Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fourteen infants with complete common atrioventricular canal (CCAVC) underwent open heart surgery under deep hypothermia and circulatory arrest. There were three operative deaths and two late deaths. Postoperative studies performed in seven of the nine survivors revealed nearly normal hemodynamics. There were no residual shunts, and excellent mitral valve function was observed in six patients. In one patient, residual mitral regurgitation was noted. The pulmonary artery pressures and pulmonary vascular resistances were normal except in one who had severe pulmonary vascular obstructive disease before surgery. The mean left ventricular end-diastolic volume changed from 175 +/- 24% (SEM) before surgery to 106 +/- 7% after surgery (P less than 0.01). The corresponding right ventricular end-diastolic volume changed from 166 +/- 16% to 102 +/- 19% (P less than 0.025). Left ventricular ejection fraction was mildly decreased before and after surgery (0.63 +/- 0.02). Surgical repair of CCAVC is possible during the first year of life, with likely normalization of cardiac size and function. Unsatisfactory results related to pulmonary vascular obstruction may be anticipated if repair is delayed much beyond the first year.
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PMID:Complete common atrioventricular canal in infancy--surgical repair and postoperative hemodynamics. 67 47

Recent studies have shown that after total coronary artery occlusion, there is impaired "reflow" of blood accompanied by myocardial and capillary endothelial cell swelling. To investigate the effect of prolonged low flow myocardial ischemia on coronary vascular resistance, regional hypoperfusion of the distal left anterior descending coronary artery was studied in 31 autonomically blocked dogs on right heart bypass. Heart rate, aortic pressure, and, during ischemia, left ventricular end-diastolic pressure were held constant. The distal left anterior descending coronary artery was perfused at a substantially reduced perfusion pressure which resulted in an antegrade coronary blood flow that usually was between 3% and 7% (0.5-1 ml/min) of control. When relative hypothermia (33-34 degrees C) was induced in nine dogs, left anterior descending coronary artery vascular resistance did not change during 2.5-3 hours of low flow ischemia. Under euthermic conditions (37-40 degrees C) in 17 dogs there was a consistent progressive increase in distal left anterior descending coronary artery vascular resistance starting at 90 minutes (median) after onset of ischemia. By 110-140 minutes ischemic antegrade flow decreased by 35 +/- 4% (SEM) (P less than 0.01). Directionally similar flow changes were observed in six euthermic experiments using the krypton-85 washout technique. Light microscopy did not reveal hemorrhage as a cause of the increased vascular resistance. The perfusion impairment did not occur in two euthermic, nonischemic hearts. In five dogs elevation of serum osmolality by 23 +/- 11 mOsmol/liter with mannitol attenuated the progressive decrease in flow. Thus, a progressive perfusion defect exists in the ischemic low flow state in the heart which presumably contributes to the extent of eventual necrosis.
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PMID:Progressive perfusion impairment during prolonged low flow myocardial ischemia in dogs. 93 13

The effect of mild hypothermia on cerebral injury was evaluated in a rat model of permanent middle cerebral artery (MCA) and ipsilateral carotid artery occlusion. The MCA occlusion was performed in rats at temporalis muscle temperatures of 30 degrees C, 33 degrees C, 34.5 degrees C and 36.5 degrees C (n = 10, 8, 10, and 13, respectively). The animals were kept at the desired temperature for 1 hour and rewarmed to 36.5 degrees C. In a separate group of animals (n = 11), the temperature was decreased to 33 degrees C 1 hour after performing the arterial occlusion at normothermia. These animals were rewarmed to 36.5 degrees C after another hour with side by side controls (n = 9) kept at 36.5 degrees C throughout the experiment. Twenty-four hours after the MCA occlusion, rats were killed and the percentage of infarcted right hemisphere was determined in coronal brain sections with 2,3,5-triphenyltetrazolium chloride. The percentage of infarcted volume at 30 degrees C, 33 degrees C, and 34.5 degrees C (9.3 +/- 2.1%, 8.2 +/- 2.2%, and 8.4 +/- 2.2%) (SEM) was significantly smaller than at 36.5 degrees C (19.6 +/- 1.6%, P < 0.01). There were no significant differences between the hypothermic groups. When rats were cooled to 33 degrees C 1 hour after the arterial occlusion, the percentage of infarcted volume was also significantly smaller than the control group (8.0 +/- 1.8% vs. 17.4 +/- 2.1%) (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of mild hypothermia on permanent focal ischemia in the rat. 147 Mar 16

