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

After a 1 hr deep prolonged immersion hypothermia, warming up of experimental rats in water (the temperature increase 0.25 degree C/min) entailed a complete recovery of all the parameters of gas exchange, haemodynamics, external respiration, and the blood. After a 3 hr hypothermia, under the same conditions of warming up, oxygen consumption, CO2 production, and 1 min blood volume were obviously decreased, and the animals died within 0.5-1.0 hr.
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PMID:[Recovery of the oxygen consumption, oxygen transport, and cardiac activity after hypothermia followed by respiration and cardiac arrest in rats]. 974 94

Intracranial pressure depends on cerebral tissue volume, cerebrospinal fluid volume (CSFV) and cerebral blood volume (CBV). Physiologically, their sum is constant (Monro-Kelly equation) and ICP remains stable. When the blood brain barrier (BBB) is intact, the volume of cerebral tissue depends on the osmotic pressure gradient. When it is injured, water movements across the BBB depend on the hydrostatic pressure gradient. CBV depends essentially on cerebral blood flow (CBF), which is strongly regulated by cerebral vascular resistances. In experimental studies, a decrease in oncotic pressure does not increase cerebral oedema and intracranial hypertension (ICHT). On the other hand, plasma hypoosmolarity increases cerebral water content and therefore ICP, if the BBB is intact. If it is injured, neither hypoosmolarity nor hypooncotic pressure modify cerebral oedema. Therefore, all hypotonic solutes may aggravate cerebral oedema and are contra-indicated in case of ICHT. On the other hand, hypooncotic solutes do not modify ICP. The osmotic therapy is one of the most important therapeutic tools for acute ICHT. Mannitol remains the treatment of choice. It acts very quickly. An i.v. perfusion of 0.25 g.kg-1 is administered over 20 minutes when ICP increases. Hypertonic saline solutes act in the same way, however they are not more efficient than mannitol. CO2 is the strongest modulating factor of CBF. Hypocapnia, by inducing cerebral vasoconstriction, decreases CBF and CBV. Hyperventilation is an efficient and rapid means for decreasing ICP. However, it cannot be used systematically without an adapted monitoring, as hypocapnia may aggravate cerebral ischaemia. Hyperthermia is an aggravating factor for ICHT, whereas moderate hypothermia seems to be beneficial both for ICP and cerebral metabolism. Hyperglycaemia has no direct effect on cerebral volume, but it may aggravate ICHT by inducing cerebral lactic acidosis and cytotoxic oedemia. Therefore, infusion of glucose solutes is contra-indicated in the first 24 hours following head trauma and blood glucose concentration must be closely monitored and controlled during ICHT episodes.
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PMID:[The internal environment and intracranial hypertension]. 975 May 95

Eight healthy horses premedicated with xylazine and induced with ketamine were used to evaluate sevoflurane in oxygen for maintenance of anaesthesia during elective exploratory laparotomy. After orotracheal intubation, horses were hoisted, placed in dorsal recumbency on a padded surgery table, and received sevoflurane in oxygen for maintenance of anaesthesia. The horses were allowed to breathe spontaneously until instrumented; then, they were mechanically ventilated to maintain the PaCO2 between 35 and 45 mmHg. Systolic (SAP), diastolic (DAP), and mean (MAP) arterial blood pressures, heart rate (HR), ECG, respiratory rate, an estimation of the saturation of haemoglobin with oxygen in peripheral arterial blood (S(p)O2), nasal temperature, end-tidal CO2(ET(CO2)), end-tidal sevoflurane (ET(SEVO)), and vaporiser concentration were recorded every 5 min post induction; arterial blood samples were obtained soon after induction, at 30 min after induction, and every hour thereafter until surgery was completed. Recovery data including times from the sevoflurane vaporiser being turned off to first movement, to sternal recumbency, and to standing, number of attempts to stand, and recovery score (between 1 = safe, smooth and 6 = stormy, major injury to horse) were collected. Analysis of variance was performed using physiological data collected over 195 min of anaesthesia, the longest time period during which all 8 horses were instrumented. Time effects (P<0.05) for HR, SAP, DAP, MAP, and nasal temperature were identified. Heart rate peaked at 45 min and declined over the course of the procedure. Arterial blood pressure generally decreased over time. Body temperature decreased over time. From 15 to 195 min mean ET(SEVO)concentration ranged from 2.0 to 3.3%, while mean vaporiser settings ranged from 3.7 to 5.5%. Three horses received intra-operative ketamine; all horses received dobutamine infusions; and 2 horses received intra-operative calcium-dextrose. Total anaesthesia time was 222-316 min (mean+/-s.d.269+/-31 min). Time from turning the sevoflurane vaporiser off to first movement was mean +/-s.d.18+/-15 min; to sternal recumbency was 54+/-22 min; to standing was 65+/-27 min; and to returning the horse to the stall in the ward was 78+/-24 min. Six horses stood on the first attempt; 2 horses stood on the second attempt. The median recovery score was one (1-3). In conclusion, sevoflurane provided a stable, easily controllable anaesthetic plane during prolonged exploratory laparotomies; horses experienced smooth, safe recoveries after maintenance of anaesthesia with sevoflurane following routine anaesthetic induction and post operative xyalzine administration.
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PMID:Maintenance of anaesthesia with sevoflurane and oxygen in mechanically-ventilated horses subjected to exploratory laparotomy treated with intra- and post operative anaesthetic adjuncts. 975 97

