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)

Thirty-one mares of Quarter Horse and Thoroughbred breeding were utilized in two experiments to evaluate the efficacy of prostaglandin F2 alpha (PGF2 alpha) for induction of equine parturition and to monitor the effects of this treatment on viability of the resulting foals. Three of five mares given 5 mg PGF2 alpha (im) on day 338 of gestation foaled 19.6+/-8.2 hr postinjection. In the second experiment immediately following 3 daily injections of 10 mg estradiol cypionate (ECP) given on days 326, 327 and 328 of gestation, seven mares were infused (iv) with PGF2 alpha at the rate of 1.3 mg/hr for 24 hr or until parturition occurred. Four of the seven mares foaled in 8.8+/-1.8 hr after the start of infusion. Side effects including sweating, hypothermia, increased respiration rate and diarrhea were evident in both injected and infused mares, but effects were transient. Neither the injection, nor infusion route of administration of PGF2 alpha adversely affected the viability of foals. However, some mares induced to foal 12 days prior to expected parturition had foals with slightly weaker pasterns than those of control mares.
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PMID:Induction of parturition in the mare with prostaglandin F2 alpha. 695 51

Staphylococcal pyrogenic exotoxin (PE) ty pe C enhanced the susceptibility of rabbits to lethal shock by endotoxin by as much as 50,000-fold. A graph of log PE type C dose used for pretreatment versus log 50% lethal dose of endotoxin gave a straight line with a slope of approximately -1. Rabbits that received PE type C alone showed fevers only, but those given both PE ty pe C and endotoxin showed initial fever followed by hypothermia, labored breathing, diarrhea, evidence of vascular collapse, and finally death. When a PE type C dose of 3 micrograms/kg was used, pretreatment of the animals with PE for 2 h before giving the endotoxin was required to obtain maximal susceptibility. However, when 15 micrograms of PE type C per kg was utilized, the endotoxin could be given before, concurrently, or after PE type C. The capacity of PE type C to prepare rabbits for enhanced susceptibility to endotoxin was lost after 24 to 48 h. Animals could be protected from enhanced susceptibility to endotoxin by prior immunization with either PE type C or endotoxin. However, 30% of the rabbits which were immunized with PE type C failed to develop immunity, and after three injections of PE type C, these animals developed gram-negative bacteremia and succumbed. In addition, rabbits with diarrhea initially, possibly caused by Pasteurella infection, died less than 24 h after a single injection of PE type C.
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PMID:Enhancement of host susceptibility to lethal endotoxin shock by staphylococcal pyrogenic exotoxin type C. 704 68

The toxicology of a potentially useful antitumor agent, 2,4-diamino-5-adamantyl-6-methylpyrimidine (DAMP), and its ethanesulfonate salt has been studied in beagle dogs after 1 to 20 doses. Two types of toxicity could be discerned: the acute central nervous system toxicity manifested by vomiting, convulsions, and minor hypothermia; and the antiproliferative toxicity, similar to that of other folate antagonists, manifested by diarrhea, anorexia, loss of body weight, and hematological changes as well as changes in blood chemistry. There is evidence of a cumulative effect of the drug with respect to antiproliferative toxicity. Characteristically, the animals could be protected against the antiproliferative toxicity by simultaneous administration of folinic acid. The pharmacokinetics of the ethanesulfonate salt of DAMP was studied after i.v. administration of sublethal doses (5 mg/kg) of tritium-labeled drug. Sixty-three % of the administered dose was excreted in the urine and 10% was excreted in the feces within 48 hr after drug administration. Thus, about 27% of the drug was not recovered, and it is possible that it persists in the tissues for a period of several days. Analysis of the plasma and urine revealed that DAMP was metabolized rapidly. At least 2 metabolites were found in plasma and urine, one lipophilic and one hydrophilic, the latter being the predominant form. Pharmacokinetic data were successfully fitted to a model consisting of central and peripheral DAMP compartments and a DAMP metabolite compartment. DAMP was very rapidly sequestered in the peripheral compartment with a rapid phase half-life of 23 sec. The slower phase of DAMP plasma disappearance had a half-life of 3 hr. The short plasma half-life and rapid metabolism distinguished this drug from other lipophilic antifolates.
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PMID:Toxicity and pharmacokinetics of a new antifolate, 2,4-diamino-5-adamantyl-6-methylpyrimidine, in dogs. 707 98

To investigate the effect of cold exposure on absorption of colostral immunoglobulins, 56 piglets were weaned at birth and placed in either a thermoneutral (35 C) or cold (21 C) environmental chamber. Thermoneutral piglets had a survival rate of 62% at 48 h, but survival among cold-exposed piglets was only 36% (P less than .10). Cold aid reduced (P less than .01) rectal temperature by more than 6 C after 24 h of exposure. A constant amount of bovine colostrum was administered orally at 4 h after initiation of thermal treatments. Bovine immunoglobulin G1 (IgG1) was readily absorbed and reached a serum level of 17 mg/ml after 24 h. Bovine IgM also was absorbed and increased to approximately 2 mg/ml at 24 h. However, absorption of colostral IgG1 and IgM was not affected by cold exposure. Cold air increased (P less than .05) incidence of diarrhea by over five fold after 72 h, and severity of diarrhea was nearly doubled (P less than .01). Hematocrit was also higher (P less than .05) in cold-exposed piglets. These data demonstrate that a cold stressor sufficient to induce hypothermia does not impair absorption of colostral macromolecules in piglets. However, cold exposure was related to increase incidence and severity of diarrhea.
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PMID:Cold exposure and absorption of colostral immunoglobulins by neonatal pigs. 714 52

