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

Exposure to a temperature of 14 degrees C was used to induce a progressive hypothermia in fourteen conscious newborn piglets. Heat production, body (rectal) and skin (between the shoulders) temperatures and shivering intensity assessed as the electromyographic activity (EMG) of longissimus thoracis muscle were measured until body temperature reached 30 degrees C and during a recovery period of 2 h at an ambient temperature of 24 degrees C (n = 7) or 34 degrees C (n = 7). During body cooling, heat production increased up to 9.67 +/- 1.28 W (kg BW)-1, but started to decrease below a body temperature threshold of 34.4 +/- 0.7 degrees C. EMG activity increased (P < 0.023) curvilinearly during body cooling; the main increase occurred between body temperatures of 38 and 33 degrees C (+142%, P < 0.001), and changes in EMG activity between 33 and 30 degrees C were not significant (+18%, P > 0.1). A marked increase in circulating levels of glucose (+312%, P < 0.001), glucagon (+76%, P < 0.05), adrenaline (+172%, P < 0.05) and noradrenaline (+113%, P < 0.05) occurred during body cooling. Insulin levels were not detectable at 2 h of life and increased during body cooling. During 2 h of rewarming at 24 degrees C, heat production and EMG activity remained elevated, changes in carbohydrate metabolism were not completely reversed and the final body temperature was only 35.6 +/- 0.9 degrees C. Rewarming of the piglets was faster at 34 degrees C. There was a net influx of heat into the animals and heat production and shivering activity decreased when body temperature reached 33.9 +/- 0.5 degrees C; the final body temperature was 37.5 +/- 0.2 degrees C. Circulating levels of lactate, glucagon and catecholamines returned to control levels. These results show that in conscious piglets exposed to a constant cold temperature there is an inverse relationship between EMG activity and body temperature during moderate hypothermia and that the thermoregulatory response and carbohydrate metabolism of the piglet are seriously impaired below a body temperature of 34 degrees C.
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PMID:Thermoregulatory responses of the newborn pig during experimentally induced hypothermia and rewarming. 979 87

We report the case of a 43-year-old schizophrenic who sustained, after 12 days of treatment including olanzapine (20 mg.day-1), carbamazepine, levomepromazine and alprazolan, a severe shock with bradycardia (HR: 40 b.min-1), circulatory collapse (SAP: 60 mmHg), hypothermia (T: 27 degrees C), coma and disseminated intravascular coagulation. A significant improvement was obtained with high doses of intravenous glucagon, whereas the normalization of central temperature, atropine, adrenaline and volume loading had been inefficient. Olanzapine, alone of associated with other psychotropics, could cause severe circulatory collapse with hypothermia and coma responding to a treatment including glucagon.
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PMID:[Severe intoxication probably from olanzapine (Zyprexa). Beneficial effect of glucagon]. 1046 38

Neonatal diabetes mellitus (NDM) is a very rare disease defined as hyperglycemia that occurs during the first month of life, requires insulin treatment, and lasts more than 2 weeks. There are 2 types of NDM: permanent neonatal diabetes mellitus (PNDM) and transient neonatal diabetes mellitus (TNDM). We report a case of PNDM in a 3-day-old female infant. This full-term neonate was born small for gestational age. Respiratory distress, poor activity, hypothermia, poor feeding, dehydration, and ketoacidosis were noted at the age of 3 days. After insulin therapy and fluid replacement, her condition became stable. Glucagon test done at the age of 26 days showed serum C-peptide level to be low for her age. During the first year of life she had catch-up growth, but insulin therapy was still required. Serum C-peptide level was undetectable at the age of 15 months. The course of this case indicates the importance of a high index of suspicion for patients with PNDM in order to correct metabolic derangement as early as possible and facilitate normal growth and development under insulin therapy.
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PMID:Permanent neonatal diabetes mellitus manifesting as diabetic ketoacidosis. 1497 69