We conducted this study to determine whether two of the physiological changes associated with non-sustainable exercise, elevated blood lactate levels and decreased arterial pH, contribute to the behavioral hypothermia exhibited by exhausted lizards. Dipsosaurus dorsalis were placed in a thermal gradient and their body temperatures were recorded from 08:00 to 14:00 h. At 14:00 h, animals were subjected to different experimental regimens. In the exercise (E) regimen, animals at 40 degrees C were forced to exercise maximally for 5 min on a treadmill. In the lactate (L) regimen, animals were infused with 11.5 ml kg-1 of 250-500 mmol l-1 sodium lactate. In the osmolarity control (O) regimen, animals were injected with 11.5 ml kg-1 of 500 mmol l-1 NaCl, and in the injection control (I) regimen, animals were injected with 11.5 ml kg-1 of 150 mmol l-1 NaCl. In the hypercapnia (H) regimen, the thermal gradient was flushed with a gas mixture containing 10 % CO2, 21 % O2 and 69 % N2, a treatment that lowers the arterial pH of D. dorsalis to a value comparable with that imposed by exhaustive exercise. A group of control (C) animals was left undisturbed in the thermal gradient for 24 h. Animals in all experimental groups were returned to the thermal gradient, and their cloacal temperatures were monitored until 08:00 h the following morning. The mean cloacal temperature of E animals underwent a significant decrease of 4-7 degrees C, relative to control animals, which persisted for 7 h. The mean cloacal temperatures of animals subjected to 2 h of regimen H also decreased by 3.5-9 degrees C and remained depressed for 12 h following the beginning of the treatment. L, O and I animals did not undergo a significant change in body temperature following treatment, and their mean body temperatures did not differ from those of C animals at any time during the experiment. The results of this study suggest that the metabolic acidosis, but not the elevated blood lactate level, that follows exhausting exercise might play a role in the behavioral hypothermia that follows exhausting exercise in D. dorsalis.
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PMID:The roles of acidosis and lactate in the behavioral hypothermia of exhausted lizards. 988 44

We assessed the seasonal variations in the effects of hypercarbia (3 or 5% inspired CO2) on cardiorespiratory responses in the bullfrog Rana catesbeiana at different temperatures (10, 20 and 30 degrees C). We measured breathing frequency, blood gases, acid-base status, hematocrit, heart rate, blood pressure and oxygen consumption. At 20 and 30 degrees C, the rate of oxygen consumption had a tendency to be lowest during winter and highest during summer. Hypercarbia-induced changes in breathing frequency were proportional to body temperature during summer and spring, but not during winter (20 and 30 degrees C). Moreover, during winter, the effects of CO2 on breathing frequency at 30 degrees C were smaller than during summer and spring. These facts indicate a decreased ventilatory sensitivity during winter. PaO2 and pHa showed no significant change during the year, but PaCO2 was almost twice as high during winter than in summer and spring, indicating increased plasma bicarbonate levels. The hematocrit values showed no significant changes induced by temperature, hypercarbia or season, indicating that the oxygen carrying capacity of blood is kept constant throughout the year. Decreased body temperature was accompanied by a reduction in heart rate during all four seasons, and a reduction in blood pressure during summer and spring. Blood pressure was higher during winter than during any other seasons whereas no seasonal change was observed in heart rate. This may indicate that peripheral resistance and/or stroke volume may be elevated during this season. Taken together, these results suggest that the decreased ventilatory sensitivity to hypercarbia during winter occurs while cardiovascular parameters are kept constant.
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PMID:Seasonal changes in the cardiorespiratory responses to hypercarbia and temperature in the bullfrog, Rana catesbeiana. 1062 62

