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)

The measurement of the plasma amino acid was made in 15 patients with chronic respiratory failure and 15 persons of control. The results showed: (1) The plasma acid model changed. Lysine increases and arginine decreases, due to hypothermia. Hypercapnia imbalance of acid and alkali and changes of hepatic dysfunction etc. (2) The prognosis of respiratory failure as well as its severity was judged according to the decreasing extent of arginine and BCAA. The more worse the condition of the disease, the more lowering of the level of arginine and BCAA. (3) The changes of blood gas analysis and hepatic dysfunction may effect on the metabolism of plasma amino acid in some degree. (4) Hypoxemia in infected patients with respiratory failure may cause peripheral deficit of energy. We suggested that patients should be given BCAA and arginine for more energy as anti-infection and oxygen therapy were used.
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PMID:[The determination and evaluation of the plasma amino acid in respiratory failure]. 191 67

During surgery under pentobarbital sodium anesthesia, 20 rats had heat exchange devices implanted into their abdominal cavity. After recovery, 14 rats underwent two sets of trials, one in which body core temperature (Tbc) was lowered to 34.5-35.5 degrees C and another in which Tbc was raised to 40.5-41.5 degrees C. Rats breathed air and hypoxic (15, 11, and 7% O2 in N2) and hypercapnic (2, 4, and 6% CO2 in air) gas mixtures. Respiratory responses were measured using a barometric method and compared with data from the same rats breathing the gas mixtures at normal Tbc (37.5-38.5 degrees C) before surgery. The six remaining rats served as controls (Tbc unchanged). Lowering Tbc increased respiration in air, whereas heating had no effect. Hypothermia and severe hypoxia combined to inhibit respiration when compared with breathing air at lowered Tbc or low O2 at normal Tbc. The CO2 response slope became steeper when Tbc was raised, suggesting an increased CO2 sensitivity. Possible sites for the hypothermia-hypoxia interaction and the hyperthermia-hypercapnia interaction are discussed.
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PMID:Body temperature effects on hypoxic and hypercapnic responses in awake rats. 211 31

The central anticholinergic syndrome (CAS) includes central signs (somnolence, confusion, amnesia, agitation, hallucinations, dysarthria, ataxia, delirium, stupor, coma) and peripheral signs (dry mouth, dry skin, tachycardia, visual disturbances and difficulty in micturition). It occurs when central cholinergic sites are occupied by specific drugs and also as a result of an insufficient release of acetylcholine. The CAS can be caused by atropine sulphate, hyoscine (scopolamine), promethazine, benzodiazepines, opioids, halothane, influrane, ketamine. The incidence of CAS during the postoperative period depends on choice and dose of anaesthetic agents, type of surgery, patient's condition and diagnostic criteria. It is close to 10% following general anaesthesia and 4% following regional anaesthesia with sedation. The differential diagnosis of CAS includes an overdose of anaesthetic drugs or an alteration in pharmacokinetics, altered hydratation, electrolyte or acid-base state, hypoglycaemia, hypoxia, hypercapnia, hypocapnia, hyperthermia, hypothermia, hormonal disorders, neurological damage resulting from surgery, embolism, haemorrhage or trauma. The diagnosis of CAS is often determined by a process of exclusion and not actually made until a positive therapeutic response to physostigmine, a centrally active anticholinesterase agent has taken place.
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PMID:[Central anticholinergic syndrome during postoperative period]. 219 41

Cerebral hemodynamics during asphyxia and reventilation were investigated in normothermic, hypothermic (35 degrees C), and indomethacin-pretreated (5 mg/kg iv) anesthetized, newborn pigs. In the normothermic group, total cerebral blood flow (CBF) measured with radioactive microspheres was 57 +/- 12 ml.min-1 x 100 g-1 during baseline, 104 +/- 19 at 1 min of asphyxia, 39 +/- 5 at 5 min of asphyxia, 186 +/- 16 at 8 min of reventilation, and 95 +/- 20 at 16 min of reventilation. During asphyxia and reventilation blood flow to brain stem was better regulated than to cerebrum or cerebellum. Baseline CBF was similar in the indomethacin and hypothermic groups (32 +/- 2 and 41 +/- 5 ml.min-1 x 100 g-1, respectively; n = 5 for each group). However, during asphyxia, blood flow was never less in either one of these groups than in the normothermic group in spite of a lack of arterial hypercapnia at 1 min in the hypothermia group. During reventilation, blood flow was sometimes lower in the hypothermic and indomethacin groups than the normothermic group but never lower when considered on a percentage change from baseline basis. We conclude that inhibition of prostanoid production with indomethacin did not limit vasodilation during these conditions.
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PMID:Role of prostanoids in cerebrovascular responses to asphyxia and reventilation in newborn pigs. 239 79

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

Studies have been made on a possibility of inducing a prolonged hypothermia by injections to albino mice of a fraction with a molecular mass 1-10 KD isolated from the small intestine of hibernating ground squirrels. Specific conditions for the onset of hibernation (hypoxia, hypercapnia, temperature) were simulated. Exposure of mice to hypoxia and hypercapnia for 2 hours in combination with injection of the mentioned fraction extended hypothermic condition in animals up to 24-36 hours as compared to 2-3 hours after sole injection of the fraction. After the injection of 5-OT under the same conditions, the prolonged hypothermia was less stable.
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PMID:[Hypothermic effect on mice of a 1-10 kD fraction of the small intestine of the hibernating suslik Citellus undulatus during hypoxia and hypercapnia]. 277 8

