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

Right heart catheterisation was undertaken in six patients with accidental deep hypothermia. Studies were carried out before and after rapid blood volume expansion, with and without Isoproterenol infusion, and were repeated at normal body temperatures. The initial haemodynamic pattern indicated a marked hypovolemia with a simultaneous decrease of both cardiac output and ventricular filling pressures, and a decreased measured total blood volume. Rapid correction of the hypovolemia revealed cardiac insufficiency, in part due to the persisting bradycardia. Left ventricular function was depressed in patients with prolonged cold exposure and normal in patients with short exposure. These abnormalities disappeared after Isoproterenol infusion during hypothermia, and spontaneously after return to normothermia. No imbalance existed between the decreased cardiac output and oxygen uptake in hypothermia, arterio-venous oxygen difference being within normal limits.
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PMID:Haemodynamic study of prolonged deep accidental hypothermia. 118 54

1. Changes in temperature were determined following injection of noradrenaline, adrenaline, isoprenaline, dopamine and 5-hydroxytryptamine (5-HT) into the cerebral ventricles of the conscious mouse.2. Noradrenaline (1-20 mug) and dopamine (10-160 mug) caused falls in body temperature. Adrenaline (1-20 mug) caused a slight and transient rise in body temperature followed by a fall. Isoprenaline (5-20 mug) caused a rise in body temperature, hypothermia only occurring after very high doses (200 mug) of this catecholamine.3. alpha- and beta-adrenergic blocking agents, phentolamine (> 2 mug) and propranolol (> 5 mug) respectively, caused falls in body temperature when injected into the cerebral ventricles of the mouse.4. Specific drug antagonism studies were limited owing to the intrinsic effects of the alpha- and beta-adrenergic blocking agents. However, some evidence was obtained to indicate that noradrenaline mediated its effects through a central alpha-type adrenergic receptor.5. 5-HT (10-160 mug) caused a fall in body temperature. The action of this indoleamine and the catecholamines in regard to thermoregulatory function is discussed.
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PMID:Temperature changes produced by the injection of catecholamines and 5-hydroxytryptamine into the cerebral ventricles of the conscious mouse. 605 3

Prodrugs of isoproterenol, 3-O-,4-O-diacetylisoproterenol (DAI) and 3-O-,4-O-dibenzoylisoproterenol (DBI), were tested for effects on colonic temperature in mice. Intraperitoneal injections of DAI or DBI (20, 50 and 125 mumol/kg) produced a dose-related hypothermia. Isoproterenol (125 mumol/kg) and its metabolite, 3-O-methylisoproterenol (125 mumol/kg), caused hypothermia of a lesser intensity. The involvement of beta-adrenergic receptors in the hypothermic effect of DAI (50 mumol/kg) was established by pretreatments with propranolol and sotalol. The results are discussed in terms of the pharmacodynamics of prodrugs, the pharmacokinetics and mechanism of action of isoproterenol, and the possible role of beta-receptors in temperature regulation. DAI and DBI may be useful as prodrugs for the activation of central beta-receptors.
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PMID:3-O-,4-O-diacetylisoproterenol and 3-O-,4-O-dibenzoylisoproterenol: hypothermic effects in mice and the involvement of beta-adrenergic receptors. 626 43

Hypothermic action of neurotropic drugs (Oxotremorine, Nicotine, Isoprenaline, Seduxene) is evaluated by means of suppression of shivering thermogenesis. The action is accounted for by their influence of the brain stem level of the postural muscular tension regulation rather than by selective action of these drugs on the hypothalamic thermoregulatory centre.
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PMID:[Analysis of the mechanism of the hypothermic action of neurotropic drugs]. 662 52

Episodic hyperhidrosis and hypothermia are the primary symptoms of a rare central nervous system disorder of thermoregulation which is often associated with agenesis of the corpus callosum and can present in childhood or adult years. During attacks, patients may exhibit confused, withdrawn, and lethargic behavior and ataxia or other neurologic symptoms. A 21-year-old man with temperature chronically between 30 and 32 degrees C transiently responded to phenobarbital and to cyproheptadine therapy. A 34-year-old woman with frequent, brief episodes of hypothermia and hyperhidrosis improved with chlorpromazine treatment. Episodic thermoregulatory disturbance has been attributed to "vagal attacks" or "diencephalic epilepsy," but the pathophysiology remains undefined.
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PMID:Episodic hyperhidrosis, hypothermia, and agenesis of corpus callosum. 668 46