The hypoxic ventilatory threshold of many mammals correlates with their hemoglobin-oxygen affinity (P50). Yet, in some small mammals ventilation actually declines, rather than increases, with exposure to decreasing PaO2; their air convection requirement (V(E)/V(O2)), however, is elevated in hypoxia. We propose that the threshold of the hypoxic V(E)/V(O2) of small mammals coincides with the inflection ('knee') of their in vivo O2 equilibrium curve (O2EC). In vivo blood gas and pH data were obtained from normoxic and hypoxic lesser-spear nosed bats, Phyllostomus discolor; in vitro blood O2EC were also generated for normoxic bats at 32 and 37 degrees C and at three P(CO2)'s. The hypoxic V(E)/V(O2) threshold of P. discolor occurs at PaO2 = 39 Torr; the corresponding in vivo O2 saturation is 0.70, approximating the inflection of the O2EC. This animal has a high blood O2 affinity (P50 = 27.5 Torr at pH 7.40 and 37 degrees C; P50 = 30.8 Torr at in vivo pH of 7.31 and TB of 37.4 degrees C). As PaO2 is reduced, a pronounced hypoxia-induced respiratory alkalosis and hypothermia help maintain SaO2 near the O2EC inflection (0.64-0.70 S(O2)).
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PMID:In vivo blood oxygen binding in hypoxic lesser spear-nosed bats: relationship to control of breathing. 1064 63

In neuronal cultures from the forebrain of 14-d-old rat embryos, transient hypoxia (95% N2/5% CO2, 37 degrees C) for 6 h has been shown to trigger delayed apoptotic death through sequential changes in protein synthesis, whereas preconditioning by a brief episode of hypoxia can rescue neurons. Because hypothermia has been reported to be neuroprotective, the present study was designed to test the influence of reduced temperature on the consequences of lethal hypoxia in our culture model, and cellular mechanisms involved were compared with those underlying preconditioning effects. After 6 d in vitro, cultures were subjected to hypoxia for 6 h. They were either placed at 32 degrees C concomitantly with hypoxia for 6 h or preconditioned the day before by a 1-h episode of hypoxia. The hypoxic insult decreased cell viability by 38% at 96 h after reoxygenation, and 23% of the neurons showed morphologic features of apoptosis. Both hypothermia and preconditioning prevented neuronal death and reduced apoptosis. Preconditioning led to time-dependent changes in leucine incorporation, with persistent overexpression of the survival proteins Bcl-2 and heat-shock protein 70. It also increased thymidine incorporation, in line with induction of the cofactor for DNA polymerase, proliferating cell nuclear antigen. Hypothermia reduced basal apoptosis and necrosis, but did not affect thymidine incorporation, and abolished hypoxia-associated protein synthesis. Therefore, both treatments were protective against neuronal injury consecutive to hypoxia in developing brain neurons in vitro. Whereas preconditioning activated a program that stimulated the expression of anti-apoptotic gene products and regulatory components of the cell cycle, hypothermia did not trigger active processes, but depressed cell activity, which in turn may impair the apoptotic phenomenon.
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PMID:Effects of hypothermia on hypoxia-induced apoptosis in cultured neurons from developing rat forebrain: comparison with preconditioning. 1070 40

