ascorbic-acid and Hypothermia

Exposure to an extremely cold environment without proper protection leading to hypothermia is an emergency, one of the several complications of which is impairment in nerve conduction. Our previous work in the rat model has shown the beneficial effect of vitamin C in modulating the effect of hypothermia on nerve conduction. The present study aimed to evaluate the effect of vitamins C and E, administered alone or in combination, in modulating the effect of mild hypothermia on human ulnar nerve conduction. The study was carried out on 26 volunteers divided into three groups: group I received vitamin C supplementation (2000 mg/day in a single dose and 1,000 mg/day for the next 6 days), group II received vitamins C and E in combination (1,000 mg and 800 mg respectively in a single dose and 500 mg and 400 mg respectively for the next 6 days) and group III received vitamin E (800 mg in a single dose and the same for the next 6 days). The recordings were carried out before and after single and weekly supplementation in each group. There was a fall in ulnar nerve conduction velocity with a reduction in the oral temperature of 2-2.5 degrees C. Vitamin C administered alone and in combination with vitamin E reduced the fall in ulnar nerve conduction velocity. Prior supplementation with vitamin C and E could help ameliorate the impairment in human ulnar nerve conduction due to hypothermia.

Topics: Adult; Ascorbic Acid; Cold Climate; Double-Blind Method; Humans; Hypothermia; Male; Neural Conduction; Ulnar Nerve; Vitamin E

Intravenous (IV) administration of ascorbic acid during cardiopulmonary resuscitation (CPR) was reported to facilitate defibrillation and improves survival in ventricular fibrillation (VF) cardiac arrest. We investigated whether IV administration of ascorbic acid after return of spontaneous circulation (ROSC) can improve outcomes in VF cardiac arrest in a rat model and its interaction with therapeutic hypothermia.. Ventricular fibrillation-induced cardiac arrest followed by CPR and defibrillation was performed in male Wistar rats. After ROSC, the animals were equally randomized to the normothermia (NormoT), hypothermia (HypoT), ascorbic acid (AA+NormoT), and ascorbic acid plus hypothermia (AA+HypoT) groups. The AA+NormoT and AA+HypoT groups received IV ascorbic acid (100 mg/kg). In the HypoT and AA+HypoT groups, therapeutic hypothermia was maintained at 32°C for 2 hours.. There were 12 rats in each group. Within 4 hours after ROSC, the HypoT, AA+NormoT, and AA+HypoT groups had significantly lower myocardial lipid peroxidation than the NormoT group. Within 4 hours following ROSC, the AA+NormoT group had a significantly better systolic function (dp/dt40 ) than the NormoT group (6887.9 mm Hg/sec, SD ± 1049.7 mm Hg/sec vs. 5953.6 mm Hg/sec, SD ± 1161.9 mm Hg/sec; p < 0.05). The AA+HypoT group also showed a significantly better diastolic function (-dp/dtmax ) than the HypoT group (dp/dt40 : 8524.8, SD ± 1166.7 mm Hg/sec vs. 7399.8 mm Hg/sec, SD ± 1114.5 mmHg/sec; dp/dtmax : -8183.4 mm Hg/sec, SD ± 1359.0 mm Hg/sec vs. -6573.7 mm Hg/sec, SD ± 1110.9 mm Hg/sec; p < 0.05) at the fourth hour following ROSC. Also at 4 hours, there was less myocytolysis in the HypoT, AA+NormoT, and AA+HypoT groups than the NormoT group. The HypoT, AA+NormoT, and AA+HypoT groups had significantly better survival rates and neurologic outcomes than the NormoT group. Compared with only five surviving animals in the NormoT group, there were nine, eight, and 10 in the HypoT, AA+NormoT, and AA+HypoT groups, respectively, with good neurologic outcomes at 72 hours.. Intravenous ascorbic acid administration after ROSC in normothermia may mitigate myocardial damage and improve systolic function, survival rate, and neurologic outcomes in VF cardiac arrest of rat. Combination of ascorbic acid and hypothermia showed an additive effect in improving both systolic and diastolic functions after ROSC.

Topics: Animals; Ascorbic Acid; Cardiopulmonary Resuscitation; Diastole; Disease Models, Animal; Electric Countershock; Heart Arrest; Hemodynamics; Hypothermia; Hypothermia, Induced; Infusions, Intravenous; Lipid Peroxidation; Male; Myocardial Contraction; Myocardium; Rats; Rats, Wistar; Survival Analysis; Systole; Ventricular Fibrillation

