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

Because deliberate hypothermia is becoming commonly used during neurosurgery, this study was performed to investigate the effects of a progressive reduction of body core temperature (T) on whole body oxygenation variables in patients undergoing elective intracranial surgery. In 13 patients (Hypothermic Group), T was reduced to 32.0 degrees C using convective-based surface cooling. In six patients (Control Group), T was maintained at 35.5 degrees C during the entire study period. The cardiac index (CI) was determined with a pulmonary artery catheter by thermodilution. Whole body oxygen delivery (DO2) was calculated from CI and arterial oxygen content. Whole body oxygen consumption (VO2), carbon dioxide production (VCO2), and energy expenditure (EE) were determined by ventilation gas analysis (indirect calorimetry). Mixed venous oxygen tension at 50% saturated hemoglobin (P50), and whole body oxygen extraction ratio (O2ER) were calculated. Repeated-measures analysis of variance and the Mann-Whitney test were used for statistical analysis. Data are expressed as means +/- SD. VO2 (from 100 +/- 13 to 77 +/- 11 ml.min-1.m-2), VCO2 (from 75 +/- 7 to 57 +/- 7 ml.min-1. m-2), EE (from 667 +/- 67 to 509 +/- 66 kcal.d-1.m-2), P50 (from 23.8 +/- 1.7 to 20 +/- 0.9 mm Hg), and O2ER (from 0.29 +/- 0.05 to 0.22 +/- 0.03%) decreased significantly in the Hypothermic Group between 35.5 and 32.0 degrees C (p < 0.05). None of these variables changed in the Control Group and at 32.0 degrees C VO2, VCO2, EE, P50, and O2ER were significantly lower in the Hypothermic Group than in the Control Group. DO2 remained unchanged in both groups. We conclude that progressive hypothermia in anesthetized patients reduces metabolic rate but does not change DO2. The significant decrease in O2ER may partly be related to a leftward shift of the oxyhemoglobin dissociation curve, as evidenced by the decrease in P50.
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PMID:Changes in oxygenation variables during progressive hypothermia in anesthetized patients. 923 80

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

Nitric oxide (NO) has high affinity to heme and by interaction with oxyhemoglobin (HbO2) is converted into nitrate to form methemoglobin (MetHb) as a side product. In combining with deoxy-Hb NO yields a stable molecule of nitrosyl-hemoglobin (HbFe(II)NO) that can further be converted into nitrate and hemoglobin (Hb). In addition, Hb was shown to transport NO in a form of S-nitrosohemoglobin (SNO-Hb). These features of the Hb and NO interaction are important for blood oxygen transport including hemoglobin-oxygen affinity (HOA). The present investigation was aimed to study the blood oxygen transport indices (pO2, pCO2, pH, HOA, etc.) in rats under hypothermia combined with a modification of L-arginine-NO pathway. To modify the L-arginine-NO pathway, rats were administered with N(G)-nitro-L-arginine methyl ester (L-NAME), L-arginine, or sodium nitroprusside (SNP) intravenously before cooling. A substantial impairment of oxygen delivery and development of hypoxia, with an important contribution of HOA into the latter accompanied the deep hypothermia in rats. All the experimental groups developed metabolic acidosis, less pronounced in rats treated with L-arginine only. In the experiments with a modification of the L-arginine-NO pathway, an enhanced cold resistance, attenuated oxygen deficiency, and a weaker oxyhemoglobin dissociation curve (ODC) shift leftwards were observed only after the administration of L-arginine. Neither SNP nor L-NAME had not any protective effects. L-Arginine lowered the value of standard P50 (pO2, corresponding to 50% Hb saturation with oxygen at 37 degrees C, pH 7.4, and pCO2 = 40 mmHg). The actual P50 (at actual pH, pCO2 and temperature) decreased by approximately 15 mmHg and was significantly higher than that under hypothermia without the drug treatment (21.03 +/- 0.35 vs 17.45 +/- 0.60 mmHg). NO also can contribute to this system through different mechanisms (HOA modification, vascular tone regulation, peroxynitrite formation, and effects).
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PMID:Blood oxygen transport in rats under hypothermia combined with modification of the L-Arginine-NO pathway. 1182 32

Hypothermia decreases cerebral metabolism and increases hemoglobin oxygen affinity. A hypothesis that the reversal of increased oxygen affinity would further attenuate hypothermic cerebral ischemia was tested by evaluating the effects of liposome-encapsulated hemoglobin (LipoHb) with low oxygen affinity (P50 = 40-50 mmHg) on hypothermic incomplete cerebral ischemia. Wistar rats were randomly assigned to one of the following two groups: (A) exchange transfusion with LipoHb solution (Hb = 6 g/dl) (LipoHb, n = 5), (B) no exchange transfusion (control, n = 5). After surface cooling to 22 degrees C, forebrain ischemia was induced for 15 min by bilateral carotid artery occlusion combined with a decrease in the mean arterial pressure (MAP) to 40 mmHg. (31)P-magnetic resonance spectroscopy was performed during ischemia and 45 min of reperfusion. After reperfusion, MAP was significantly higher in the control group than in the LipoHb group (P < 0.01), although there were no significant differences during ischemia. Intracellular pH and phosphocreatine (PCr) levels decreased during ischemia and returned to the preischemic level in both groups following reperfusion. The LipoHb group had a significantly larger decrease and smaller recovery in PCr than the control group (P < 0.0001). Althouth beta-adenosine triphosphate decreased during ischemia in the LipoHb group, it increased in the control group (P < 0.0001). Inorganic phosphate (Pi) increased during ischemia and decreased to the normal value after reperfusion. The LipoHb group experienced a significantly larger production of Pi than the control group (P = 0.02). Hemodilution with high-P50 LipoHb does not reduce ischemic energy depletion induced by hypothermic incomplete forebrain ischemia in rats.
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PMID:Hemodilution with liposome-encapsulated low-oxygen-affinity hemoglobin does not attenuate hypothermic cerebral ischemia in rats. 1636 25


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