Rats infused centrally with bombesin become hypothermic at normal ambient temperatures when acutely deprived of food, but not while allowed unrestrained access to food. Ad lib-fed rats, tested at normal ambient temperatures, become hypothermic after receiving intracerebroventricular (ICV) bombesin when they have ventromedial hypothalamic lesions or when administered insulin or 2-deoxy-D-glucose peripherally. All of these conditions have been linked to reductions of sympathetic nervous system activity to brown adipose tissue (BAT), a major thermogenic mechanism of many homeotherms. A between group design was used to examine the effects of ICV bombesin infusions on the response to peripheral injections of a) the sympathetic ganglionic blocker chlorisondamine (2.5 mg/kg, IP) in ad lib-fed rats, b) the nonspecific beta-agonist isoproterenol (30 mg/kg, IP) in food-deprived rats, and c) the combination of isoproterenol and chlorisondamine in ad lib-fed rats. Ad lib-fed rats receiving ICV bombesin (100 ng/5 microliters), in combination with peripheral chlorisondamine injection, became hypothermic 60 min postbombesin administration (-2.84 +/- 0.33 degrees C), while ad lib-fed rats receiving ICV bombesin infusion and peripheral injections of saline did not (-0.08 +/- 0.37 degrees C). Isoproterenol blocked hyperthermia in ad lib-fed rats injected with chlorisondamine and ICV bombesin. Food-derived rats receiving ICV bombesin infusion and peripheral saline injection exhibited hypothermia 60 min postbombesin administration (-2.51 +/- 0.29 degrees C). Peripheral injections of isoproterenol prevented bombesin-induced hypothermia in food-deprived rats. These data suggest that bombesin induces hypothermia at normal ambient temperatures when the sympathetic nervous system drive to BAT cannot be (or is not) activated.
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PMID:Bombesin-induced hypothermia in rats tested at normal ambient temperatures: contribution of the sympathetic nervous system. 760 92

1. The study was carried out in adult patients having normal cardiovascular reflexes and no brain stem lesions. They were exposed to ambient temperature of 72-74 degrees F. Injections of agonists and antagonists of receptors were made into the lateral cerebral ventricles of these patients through diagnostic burr hole in the skull. 2. Noradrenaline, adrenaline and dopamine evoked hypotension and bradycardia. While the core temperature was reduced by nor-adrenaline and adrenaline, dopamine evoked hyperthermia. Isoprenaline elicited hypertension, tachycardia and hyperthermia. Opposite cardiovascular and thermal effects were observed with blockade of alpha 1-, beta-and dopamine receptors with prazosin, propranolol and haloperidol respectively. 3. Injection of 5-hydroxytryptamine resulted in hypertension, tachycardia and hyperthermia but hypotension, bradycardia and hypothermia were seen with methysergide. 4. Similarly, carbachol injection caused initial excitatory followed by inhibitory cardiovascular responses. These were associated with hypothermia. On the contrary atropine per se elicited hypertension, tachycardia and hyperthermia. 5. Thus, alpha 1- and beta-adrenoceptors, dopaminergic, serotonergic and muscarinic cholinergic receptors are present in human brain which appear to modulate cardiovascular activity and core temperature.
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PMID:A study of effects of putative neurotransmitters injected into the lateral cerebral ventricle of man. 790 93