A 60-year-old woman presented to her primary care physician with fatigue and anemia. Laboratory evaluation revealed a hemoglobin level of 9.8 g/dL and an erythrocyte sedimentation rate (ESR) of 64 mm/hour. She subsequently developed nocturnal episodes of diaphoresis, confusion, and hypothermia. Capillary glucose measurements during the spells revealed hypoglycemia. During two supervised fasts, the patient's plasma glucose levels fell to 35 mg/dL and 32 mg/dL, respectively. Plasma insulin and C-peptide levels were appropriately suppressed, but a low concentration of beta-hydroxy-butyrate and normal increase of plasma glucose concentration after a glucagon injection suggested the presence of an insulin-like substance. Computed tomographic (CT) scan of the abdomen and subsequent positron emission tomographic (PET) scan revealed extensive lymphadenopathy. Biopsy of periaortic lymph nodes revealed Hodgkin's disease of the mixed cellularity type. Following chemotherapy, a complete remission ensued, the spells abated, and hypoglycemia was not induced by a 23-hour fast. We believe that the patient's Hodgkin's disease was producing an insulin-like substance. The observations of others suggest that this substance may be an autoantibody to the insulin receptor.
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PMID:Recurrent hypoglycemia and hypothermia in a patient with Hodgkin's disease. 1719 56

The effects of peripheral glucagon like peptide-1 receptor (GLP-1R) stimulation on feeding, gastric emptying, and energetic responses involve vagal transmission and central nervous system processing. Despite a lack of studies aimed at determining which central nervous system regions are critical for the GLP-1R response production, hypothalamic/forebrain processing is regarded as essential for these effects. Here the contribution of the caudal brainstem to the control of food intake, core temperature, heart rate, and gastric emptying responses generated by peripheral delivery of the GLP-1R agonist, exendin-4 (Ex-4), was assessed by comparing responses of chronic supracollicular decerebrate (CD) rats to those of pair-fed intact control rats. Responses driven by hindbrain intracerebroventricular (fourth i.c.v) delivery of Ex-4 were also evaluated. Intraperitoneal Ex-4 (1.2 and 3.0 microg/kg) suppressed glucose intake in both CD rats (5.0+/-1.2 and 4.4+/-1.1 ml ingested) and controls (9.4+/-1.5 and 7.7+/-0.8 ml ingested), compared with intakes after vehicle injections (13.1+/-2.5 and 13.2+/-1.7 ml ingested, respectively). Hindbrain ventricular Ex-4 (0.3 microg) also suppressed food intake in CD rats (4.7+/-0.6 ml ingested) and controls (11.0+/-2.9 ml ingested), compared with vehicle intakes (9.3+/-2.1 and 19.3+/-4.3 ml ingested, respectively). Intraperitoneal Ex-4 (0.12, 1.2, 2.4 microg/kg) reduced gastric emptying rates in a dose-related manner similarly for both CD and control rats. Hypothermia followed ip and fourth i.c.v Ex-4 in awake, behaving controls (0.6 and 1.0 C average suppression) and CD rats (1.5 and 2.5 C average suppression). Intraperitoneal Ex-4 triggered tachycardia in both control and CD rats. Results demonstrate that caudal brainstem processing is sufficient for mediating the suppression of intake, core temperature, and gastric emptying rates as well as tachycardia triggered by peripheral GLP-1R activation and also hindbrain-delivered ligand. Contrary to the literature, hypothalamic/forebrain processing and forebrain-caudal brainstem communication is not required for the observed responses.
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PMID:Caudal brainstem processing is sufficient for behavioral, sympathetic, and parasympathetic responses driven by peripheral and hindbrain glucagon-like-peptide-1 receptor stimulation. 1842 Jul 40

