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)

A 19-year old woman ingested an unknown amount of sodium azide (NaN3). The earliest symptoms were nausea and loss of vision. Within a few hours her clinical features were dominated by central nervous system signs, acute pulmonary edema, lactic acidosis, and hypothermia. The patient died within 12 hours, hypotension and shock occurring as preterminal events. This was the first recorded case in which antidotal methemoglobin production was attempted. Sodium nitrite administration resulted in methemoglobinemia but did not appreciably alter the clinical course and may not be of major benefit. Gross examination post-mortem showed marked pulmonary edema, visceral hemorrhage and congestion, and slight cerebral edema. Microscopically, the lungs showed alveolar and interstitial edema and a polymorphonuclear infiltrate. There were petechial hemorrhages and severe nonspecific changes in the brain.
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PMID:Fatal self-administration of sodium azide. 114 58

Previous reports from our laboratory indicated that prophylactic protection against cyanide intoxication in mice can be enhanced by administration of chlorpromazine when it is given with sodium thiosulfate. The mechanism of potentiation of sodium thiosulfate by chlorpromazine was studied alone and in combination with sodium nitrite. Although chlorpromazine was found to induce a hypothermic response, the mechanism of enhancement of the antagonism of cyanide by chlorpromazine does not correlate with the hypothermia produced. Various other possible mechanisms were investigated, such as rate of methemoglobin formation, enzymatic activity of rhodanese and cytochrome oxidase, and alpha-adrenergic blockade. The alpha-adrenergic blocking properties of chlorpromazine may provide a basis for its antidotal effect, since this protective effect can be reversed with an alpha-agonist, methoxamine.
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PMID:Effect of chlorpromazine on cyanide intoxication. 631 90

To assess the oxygen transport capacity and safety of Neo Red Cells (NRC) with the enzymatic reduction system of methemoglobin in vitro and in experimental animals. Stroma free hemoglobin (SFH) prepared without damage of enzymes from outdated human red blood cells, together with inositol hexaphosphate as an allosteric effector, NAD as a coenzyme and glucose, adenine and inosine as a substrate was encapsulated within liposomes composed of hydrogenated soy phosphatidylcholine, cholesterol, myristic acid and alpha-tocopherol in the ratio of 7:7:2:0.28 respectively. NRC thus prepared with a mean diameter of 220 nm, encapsulation efficiency of 1.3 g-Hb:1 g-lipid and P50O2 of 50-60 mmHg were then coated with polyethylene glycol bound to hydrogenated soy phosphatidylethanolamine as a surface modifier to prevent aggregation of NRC in plasma. The methemoglobin formation of the NRC with enzymatic reduction system were evaluated by in-vitro examination and exchange transfusion with rats as in-vivo examination, then the methemoglobin formation was reduced from 1%/hr to 0.4%/hr by the addition of methemoglobin reduction system. The generation of the pyruvate and the lactate were observed within the NRC with enzymatic reduction system, then the activation of the Embden-Meyerhof pathway was confirmed. And we concerned about the availability of the NRC as a perfusate for the cardiopulmonary bypass during moderate or profound hypothermia, then we evaluated the oxygen transporting efficiency and capacity of the NRC under the using of the artificial lung system in vitro examination. The present investigation suggest that the effectiveness of the NRC with enzymatic reduction system, they restrained the formation of methemoglobin and they are efficient oxygen carriers as a perfusate of the artificial lung, and we suggest the new extracorporeal circulation system using of the NRC as a perfusate for the cardiopulmonary bypass.
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PMID:Development of neo red cells (NRC) with the enzymatic reduction system of methemoglobin. 924 36

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

In newborn and premature infants whose lung immaturity entails a limited capacity for O2 detoxification, the use of supplemental oxygen should be continuously and non-invasively monitored. Pulse oximetry and transcutaneous O2 monitoring are the systems most used in the NICU. Major limitations of pulse oximetry are motion artifact, sensitivity to excessive light, cutaneous hypoperfusion, hypothermia, venous congestion, arterio-venous shunting, strong skin pigmentation, anemia and high percentage of abnormal hemoglobin. Alarm habituation is a further major risk. New oxymeters show less motion, artifact and higher accuracy during low oxygen saturation. The accuracy during high oxygen saturation is very dependent on the specific oxymeter model used. Transcutaneous O2 monitoring is usually combined with transcutaneous PCO2 monitoring, hence enabling evaluation of oxygenation as well as ventilation. A major risk of this method is related to the heated electrode sensor, which can induce skin burns. A combined ear sensor for pulse oximetry and PCO2 monitoring seems promising.
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PMID:[Oxygen therapy in newborn: equipments for non-invasive monitoring]. 1576 30

In performing pulmonary endarterectomy (PEA) for a patient with chronic thromboembolic pulmonary hypertension (CTEPH), we encountered methemoglobinemia that was unmasked by hypothermia while on cardiopulmonary bypass (CPB). The patient on dapsone therapy for antiphospholipid antibody syndrome had developed acquired methemoglobinemia that went undiagnosed because her cyanosis was believed to be due to CTEPH and the resulting ventilation-perfusion (V/Q) mismatch. Although pharmacological triggers for methemoglobin are well known, causation by hypothermia is not described. Monitoring saturation while on CPB was challenging because of nonpulsatile blood flow but was overcome using cerebral oximetry.
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PMID:Methemoglobinemia Unmasked by Use of Sodium Nitroprusside and Hypothermia in a Case of Chronic Thromboembolic Pulmonary Hypertension During Pulmonary Endarterectomy: A Case Report. 3298 47