Acute postoperative left ventricular dysfunction after hypothermic, crystalloid potassium cardioplegia occasionally occurs. This project examined myocyte contractility and inotropic responsiveness after hypothermic arrest with and without potassium cardioplegia. Isolated swine left ventricular myocytes were placed in a thermostatically controlled chamber (37 degrees C) that contained a standard cell medium, pulse stimulated at 1 Hz, and steady-state contractions were measured by computer-assisted video microscopy with and without isoproterenol (25 nmol/L). After baseline measurements were taken the myocytes were randomly assigned to the following treatments: (1) control group with infusion of 37 degrees C crystalloid solution and maintained at 37 degrees C for 3 hours (n = 23), (2) hypothermia group with infusion of 4 degrees C crystalloid without potassium and stored at 4 degrees C for 3 hours (n = 22), (3) hypothermic cardioplegia group with infusion of a crystalloid cardioplegia (oxygenated, buffered 4 degrees C Ringer's solution with 24 mEq/L K+) and then stored at 4 degrees C for 3 hours (n = 35). After treatment the myocytes were then rewarmed to 37 degrees C by infusion of medium, and contractile measurements were repeated. In the control group, the percent and velocity of shortening were identical to those in baseline measurements: 6.4% +/- 0.4% and 53 +/- 5 microns/sec, respectively, and these values remained unchanged in the hypothermia group: 6.5% +/- 0.4% and 51 +/- 3 microns/sec, respectively. However, in the hypothermic cardioplegia group, the percent and velocity of shortening were significantly lower with rewarming: 4.8% +/- 0.4% and 35 +/- 3 microns/sec, respectively, p < 0.05). Isoproterenol caused increased percent and velocity of shortening in both the control and hypothermia groups: 10.0% +/- 0.6% and 9.5% +/- 0.9% and 81.6 +/- 8 microns/sec and 71.4 +/- 8 microns/sec, respectively. This response was significantly blunted in the cardioplegia group (8.9% +/- 0.8% and 56.9 +/- 7 microns/sec, p < 0.05). With an isolated myocyte system that is independent of extracellular and perfusion effects, hyperkalemic cardioplegic solution resulted in depressed myocyte contractile performance after rewarming. Potassium cardioplegia also caused a blunted inotropic responsiveness on rewarming. A potential contributory factor for the depressed left ventricular function after the use of potassium cardioplegia is a direct depression in myocyte contractility.
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PMID:Hypothermic potassium cardioplegia impairs myocyte recovery of contractility and inotropy. 815 26

The aim of this study was to investigate the effects of beta-stimulation in deep (25 degrees C) hypothermia. Cardiac catheterization was performed on seven anesthetized beagle dogs. They were cooled between ice bags down to 25 degrees C and received isoproterenol administered intravenously three times: at the normal body temperature (37 degrees C) before cooling, after cooling at 25 degrees C, and after rewarming at 37 degrees C. Circulatory function was measured for every 1 degree C of temperature change. Isoproterenol infusion at 37 degrees C induced cardiac acceleration, including the increases of heart rate, cardiac output, and peak first derivative of the left ventricular pressure curve. Systemic vascular and mean outflow resistances and mean aortic pressure decreased. During cooling, shivering thermogenesis continued, even down to 25 degrees C. At 25 degrees C, cardiac acceleration after isoproterenol infusion did not exist but relaxation rate increased slightly. Systemic vascular and mean outflow resistances decreased, but left ventricular end-diastolic and filling pressures increased. beta-Stimulation at normal body temperature increases shivering thermogenesis during cooling. The venous return to the left ventricle at 25 degrees C increased after isoproterenol infusion while systemic vascular resistance decreased, indicating systemic vasodilatation. This increase in preload is probably due to vasoconstriction in pulmonary vessels, which may be mediated by prejunctional beta-adrenoceptors. For cardiac inotrophy, the isoproterenol had no physiologically significant effects at 25 degrees C. After rewarming at 37 degrees C, the effects of isoproterenol were physiologically similar to the effects at the same temperature before cooling.
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PMID:Cardiovascular responses to beta-stimulation with isoproterenol in deep hypothermia. 887 20

A 21-year-old male patient had suffered from palpitation and exertional dyspnea since October, 1997. He was admitted to our hospital, and a series of examinations were performed. Chest computed tomography (CT) revealed marked dilatation of the ascending aorta (about 7.5 cm at the proximal portion) and aortic annulus, an intimal flap in the ascending aorta and aortic arch was also noted. Cardiac catheterization revealed the pulmonary capillary wedge pressure was 33 mmHg, pulmonary artery pressure was 47/38 mmHg with a mean of 35.4. The cardiac index was 1.01 l/min/m2. Poor left ventricular contractility was shown by a left ventricular ejection fraction (LVEF) of 13.8% and a right ventricular ejection fraction (RVEF) of 5.13% by a radionuclide angiogram (RNA) study. Under the diagnosis of dilated cardiomyopathy and dissecting aortic aneurysm of the ascending aorta and aortic arch, he was put on a waiting list for heart transplantation. On November 11, 1997 he received heart transplantation. Resection of the dissecting aneurysm of the ascending aorta and the aortic arch and replacement with a 26 mm Vascutek graft were performed first under deep hypothermia and retrograde cerebral perfusion. Then while he was rewarming up, heart implantation was performed. He was discharged 30 days after surgery and has been doing well since then. As far as we know, no literature regarding combined heart transplantation and resection of a dissecting aneurysm of the ascending aorta and aortic arch has been reported.
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PMID:Combined heart transplantation and resection of dissecting aneurysm of ascending aorta and aortic arch: a case report. 1074 63


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