Thyronamines are naturally occurring, chemical relatives of thyroid hormone. Systemic administration of synthetic 3-iodothyronamine (T(1)AM) and - to a lesser extent - thyronamine (T(0)AM), leads to acute bradycardia, hypothermia, decreased metabolic rate, and hyperglycemia. This profile led us to hypothesize that the central nervous system is among the principal targets of thyronamines. We investigated whether a low dose i.c.v. infusion of synthetic thyronamines recapitulates the changes in glucose metabolism that occur following i.p. thyronamine administration. Plasma glucose, glucoregulatory hormones, and endogenous glucose production (EGP) using stable isotope dilution were monitored in rats before and 120 min after an i.p. (50 mg/kg) or i.c.v. (0.5 mg/kg) bolus infusion of T(1)AM, T(0)AM, or vehicle. To identify the peripheral effects of centrally administered thyronamines, drug-naive rats were also infused intravenously with low dose (0.5 mg/kg) thyronamines. Systemic T(1)AM rapidly increased EGP and plasma glucose, increased plasma glucagon, and corticosterone, but failed to change plasma insulin. Compared with i.p.-administered T(1)AM, a 100-fold lower dose administered centrally induced a more pronounced acute EGP increase and hyperglucagonemia while plasma insulin tended to decrease. Both systemic and central infusions of T(0)AM caused smaller increases in EGP, plasma glucose, and glucagon compared with T(1)AM. Neither T(1)AM nor T(0)AM influenced any of these parameters upon low dose i.v. administration. We conclude that central administration of low-dose thyronamines suffices to induce the acute alterations in glucoregulatory hormones and glucose metabolism following systemic thyronamine infusion. Our data indicate that thyronamines can act centrally to modulate glucose metabolism.
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PMID:Central effects of thyronamines on glucose metabolism in rats. 1927 99

Cocaine- and amphetamine-regulated transcript (CART) peptides are widely distributed throughout the neuraxis, including regions associated with energy balance. CART's classification as a catabolic neuropeptide is based on its inhibitory effects on feeding, coexpression with arcuate nucleus proopiomelanocortin neurons, and on limited analysis of its energy expenditure effects. Here, we investigate whether (1) caudal brainstem delivery of CART produces energetic, cardiovascular, and glycemic effects, (2) forebrain-caudal brainstem neural communication is required for those effects, and (3) glucagon-like peptide-1 receptors (GLP-1Rs) contribute to the mediation of CART-induced effects. Core temperature (Tc), heart rate (HR), activity, and blood glucose were measured in rats injected fourth intracerebroventricularly with CART (0.1, 1.0, and 2.0 microg). Food was withheld during physiologic recording and returned for overnight measurement of intake and body weight. CART induced a long-lasting (>6 h) hypothermia: a 1.5 degrees C and 1.6 degrees C drop in Tc for the 1.0 and 2.0 microg doses. Hindbrain CART application reduced food intake and body weight and increased blood glucose levels; no change in HR or activity was observed. Supracollicular decerebration eliminated the hypothermic response observed in intact rats to hindbrain ventricular CART, suggesting that forebrain processing is required for hypothermia. Pretreatment with the GLP-1R antagonist (exendin-9-39) in control rats attenuated CART hypothermia and hypophagia, indicating that GLP-1R activation contributes to hypothermic and hypophagic effects of hindbrain CART, whereas CART-induced hyperglycemia was not altered by GLP-1R blockade. Data reveal a novel function of CART in temperature regulation and open possibilities for future studies on the clinical potential of the hypothermic effect.
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PMID:Hindbrain cocaine- and amphetamine-regulated transcript induces hypothermia mediated by GLP-1 receptors. 1947 24

