severe migraine without aura since she was 23. The patient has been taking 1-3 suppositories of Virdex (2 mg of ergotamine tartrate, 250 mg of aminophenazone, caffeine) every day for the past three years. In addition to headache, the onset of short, sporadic cramps in the limbs together with paresthesia, hyposthenia, hypothermia and skin pallor with a slight increase in diastolic pressure, made hospital treatment necessary. Instrumental investigation through a stress test on a moving carpet, doppler, echo-doppler and digitalized angiography of the arterial vessels of the lower limbs shows the presence of bilateral impairment attributable to the chronic intake of ergotamine.
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PMID:Vascular injuries in ergotamine abuse: a case report. 831 18

This paper reviews the use of ephedrine (E) and xanthines (X) to improve thermogenesis and cold tolerance. Recent experiments in cold-exposed subjects have shown that the beneficial effects of ingesting an E/caffeine (C) capsule on metabolic rate (M), heat debt, deep body core temperature (Tre) (P < 0.05) is entirely comparable to that observed with an E/C/theophylline (T) capsule. Although T has been reported to reduce the drop in Tre in several studies, these improvements are difficult to explain in the absence of changes in M. A theobromine-based commercial sports bar (Cold Buster) has been similarly shown to reduce the drop in Tre. However, such a claim could not be confirmed in our lab, even in two studies performed under different environmental conditions. Despite an increase in M in some studies, C had no effect on Tre in the cold. It is concluded that E/X represent, at the moment, the best pharmacological agents to enhance cold thermogenesis and to delay the onset of hypothermia in humans.
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PMID:Effects of ephedrine/xanthines on thermogenesis and cold tolerance. 838 82

To study the role of adenosine in sleep regulation, the adenosine A1 receptor agonist N6-cyclopentyladenosine (CPA) and the antagonist caffeine were administered to rats. Intraperitoneal (i.p.) CPA 1 mg/kg but not 0.1 mg/kg, suppressed rapid-eye-movement (REM) sleep and enhanced electroencephalographic (EEG) slow-wave activity (power density 0.75-4.0 Hz) in non-REM sleep. The latter effect was remarkably similar to the response to 6-h sleep deprivation. The effects persisted when CPA-induced hypothermia was prevented. Caffeine (10 and 15 mg/kg i.p.) elicited a dose-dependent increase in waking followed by a prolonged increase of slow-wave activity in non-REM sleep. The combination of caffeine (15 mg/kg) and sleep deprivation caused less increase in slow-wave activity than sleep deprivation alone, indicating that caffeine may reduce the buildup of sleep pressure during waking. The results are consistent with the involvement of adenosine in the regulation of non-REM sleep.
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PMID:Effects of N6-cyclopentyladenosine and caffeine on sleep regulation in the rat. 873 4

To determine the relationship between cardiac hypothermia tolerance and the sources of activator calcium, we selectively modified either the sarcolemmal calcium permeability by nifedipine or the sarcoplasmic reticulum function by caffeine in papillary muscles from both the rat, as a cold sensitive model, and the ground squirrel, Citellus dauricus, a deep hibernator. Both force-interval relationship and cooling performance were investigated. At 25 degrees C, the slope of the force-interval curve of the ground squirrel was nearly double that of the rat. At shorter test intervals 0.5 muM nifedipine moved the curve down with little effect at longer intervals, and the curve slope increased. Caffeine (1 mM) decreased the peak force and eliminated its dependence upon test interval. When the temperature was lowered, rat preparations showed a marked increase of resting tension and aftercontraction between 7 and 12 degrees C and became inexcitable. In contrast, they maintained contractility down to a few degrees above 0 degrees C without aftercontraction and increased resting tension in the ground squirrel. In the rat nifedipine shortened the contractions, prevented the increase of resting tension, and minimized aftercontractions, with little improvement of contractility. Caffeine prolonged the contractions, caused a striking increase of resting tension and aftercontractions, and finally disabled the contractility at about 5-10 degrees C, even in the ground squirrel. We conclude that depressed calcium influx helps to prevent hypothermic calcium overload of the cardiac cells. Good function of the sarcoplasmic reticulum is essential for tolerance of hypothermia by cardiac cells. A suggestion that may improve the hypothermic tolerance of the myocardium from nonhibernators is postulated.
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PMID:Dependence of myocardial hypothermia tolerance on sources of activator calcium. 936 7

Almotriptan (3-[2-(dimethylamino) ethyl]-5-(pyrrolidin-1-ylsulfonylmethyl)-1H-indole, CAS 154323-57-6) is a new 5-HT1B/1D agonist whose clinical efficacy has been demonstrated in Phase III clinical trials. This study aimed to evaluate the safety of almotriptan with respect to the central nervous system, renal function and respiratory dynamics using preclinical animal models. The results indicate that almotriptan does not cross the blood-brain barrier, since no effects on/interaction with spontaneous locomotor activity, hexobarbital-induced sleeping time, caffeine-induced increase of spontaneous locomotor activity, or hypothermia (caused by stimulation of central 5-HT1D receptors) was observed following treatment. Almotriptan had a mild antiemetic effect and a slight, transient diuretic effect in dogs, although the latter effect is probably of no clinical relevance. In addition, no effect on the respiratory system of conscious guinea pigs was observed following almotriptan treatment. These results indicate that almotriptan has a favourable safety profile with respect to the central nervous, renal and respiratory systems.
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PMID:Safety profile of almotriptan, a new antimigraine agent. Effects on central nervous system, renal function and respiratory dynamics. 1164 4

OBJECTIVE: To review medical literature related to apnea of prematurity. SOURCES: Extensive literature search and clinical practice-oriented concepts. SUMMARY OF THE FINDINGS: Apnea is one of the most common respiratory disorders in the neonatal period. Immaturity of the central nervous system is associated with instability of respiration. Therefore, apnea manifests itself in other systems, causing problems such as hypoglycemia, hypothermia, infection, or patent ductus arteriosus. Apnea may be central, obstructive or mixed depending on the presence of air flow through the upper airways. Diagnosis should involve careful observation by unit personnel and the monitoring of heart rate, respiratory frequency or arterial oxygen saturation. Initially, the treatment consists of xanthines (caffeine and aminophylline). If respiratory failure occurs, then continuous positive airway pressure (CPAP), and mechanical ventilation should be used. CONCLUSIONS: Preterm newborns are susceptible to respiratory problems, having apnea as a clinical manifestation of disorders in many organs and systems.
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PMID:[Neonatal apnea] 1467 97


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