Increased intracranial pressure (ICP) is a pathological state common to a variety of neurological diseases, all of which are characterized by the addition of volume to the skull contents. Elevated ICP may lead to brain damage or death by two principle mechanisms: 1) global hypoxic-ischemic injury, as a consequence of reduced cerebral perfusion pressure (CPP) and cerebral blood flow; and 2) mechanical distortion and compression of brain tissue as a result of intracranial mass effect and ICP compartmentalization. All ICP therapies have as a goal, reduction of intracranial volume. In unmonitored patients with acute neurological deterioration, head elevation, hyperventilation, and mannitol (1g/kg) can rapidly lower ICP. Fluid-coupled ventricular catheters and fiberoptic transducers are the most accurate and reliable instruments for measuring ICP. In monitored patients, the treatment of critically raised ICP should proceed in an orderly step-wise fashion: 1) consideration of neuroimaging to exclude a new surgically operable lesion; 2) intravenous sedation to attain a quiet motionless state; 3) manipulation of blood pressure to keep CPP >70 and <120; 4) mannitol infusion; 5) moderate hyperventilation (P(CO2) 26 to 30 mmHg); and 6) high-dose pentobarbital therapy. Application of moderate hypothermia (32 to 33 degrees C) shows promise as a newer method for treating refractory ICP. Placement of an ICP monitor is the critical first step in management of ICP. Treatment is best done using a stepwise protocol, with careful attention to sedation and CPP control prior to using mannitol and hyperventilation.
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PMID:Diagnosis and management of increased intracranial pressure. 1188 75

Over the last decade, a proliferation of interest has emerged in the area of avalanche survival, yielding both an improved understanding of the pathophysiology of death after avalanche burial and technological advances in the development of survival equipment. The dismal survival statistics born out of the modern era of winter recreation unmistakably reveal that elapsed time and depth of burial are the most critical variables of survival and the focus of newer survival devices on the market. Although blunt trauma may kill up to one third of avalanche victims, early asphyxiation is the predominant mechanism of death, and hypothermia is rare. A survival plateau or delay in asphyxiation may be seen in those buried in respiratory communication with an air pocket until a critical accumulation of CO2 or an ice lens develops. The newest survival devices available for adjunctive protection, along with a transceiver and shovel, are the artificial air pocket device (AvaLung), the avalanche air bag system (ABS), and the Avalanche Ball. The artificial air pocket prolongs adequate respiration during snow burial and may improve survival by delaying asphyxiation. The ABS, which forces the wearer to the surface of the avalanche debris by inverse segregation to help prevent burial, has been in use in Europe for the last 10 years with an impressive track record. Finally, the Avalanche Ball is a visual locator device in the form of a spring-loaded ball attached to a tether, which is released from a fanny pack by a rip cord. Despite the excitement surrounding these novel technologies, avalanche avoidance through knowledge and conservative judgment will always be the mainstay of avalanche survival, never to be replaced by any device.
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PMID:Technological advances in avalanche survival. 1265 51

Although gastric mucosal tonometry has been reported as a useful method to assess splanchnic perfusion during cardiovascular surgery, the conventional discontinuous method of tonometry (saline tonometry) was cumbersome and prone to systematic errors. A new automated system of air tonometry (Tonocap; Datex Ohmeda, Helsinki, Finland) allows for frequent (every 10 minutes) measurement of gastric regional CO2 (PrCO2) and may be more suitable as a monitoring system in cardiac patients. We evaluated the usefulness of continuous air tonometry as a marker of splanchnic perfusion during cardiopulmonary bypass (CPB). In 19 patients (53-79 years, mean 63 years) who underwent cardiovascular surgery under standard CPB with mild hypothermia (32 degrees C) from January 2001 to May 2002, the PrCO2 and calculated intramucosal pH (pHi) of gastric tonometry was monitored using Tonocap, and their relation to postoperative visceral organ function was evaluated. The pHi significantly increased after initiation of CPB from 7.32 +/- 0.07 to 7.43 +/- 0.10 (p < 0.05) and then consistently decreased in all patients to 7.39 +/- 0.09 at the end of CPB. The value of PrCO2 significantly (p < 0.01) correlated with the value of pHi. The lowest value of pHi during CPB was significantly related to blood urea nitrogen (r = -0.75, p < 0.05), serum creatinine (r = -0.78, p < 0.05), creatinine clearance (r = 0.68, p < 0.05) on postoperative day 1, and blood urea nitrogen (r = -0.84, p < 0.01) on day 3. In contrast, arterial blood lactate level, venous oxygen saturation, and routinely measured hemodynamics (e.g., pump flow, arterial pressure) during CPB were unrelated to the postoperative visceral organ function. These results suggest that continuous monitoring of gastric regional CO2 and pHi by air tonometry system is useful for the evaluation of splanchnic perfusion during CPB and may contribute to improve CPB technique by allowing the early detection of visceral malperfusion.
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PMID:Usefulness of continuous air tonometry for evaluation of splanchnic perfusion during cardiopulmonary bypass. 1255 16


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