It is well known that abnormally elevated glutamate levels in the brain are associated with secondary brain injury following acute and chronic brain insults. As such, a tight regulation of brain glutamate concentrations is of utmost importance in preventing the neurodegenerative effects of excess glutamate. There has been much effort in recent years to better understand the mechanisms by which glutamate is reduced in the brain to non-toxic concentrations, and in how to safely accelerate these mechanisms. Blood glutamate scavengers such as oxaloacetate, pyruvate, glutamate-oxaloacetate transaminase, and glutamate-pyruvate transaminase have been shown to reduce blood glutamate concentrations, thereby increasing the driving force of the brain to blood glutamate efflux and subsequently reducing brain glutamate levels. In the past decade, blood glutamate scavengers have gained increasing international interest, and its uses have been applied to a wide range of experimental contexts in animal models of traumatic brain injury, ischemic stroke, subarachnoid hemorrhage, epilepsy, migraine, and malignant gliomas. Although glutamate scavengers have not yet been used in humans, there is increasing evidence that their use may provide effective and exciting new therapeutic modalities. Here, we review the laboratory evidence for the use of blood glutamate scavengers. Other experimental neuroprotective treatments thought to scavenge blood glutamate, including estrogen and progesterone, beta-adrenergic activation, hypothermia, insulin and glucagon, and hemodialysis and peritoneal dialysis are also discussed. The evidence reviewed here will hopefully pave the way for future clinical trials.
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PMID:Brain to blood glutamate scavenging as a novel therapeutic modality: a review. 2462 40

After birth, the newborn must adapt to the acute challenges of circulatory changes, active respiration, thermoregulation, microbial colonization, and enteral nutrition. Whereas these processes normally occur without clinical complications in neonates born at term, birth at a preterm state of gestation is associated with high morbidity and mortality. In commercial pig production, perinatal mortality is higher than in any other mammalian species. Asphyxia, hypothermia, hypoglycemia, sepsis, and gut dysmotility, represent some of the most common findings. The intestine is a particularly sensitive organ after birth, as it must adapt acutely to enteral nutrition and microbial colonization. Likewise, during the weaning phase, the intestine must adapt to new diet types. Both critical phases are associated with high morbidity. This review focuses on the endocrine changes occurring around birth and weaning. There are a number of endocrine adaptations in late gestation and early postnatal life that are under influence of development stage and environmental factors such as diet. The review discusses general endocrine changes in perinatal life but specifically focuses on the role of glucagon-like peptide-2. This gut-derived hormone plays a key role in development and function of the intestine in early life.
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PMID:Endocrine regulation of gut maturation in early life in pigs. 2734 27

A severely malnourished, Japanese female in her twenties was found dead in her apartment. On autopsy, most of the findings from the internal examination were suggestive of hypothermia. Postmortem biochemistry, however, showed severely increased levels of glycated hemoglobin (HbA1c) and blood and urine glucose levels. Levels of acetone, 3-hydroxybutyric acid, and acetoacetate in various body fluids were also highly increased, indicating ketosis. The serum insulin and c-peptide levels were severely low, and subsequent testing was positive for anti-GAD antibodies. Immunohistochemical examination of the pancreatic islet cells revealed few insulin-positive cells but many glucagon-positive cells on staining. Furthermore, slight invasion of CD8-positive lymphocytes in the pancreatic islets of Langerhans was observed. Results of immunostaining of the pancreatic and bronchial epithelial tissues were partly positive for the Influenza A virus. We concluded that severe ketoacidosis associated with rapid-onset hyperglycemia due to autoimmune type 1 diabetes (AT1D) had occurred shortly before death. However, the ketosis was accompanied by hypothermia and malnutrition as well as diabetic ketoacidosis (DKA). Therefore, we retrospectively collected biochemical data on cases of hypothermia and malnutrition and compared them with the present case. Serum glucose, acetone, 3-hydroxybutyric acid, and acetoacetic acid can be used for screening and diagnosis to distinguish DKA from ketosis due to hypothermia and malnutrition. Therefore, in the present case, we diagnosed that the natural cause of death was due to AT1D. In conclusion, screening investigations for relevant biochemical markers can provide essential information for the diagnosis of metabolic disturbances, which fail to demonstrate characteristic autopsy findings.
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PMID:Usefulness of postmortem biochemistry in identification of ketosis: Diagnosis of ketoacidosis at the onset of autoimmune type 1 diabetes in an autopsy case with cold exposure and malnutrition. 2759 35


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