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

Blood gases were measured in hibernating and hypothermic animals as a biological model of clinical hypothermia. Blood gas analyses from hamsters and dormice were carried out with the aid of permanent arterial catheters during normothermia and hibernation. In golden hamster pH increased from 7.30 to 7.46 during hibernation and PaCO2 decreased from 59.7 to 40.5 mm Hg. In dormice pH increased from 7.24 to 7.44 and PaCO2 decreases from 38.5 to 27.4 mm Hg. The actual bicarbonate concentration increased from 29 to 52 mMol in golden hamsters and from 16 to 34 mMol in dormice during hibernation. In experiments with induced hypothermia in golden hamsters under ketamine-anaesthesia there was no correlation between temperature and PaCO2. Despite the slight decrease in PaCO2 during hibernation we conclude that PaCO2 rather than total carbon dioxide content is held constant when temperature is changed. During clinical hypothermia it will probably be safe to keep PaCO2 constant.
 ...
PMID:Blood gas analyses of hibernating hamsters and dormice. 1 44

Unanesthetized and unrestrained rats, chronically cannulated in the carotid artery, were exposed to normal air (NA) and Helox (21% O2, 79% He) at ambient temperatures (Ta) of 22 and -10 degrees C. In Helox at Ta = 22 degrees C, the Vo2 was 1.39 ml O2/g-h and the Vco2 0.98 ml CO2/g-h, 145 and 126%, respectively, of the values in NA at Ta = 22 degrees C. The arterial Pao2, Paco2, and pH were comparable in Helox and NA at Ta = 22 degrees C. In Helox at Ta = -10 degrees C, rats invariably became hypothermic after exposure of 0.75 to 1.5 h. During the induction of hypothermia the decrease of Vo2 and Vco2 was oscillatory, Pao2 and pH increased, and Paco2 decreased significatnly (P less than 0.05). Minimum Vo2 and Vco2 during hypothermia averaged 0.71 ml O2/g-h and 0.50 ml CO2/g-h, 23 and 22%, respectively, of the values in normothermic animals at Ta = -10 degrees C. Minimum body temperature during hypothermia was clamped at 21.7 +/- 0.3 degrees C (X +/- SE) by increasing Ta to 19 degrees C. When Helox was replaced by NA, hypothermic rats rewarmed spontaneously, returning to normothermia within 4 h. The data suggest that hypothermia induced by Helox plus cold does not seem to be due to respiratory failure, as systemic hypoxia or hypercapnia were not observed. The controlled hypothermia cycle reported here provides a model for dynamic studies of thermogenic mechanisms both at the normothermic and hypothermic states without the interference of drugs and other nonphysiological treatments.
 ...
PMID:Metabolic and respiratory responses during Helox-induced hypothermia in the white rat. 24 22

The alterations in tissue metabolism induced by hypothermic cardiopulmonary bypass are not completely known. Phosphorus-31 nuclear magnetic resonance spectroscopy was used to determine the effect of hypothermic cardiopulmonary bypass on energy states and intracellular pH of the heart and brain. Sheep were instrumented for cardiopulmonary bypass and had a radiofrequency coil placed over either the heart or skull. The animals were placed in a 4.7-T magnet at 37 degrees C and spectra obtained. The animals were cooled on cardiopulmonary bypass to either 26 degrees C (n = 17) or 18 degrees C (n = 14) for brain studies and to 26 degrees C (n = 12) for heart studies. Hypothermia increased the phosphocreatine/adenosine triphosphate ratio in the heart (2.38 +/- 0.23 versus 3.18 +/- 0.37, 37 degrees versus 26 degrees C, respectively, p = 0.03). The brain phosphocreatine/adenosine triphosphate ratio increased from 1.70 +/- 0.09 at 37 degrees C to 2.00 +/- 0.12 at 26 degrees C (p = 0.009) and 2.10 +/- 0.07 at 18 degrees C (p = 0.0001). Intracellular pH increased during hypothermia (heart: 7.05 +/- 0.02 to 7.18 +/- 0.02, 37 degrees versus 26 degrees C, p = 0.0001; and brain: 7.07 +/- 0.02 versus 7.32 +/- 0.02, 37 degrees versus 18 degrees C, p = 0.0001). The adenosine triphosphate resonance position is known to be sensitive to magnesium binding as well as temperature and was shifted upfield (p less than 0.01) in both the heart and brain. This effect could be totally explained by the temperature dependence of this process.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Metabolism of the heart and brain during hypothermic cardiopulmonary bypass. 198 46