The infant's state immediately after delivery is characterized by critical shifts of homeostasis parameters: decompensated mixed acidosis, pathologic indices of gaseous blood condition (arterial hypoxemia and hypercapnia), spontaneous postnatal hypothermia. Qualitative change of functional systems after delivery is accompanied by expressed tense of adaptation and regulation mechanisms and by centralization of cardiac rhythm control. The use of mathematical analysis of cardiac rhythm made it possible to find out that the change of degree of adaptation tense in the process- of postnatal period obeys the exponential dependence; moreover, the duration of transitional process of healthy newborns is 1 hour, but it considerably increases in case of hypoxia. After comparison of cardiac rhythm indices of these two groups of newborns it has been pointed out that mechanisms of adaptation after delivery are equal and they are based on the growing activity of central regulation processes. The dynamics of transitional process such as the period of postnatal adaptation indicates the reserve possibilities of infant and helps to reveal pre-nosological forms of disadaptational syndrome.
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PMID:[A period of urgent postnatal adaptation as a critical stage of human ontogenesis]. 308 37

Ventilation and breathing pattern were recorded in a group of seven anesthetized cats during rewarming from 24 to 38 degrees C of esophageal temperature. It was found that at 24 degrees C, ventilation was very much depressed accounting for an alveolar hypoventilation resulting in hypoxia and hypercapnia. During rewarming, ventilation increased steadily; this was caused by sequential changes in central inspiratory activity (VT/Ti) and Ti/Tt ratio reflecting breath timing. Changes in VT/Ti have been initially attributed to an improvement in chemoresponsiveness and subsequently, to an involvement of supra-pontine thermoregulatory control areas during rewarming. Marked changes in breath timing, especially observed between 28 and 34 degrees C, have been attributed to a direct effect of rewarming upon the brain stem respiratory network. It has the result, that during hypothermia, several components of the respiratory control system are differently affected causing marked changes in breathing pattern and ventilation. They are accompanied by modifications in arterial blood pressure and heart rate.
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PMID:Ventilatory recovery from hypothermia in anesthetized cats. 309 Jun 66

1. The role of chemoreceptors in the control of heart rate and behaviour during diving activity in the tufted duck was investigated in two ways. In a closed-loop experiment, ducks were exposed to ambient gas mixtures of varied composition during diving activity in an indoor tank. Characteristics of diving behaviour, heart rate and deep body temperature were monitored under hypoxic, hyperoxic and hypercapnic conditions and compared with those in air. Secondly, in an open-loop experiment the role of the carotid body (CB) chemoreceptors in the control of the responses to altered inspired gas composition and in the cardiac responses to extended and enclosed dives (Stephenson, Butler & Woakes, 1986) was investigated by chronic bilateral denervation of these receptors. 2. Heart rate during submersion was unaffected by inspired gas composition in control (data from intact and sham-operated ducks combined) and CB-denervated ducks, though diving behaviour was significantly modified in both groups of animals in response to altered inspired gas composition. Hypoxia and hypercapnia resulted in an increase in the proportion of total diving time spent breathing at the surface. The main effect of hypoxia (9-10% O2) was to reduce dive duration in control ducks and this effect was almost completely abolished after CB denervation. Hypercapnia (5-6% CO2) reduced dive duration less markedly than hypoxia but it greatly increased the duration of the inter-dive interval, effects which were not significantly influenced by CB denervation. Hyperoxia (40-45% O2) had very little effect on either behaviour or heart rate during diving, although deep body temperature was significantly elevated in this gas mixture during diving activity. There was also a less marked, but nevertheless significant, apparent hyperthermia during diving activity in air on an indoor tank but not on an outdoor pond. Conversely, there was a significant apparent hypothermia during diving activity under hypoxic conditions. 3. The CB chemoreceptors were shown to play a role in cardiac control during diving under certain circumstances. The duration of pre-dive tachycardia was significantly increased in hypoxia and this increase was abolished after CB denervation. The rate of development of bradycardia during extended and enclosed dives was slowed following CB denervation, though the initiation of the responses in extended and enclosed dives and the eventual attainment of sub-resting heart rates in enclosed dives were not prevented, indicating that other, as yet unidentified, sensory inputs are involved in cardiac control under these conditions.
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PMID:Chemoreceptor control of heart rate and behaviour during diving in the tufted duck (Aythya fuligula). 313 33

We studied 49 consecutively admitted infants of less than 34 weeks' gestation to analyze the role of several maternal, intrapartum, and neonatal factors associated with the occurrence of periventricular-intraventricular hemorrhage (PIVH). To detect PIVH, ultrasound studies were performed every eight hours during the first three days of life and every 12 hours during the following four days. In 20 infants (41%) PIVH was detected. Of these 20 cases, 30% were diagnosed immediately after birth and 55%, 70%, 90%, and 100% after 24, 48, 72, and 108 hours, respectively. Hypoxia, hypercapnia, and acidosis were the most important factors associated with the development of PIVH. Hypothermia was also an antecedent. Suctioning, serum osmolality, weight loss, transfusions, pneumothorax, patent ductus arteriosus, and bolus infusions with sodium bicarbonate were not associated with the onset of PIVH.
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PMID:Perinatal factors and periventricular-intraventricular hemorrhage in preterm infants. 353 62


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