The increased metabolic and respiratory demand during naloxone recovery from opioid-based anesthesia could be related to the return of thermoregulation in hypothermic patients and thus be avoided by preventing intraoperative hypothermia. In this study, we measured O2 uptake (VO2) during naloxone-induced recovery in two groups of patients to determine the effect of intraoperative heat loss on postoperative VO2 changes. In seven patients, intraoperative hypothermia was prevented (normothermic group), whereas hypothermia was allowed to develop in seven other patients (hypothermic group). Core and skin temperatures were measured throughout the study to calculate changes in body heat content. Before naloxone antagonism of fentanyl-supplemented anesthesia, core temperature (mean +/- SEM) was 36.8 +/- 0.1 degrees C in the normothermic group and 34.2 +/- 0.2 degrees C in the hypothermic group (P less than 0.001). After titrated administration of naloxone during recovery, VO2 and minute ventilation (VE) increased in the hypothermic group, by 114 +/- 37% and 97 +/- 52% respectively (P less than 0.05), with a three-fold increase in four patients. In the normothermic group, VO2 increased significantly less (25 +/- 5%), without any significant change in VE. The change in VO2 and VE was significantly greater in patients who were hypothermic. VO2 was integrated throughout the recovery period to calculate recovery energy expenditure. Recovery energy expenditure and intraoperative heat loss were highly correlated (r = 0.88; P less than 0.01). This study demonstrates that the metabolic and respiratory stresses associated with naloxone-induced recovery from opioid-based anesthesia depend on the intraoperative heat loss and can therefore be reduced by preventing intraoperative hypothermia.
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PMID:Oxygen uptake during recovery following naloxone. Relationship with intraoperative heat loss. 172 37

Sublingual body temperatures were measured before and at 0.5, 1, 2, 3, 4, 8, 12, and 24 hours after administration of epidural or subarachnoid morphine in four groups of patients (n = 15 in each group) undergoing cesarean delivery with regional anesthesia. All patients were acutely hydrated with 1200 ml warmed lactated Ringer's solution. Group 1 received 5 mg epidural morphine; Group 2, 5 ml epidural saline; Group 3, 0.5 mg subarachnoid morphine, and Group 4, 0.5 ml subarachnoid saline. The results were expressed as means +/- SEM and analyzed using analysis of variance at p less than 0.05. Body temperature decreased significantly in all the four groups after anesthesia. The maximum decreases in Groups 1, 2, 3, and 4, respectively, were 0.95 +/- 0.1, 0.9 +/- 0.1, 1.4 +/- 0.2, and 0.8 +/- 0.13 degrees C and occurred at 0.5, 1, 2, and 1 hour, respectively. The decrease was greater in the subarachnoid morphine group than in the other groups (p less than 0.03). At any of the measurement periods, the temperatures in the two epidural groups did not differ from each other. However, the temperature in the subarachnoid morphine group remained significantly lower than the corresponding temperature in the control group for up to 24 hours. It is concluded that subarachnoid morphine intensifies the hypothermic action of spinal anesthesia in parturients.
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PMID:The hypothermic action of epidural and subarachnoid morphine in parturients. 177 16