The 1910-1913 Terra Nova Expedition to the Antarctic, led by Captain Robert Falcon Scott, was a venture of science and discovery. It is also a well-known story of heroism and tragedy since his quest to reach the South Pole and conduct research en route, while successful was also fateful. Although Scott and his four companions hauled their sledges to the Pole, they died on their return journey either directly or indirectly from the extreme physiological stresses they experienced. One hundred years on, our understanding of such stresses caused by Antarctic extremes and how the body reacts to severe exercise, malnutrition, hypothermia, high altitude, and sleep deprivation has greatly advanced. On the centenary of Scott's expedition to the bottom of the Earth, there is still controversy surrounding whether the deaths of those five men could have, or should have, been avoided. This paper reviews present-day knowledge related to the physiology of sustained man-hauling in Antarctica and contrasts this with the comparative ignorance about these issues around the turn of the 20th century. It closes by considering whether, with modern understanding about the effects of such a scenario on the human condition, Scott could have prepared and managed his team differently and so survived the epic 1,600-mile journey. The conclusion is that by carrying rations with a different composition of macromolecules, enabling greater calorific intake at similar overall weight, Scott might have secured the lives of some of the party, and it is also possible that enhanced levels of vitamin C in his rations, albeit difficult to achieve in 1911, could have significantly improved their survival chances. Nevertheless, even with today's knowledge, a repeat attempt at his expedition would by no means be bound to succeed.

Topics: Altitude Sickness; Antarctic Regions; Ascorbic Acid; Exercise; Expeditions; History, 20th Century; History, 21st Century; Humans; Hypothermia; Male; Malnutrition; Physiology; Science; Sleep Deprivation; Stress, Physiological; Survival

Iron chelators and antioxidants have been shown to prevent hypothermia-induced apoptosis in hepatocytes. This study examined whether iron chelation and antioxidants could also prevent hypothermia-induced necrosis. Isolated rat hepatocytes were incubated at 4 degrees C for 6 hours and then rewarmed at 37 degrees C for 18 hours with or without the iron chelator deferoxamine and a selection of antioxidants. There was no evidence of increased cell death or adenosine triphosphate depletion during hypothermic incubation. After hypothermia and rewarming, the majority of rat hepatocytes died of necrosis as indicated by the absence of DNA fragmentation, caspase 3 activity, and apoptotic bodies. Cell death was significantly reduced if deferoxamine or a selection of antioxidants were present during hypothermia and rewarming. Deferoxamine was more effective in preventing cell death when added prior to hypothermia, indicating cell death processes were likely initiated during hypothermia.

Topics: Adenosine Triphosphate; Animals; Apoptosis; Ascorbic Acid; Caspase 3; Cell Culture Techniques; Cell Death; Hepatocytes; Hypothermia; Iron; L-Lactate Dehydrogenase; Lactates; Necrosis; Oxidative Stress; Rats

Topics: Aged; Anti-Bacterial Agents; Ascorbic Acid; Bronchitis; Female; Humans; Hypothermia; Male; Nutrition Disorders; Respiratory Tract Infections; Seasons

Topics: Acoustic Stimulation; Adrenal Glands; Alcoholic Intoxication; Animals; Ascorbic Acid; Body Temperature; Chlorpromazine; Corticosterone; Depression, Chemical; Ethanol; Female; Growth Disorders; Humans; Hypothalamus; Hypothermia; Rats

Topics: Aminocaproates; Aminopyrine; Anaphylaxis; Animals; Aprotinin; Ascorbic Acid; Bordetella pertussis; Drug Synergism; Fever; Histamine H1 Antagonists; Hypothermia; Methysergide; Mice; Phenylbutazone; Temperature

Topics: Animals; Ascorbic Acid; Electron Transport Complex IV; Hyperthyroidism; Hypothermia; Hypothermia, Induced; Hypothyroidism; Iodine Isotopes; Oxidoreductases; Phosphoric Monoester Hydrolases; Rats; Thyroid Gland

Topics: Adrenal Glands; Analgesics; Animals; Ascorbic Acid; Butyrophenones; Caffeine; Drug Synergism; Hypothermia; Rats; Salicylamides; Thiamine

Topics: Ascorbic Acid; Blood Circulation; Blood Proteins; Chemical Phenomena; Chemistry; Dextrans; Dogs; Electroencephalography; Erythrocyte Aggregation; Extracorporeal Circulation; Heart, Artificial; Hypothermia; Hypothermia, Induced; Oxygen; Plasma; Research; Surface-Active Agents

Topics: Ascorbic Acid; Asphyxia; Carbohydrate Metabolism; Glutathione; Hypothermia; Hypothermia, Induced

Topics: Aqueous Humor; Ascorbic Acid; Hypothermia; Hypothermia, Induced; Sodium

Topics: Adrenal Cortex; Ascorbic Acid; Body Temperature; Carbohydrate Metabolism; Hypothermia

Topics: Adrenal Cortex; Adrenocorticotropic Hormone; Animals; Ascorbic Acid; Carbohydrate Metabolism; Cholesterol; Hypothermia; Lipid Metabolism; Rats