To study the respiratory function and acid-base status in hypothermia, we retrospectively reviewed data of arterial blood gas analysis obtained from 63 patients with accidental hypothermia on admission. Twenty-nine showed acidemia and 16 showed alkalemia. The following results were obtained from 57 patients in whom blood gas analysis was performed in room air. PaCO2 was 46 mmHg or more in 2 and 34 mmHg or less in 46. Most of the patients exhibiting acidemia had metabolic acidosis except 2 with severe pneumonia or subdural hematoma. PaCO2 was low even in the patients with alkalemia. PaO2 was 60 mmHg or less in 8, of whom 7 had pneumonia, and 70 mmHg or more in most of the patients without pneumonia. We found that patients with accidental hypothermia generally showed a respiratory function proportionate to their decreased metabolism or hyperventilation, and most of the patients with acidemia exhibited metabolic acidosis.
 ...
PMID:Respiratory function and acid-base status in accidental hypothermia assessed by arterial blood gas analysis. 212 23

Recent experimental and clinical studies from our institution have shown that the administration of cold, bicarbonate-buffered, hyperkalemic crystalloid cardioplegic solution resulted in a significant rise in intramyocardial pH. This rise could theoretically be caused by (1) the alkalinity of the solution administered (pH 8.2 at 25 degrees C), (2) the washout of acid metabolites with each administration, and (3) hypothermia per se. To investigate the relative effects of each of these three factors on intramyocardial pH, dogs on cardiopulmonary bypass received crystalloid cardioplegic solution either at 10 degrees C (n = 9) or at 37 degrees C (n = 8) every 30 min during 2 hr of aortic cross-clamping. Myocardial temperature, intramyocardial pH, and CO2 tension (Pmco2) were measured continuously. Needle biopsy specimens were taken every 30 min for biochemical and ultrastructural analysis. Before aortic cross-clamping, intramyocardial pH was 7.07 +/- 0.06 in both groups (+/- SEM). Upon each administration of cardioplegic solution, hearts in the 10 degrees C group cooled to 10 degrees to 15 degrees C and intramyocardial pH increased on the average by 0.31 +/- 0.03 units (p less than .001). In the 37 degrees C group intramyocardial pH was unaffected by cardioplegic solution. At the end of the cross-clamping period, intramyocardial pH had declined to 6.49 +/- 0.13 in the 10 degrees C group and to 5.60 +/- 0.08 in the 37 degrees C group, the fall in pH being significantly greater in the 37 degrees C group than in the 10 degrees C group (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The relative importance of alkalinity, temperature, and the washout effect of bicarbonate-buffered, multidose cardioplegic solution. 643 May 94

The metabolic status of rat livers during hypothermia has been studied using 31P magnetic resonance spectroscopy. Perfusion with oxygenated buffer at 6-8 degrees C allowed maintenance of ATP, while pH increased to values in the range 7.7-7.9. In organs depleted of ATP by a short (2 h) period of cold ischemia, pH fell to 6.92 +/- 0.10. If these livers were reperfused with hypoxic buffer at hypothermia, two distinct responses were noted. In one group (responders), there was evidence of ATP resynthesis and in these organs pH returned to 7.90 +/- 0.28. In the second group (non-responders), there was no recovery of ATP synthesis and pH remained depressed at 6.97 +/- 0.07. In another group, adenine nucleotides were severely depleted by 24 h of cold ischemia, and in these livers there was again no significant recovery of ATP synthesis during hypoxic reperfusion and pH remained at 7.03 +/- 0.25. These results suggest that (a) there is an apparent relationship between energy metabolism and control of intracellular pH in the hypothermic mammalian liver, and (b) that intracellular pH may shift in liver at hypothermia to values predicted by the alpha-stat hypothesis.
 ...
PMID:Control of intracellular pH in mammalian liver at hypothermia: evidence for a relationship with energy metabolism. 830 3

Nitric oxide (NO) is a key regulator of vascular tone. Endothelial nitric oxide synthase (eNOS) is responsible for NO generation under normoxic conditions. Under hypoxia however, eNOS is inactive and red blood cells (RBC) provide an alternative NO generation pathway from nitrite to regulate hypoxic vasodilation. While nitrite reductase activity of hemoglobin is well acknowledged, little is known about generation of NO by intact RBC with physiological hemoglobin concentrations. We aimed to develop and apply a new approach to provide insights in the ability of RBC to convert nitrite into NO under hypoxic conditions. We established a novel experimental setup to evaluate nitrite uptake and the release of NO from RBC into the gas-phase under different conditions. NO measurements were similar to well-established clinical measurements of exhaled NO. Nitrite uptake was rapid, and after an initial lag phase NO release from RBC was constant in time under hypoxic conditions. The presence of oxygen greatly reduced NO release, whereas inhibition of eNOS and xanthine oxidoreductase (XOR) did not affect NO release. A decreased pH increased NO release under hypoxic conditions. Hypothermia lowered NO release, while hyperthermia increased NO release. Whereas fetal hemoglobin did not alter NO release compared to adult hemoglobin, sickle RBC showed an increased ability to release NO. Under all conditions nitrite uptake by RBC was similar. This study shows that nitrite uptake into RBC is rapid and release of NO into the gas-phase continues for prolonged periods of time under hypoxic conditions. Changes in the RBC environment such as pH, temperature or hemoglobin type, affect NO release.
...
PMID:The capacity of red blood cells to reduce nitrite determines nitric oxide generation under hypoxic conditions. 2500 72