Urethane-anesthetized rats were used to study the mechanism of cocaine-induced death. Continuous recording of the changes in five physiological parameters, including respiratory rate (RR), electroencephalogram (EEG), blood pressure (BP), electrocardiogram (ECG), and body temperature (BT), were conducted after intraperitoneal (IP) administration of a single dose of cocaine HCl (70 mg/kg). In the control group (normothermic with core body temperature 37.7 +/- 0.1 degree C and spontaneously breathing), the death rate was 88% (15/17), and the average time to respiratory arrest was 12.99 +/- 1.40 min (mean +/- SEM). The first set of experiments investigated the contribution of hypothermia to cocaine-induced death. The hypothermic group (core body temperature 33.9 +/- 0.3 degrees C and spontaneously breathing) had a death rate of 81.5% (22/27), and an average time to respiratory arrest of 16.70 +/- 1.24 min, which was significantly (p les than 0.05) prolonged. A substantial decrease in respiratory rate was seen in normothermic group, while all the other measured parameters remained relatively stable until respiratory arrest. Sequential arterial blood gas data in this group showed a decrease in PaO2 from 116.0 +/- 5.7 mmHg to 57.7 +/- 4.6 mmHg, an increase in PaCO2 from 27.7 +/- 2.2 mmHg to 42.7 +/- 3.0 mmHg, and a decrease in pH from 7.467 +/- 0.039 to 7.357 +/- 0.003. To confirm that respiratory depression was an important mechanism of cocaine-induced death in this model, ten normothermic rats underwent mechanical ventilation, and all survived cocaine exposure. This study points to the important role of respiratory depression as a cause of cocaine-induced death.
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PMID:Cocaine-induced respiratory depression in urethane-anesthetized rats: a possible mechanism of cocaine-induced death. 178 91

Microneurographic measurements of muscle sympathetic nerve activity (SNA) have suggested that, during static exercise, central command is much less important than skeletal muscle afferents in causing sympathetic neural activation. The possibility remains, however, that the sympathetic discharge produced by central command is targeted mainly to tissues other than skeletal muscle. To examine this possibility, we recorded SNA with microelectrodes placed selectively in skin, as well as in muscle, nerve fascicles of the peroneal nerve during static handgrip maneuvers designed to separate the effects of central command from those of muscle afferents. To study the relative effects of cutaneous sympathetic activation on sudomotor versus vasomotor function, we simultaneously estimated changes in skin blood flow (laser Doppler velocimetry) and in sudomotor (electrodermal) activation in the region of skin innervated by the impaled nerve fascicle. Two minutes of static handgrip at 10%, 20%, and 30% of maximal voluntary contraction caused large and intensity-dependent increases in skin SNA. These increases in SNA immediately preceded the onset of muscle tension, accelerated progressively during sustained handgrip, and resolved promptly with the cessation of motor effort. The handgrip-induced increases in skin SNA were not maintained when handgrip was followed by arrest of the forearm circulation, a maneuver that maintains the stimulation of chemically sensitive muscle afferents while eliminating the influences of central command and mechanically sensitive muscle afferents. During normothermia, static handgrip at 30% maximal voluntary contraction caused sustained increases in skin SNA (+400 +/- 83%, mean +/- SEM, p less than 0.05) and in electrodermal activity (+276 +/- 56%, p less than 0.05) but only transient increases in estimated skin vascular resistance (+11 +/- 2%, p less than 0.05). When skin temperature was increased or decreased to a new stable baseline level, subsequent increases in skin SNA during handgrip were accompanied by sustained but directionally opposite changes in estimated skin vascular resistance, with exercise-induced vasodilation during hyperthermia but exercise-induced vasoconstriction during hypothermia. From these observations, we conclude the following: 1) static exercise markedly increases sympathetic outflow to skin as well as to skeletal muscle; 2) the increases in skin SNA, unlike muscle SNA, appear to be caused mainly by central command rather than by muscle afferent reflexes; and 3) this cutaneous sympathetic activation appears to be targeted both to sweat glands and to vascular smooth muscle, with the relative targeting being temperature dependent.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Stimulation of skin sympathetic nerve discharge by central command. Differential control of sympathetic outflow to skin and skeletal muscle during static exercise. 205 36

The oxyhemoglobin dissociation curve was quantified in 15 patients subjected to hypothermic cardiopulmonary bypass under opiate-benzodiazepine anesthesia using the alpha-stat approach to control blood acid-base status. The P50 was calculated from a single measurement of oxygen tension and hemoglobin saturation in blood obtained from the pulmonary artery or the venous line from the cardiopulmonary bypass circuit. In addition, the P50 was directly determined at the registered patient temperature. The P50 decreased from 3.87(+/- 0.15) kPa (mean, SEM) before anesthesia to 1.55(+/- 0.16) kPa during hypothermic (25.43 +/- 1.99 degrees C) cardiopulmonary bypass (p less than 0.001). On rewarming, the P50 increased to 4.89 +/- 0.27 kPa (at 36.14 +/- 0.14 degrees C, p less than 0.001 compared to the preinduction and hypothermic values). Eight hours after cardiopulmonary bypass the P50 returned to the preinduction value (3.72 +/- 0.22 kPa). The relationship between temperature and P50 is described by the regression equation: P50 = 0.22(+/- 0.02).Temperature--3.78(+/- 0.62). The correlation was 0.78 (p less than 0.001). It is concluded that (1) the leftward shift of the oxyhemoglobin dissociation curve during hypothermia may be detrimental to oxygen delivery and (2) the oxygen saturation of the venous blood should not be used indiscriminately to evaluate cellular oxygen status.
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PMID:The oxyhemoglobin dissociation curve before, during and after cardiac surgery. 208 10

The flow velocity in the middle cerebral artery was measured continuously with a noninvasive transcranial Doppler in 18 patients during coronary artery surgery. Neurolept anesthesia and alpha-static acid-base management were employed. The flow velocity data were expressed as a percent of the awake level. During intubation, there was a transient flow velocity increase, which was related to a concomitant increase in mean arterial pressure (r = 0.67, p less than 0.01). Prior to cardiopulmonary bypass, flow velocity had decreased to 52.4% +/- 3.0% (mean +/- SEM). At the onset of cardiopulmonary bypass, flow velocity values were transiently doubled. Flow velocity then reached a stable level of 63% to 65% during hypothermia (25 degrees C to 30 degrees C). The increase from 52.4% to 63% to 65% was related to the reduction in hematocrit (r = -0.62, p less than 0.02). With rewarming, flow velocity increased to 101% +/- 5.2%. Flow velocity was found to correlate with temperature during cardiopulmonary bypass (median rs = 0.84, range 0.61 to 0.99, p less than 0.0001). No positive correlation was found between mean arterial pressure (MAP) and flow velocity during cardiopulmonary bypass. Although no direct metabolic measurements were performed, it is concluded that these findings are compatible with a maintained cerebral blood flow/metabolic coupling during cardiopulmonary bypass.
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PMID:Middle cerebral artery flow velocity during coronary surgery; influence of clinical variables. 213 21

This study measured the velocity of fast orthograde axonal transport of incorporated 3H-proline in motoneurones of the sciatic nerve in control rats and in rats with streptozotocin-induced diabetes of 3 weeks duration. Sciatic nerve and abdominal cavity temperatures were monitored throughout the period of measurement of transport velocity, and the rats were warmed to minimise hypothermia at both sites. There was marked abdominal and sciatic nerve hypothermia immediately after operation, and this effect was more intense in diabetic rats than in control rats. In steady state, abdominal cavity temperature (mean +/- SEM) was 38.1 +/- 0.1 degree C in both control and diabetic rats, and the sciatic nerve temperatures were 37.8 +/- 0.1 degree C in controls and 37.1 +/- 0.3 degrees C in diabetic rats. The difference was not statistically significant. The velocities of orthograde axonal transport for the fastest molecules containing 3H-proline were 14.0 +/- 0.9 (SEM)mm/h for controls and 13.9 +/- 1.1 (SEM)mm/h for diabetic rats. Thus, no velocity difference was observed. The findings are discussed in relation to measurements of fast orthograde transport velocity in experimental diabetes in other studies. It is suggested that, where velocity deficits have been seen in diabetic rats, nerve hypothermia should be considered as a contributory factor.
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PMID:Fast orthograde axonal transport in sciatic motoneurones and nerve temperature in streptozotocin-diabetic rats. 241 4


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