Aziridinylbenzoquinone (AZQ: NSC-182986), is a quinone derivative which has been shown to have activity in implanted murine tumor systems. Toxicity in small and large animals included hypothermia, diarrhea, anorexia, emesis, weight loss, and gastrointestinal bleeding. In addition, there was myelosuppression and elevated liver function tests. In a phase I study at the Mayo Clinic, dose-limiting toxicity was myelosuppression. Patients with prior radiation therapy or prior chemotherapy were more sensitive to this toxicity. A dose schedule of 27.5 mg/m2 q4 weeks was recommended for patients who had had no previous chemotherapy and 22.5 mg/m2 for previously treated patients or for patients who had had extensive prior radiation therapy. The objective of this study was to determine therapeutic activity for AZQ in patients with advanced colorectal adenocarcinoma.
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PMID:A phase II study of aziridinylbenzoquinone (AZQ) in advanced large bowel carcinoma. 718 Aug 32

The injection of high dose of naloxone 15 minutes after a single injection of morphine in mice was found to produce a jumping response which was behaviorly similar to the jumping response observed during the withdrawal from chronic morphine administration. In addition the jumping response following the acute administration of morphine-naloxone was increased by the injection of atropine and attenuated by oxotremorine. These data are consistent with the reports of effect of these cholinergic drugs on the jumping response which occurred during withdrawal after chronic morphine administration. However, other symptoms associated with opiate withdrawal (hypothermia, weight loss and diarrhea) were not produced by the acute injection of morphine-naloxone. It is therefore suggested that this single injection paradigm is particular to the jumping response rather than a demonstration of the rapid development of opiate dependence.
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PMID:Opiate dependence following acute injections of morphine and naloxone: the assessment of various withdrawal signs. 719 40

Beagle bitches were treated on days 20-22 of pregnancy with TPT as an aqueous solution administered subcutaneously via a minipump at a rate of 10 micrograms per hour for either 24 (I) or 48 hours (II). Additional animals received a single subcutaneous injection of 200 micrograms of TPT as an aqueous solution (III) or dissolved in polyethylene glycol 400 (IV) or the methyl ester of TPT dissolved in polyethylene glycol 400 (V). The duration of action was assessed by the nadir in circulating progesterone levels. By this criterion the duration of action in the different groups ranked I=III<II=IV<V, the nadir occurring at 2, 3 and 3-4 days post treatment, respectively. Duration of action correlated with the incidence of abortion. Salivation, emesis and diarrhea or hypothermia side effects, previously noted for this agent, were not affected by the manipulations of duration of action.
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PMID:Manipulation of duration of action of a synthetic prostaglandin analogue (TPT) assessed in the pregnant beagle bitch. 741 48

Following the Exxon Valdez oil spill, 347 oiled sea otters (Enhydra lutris) were treated in rehabilitation centers. Of these, 116 died, 94 within 10 days of presentation. Clinical records of 21 otters dying during the first 10 days of rehabilitation were reviewed to define the laboratory abnormalities and clinical syndromes associated with these unexpected deaths. The most common terminal syndrome was shock characterized by hypothermia, lethargy, and often hemorrhagic diarrhea. In heavily and moderately oiled otters, shock developed within 48 hours of initial presentation, whereas in lightly oiled otters shock generally occurred during the second week of captivity. Accompanying laboratory abnormalities included leukopenia with increased numbers of immature neutrophils (degenerative left shift), lymphopenia, anemia, azotemia (primarily prerenal), hyperkalemia, hypoproteinemia/hypoalbuminemia, elevations of serum transaminases, and hypoglycemia. Shock associated with hemorrhagic diarrhea probably occurred either as a direct primary effect of oiling or as an indirect effect secondary to confinement and handling in the rehabilitation centers. Lightly oiled otters were less likely to die from shock than were heavily oiled otters (22% vs. 72%, respectively). Heavily oiled otters developed shock more rapidly and had greater numbers of laboratory abnormalities, suggesting that exposure to oil was an important contributing factor.
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PMID:Clinical and clinical laboratory correlates in sea otters dying unexpectedly in rehabilitation centers following the Exxon Valdez oil spill. 748 8

Butorphanol has been shown to act on mu-, delta-, and kappa-opioid receptors. However, the relative involvement of different opioid receptor subtypes in butorphanol dependence is not known. In the present study, nor-binaltorphimine, a long-acting non-peptide kappa-opioid receptor antagonist, was employed to mask central kappa-opioid receptors before and during the induction of butorphanol dependence in rats, so that the involvement of kappa-opioid receptors could be elucidated. The results revealed that treatment with nor-binaltorphimine markedly blocked naloxone-precipitated withdrawal signs of escape behavior, teeth-chattering, wet shakes, ptosis, body weight loss, and hypothermia at all doses tested, and attenuated the withdrawal symptoms of forepaw tremors (24 nmol: P < 0.001) and diarrhea (12 nmol: P < 0.05; 24 nmol: P < 0.01). In contrast, nor-binaltorphimine had no effect on yawning, ejaculation, nor urination in butorphanol-infused rats undergoing withdrawal. Three days of butorphanol infusion significantly increased KD values (in the cortex and striatum), decreased Bmax (in the cortex only) of [3H]U-69,593 binding, and shifted Ki of nor-binaltorphimine against [3H]U-69,593 (4.5 nM) binding in the cortex by more than 10-fold. Treatment with nor-binaltorphimine blocked the effects of butorphanol on kappa-opioid receptors. It is therefore concluded that kappa-opioid receptors are involved in mediating escape behavior, teeth-chattering, wet shakes, forepaw tremors, ptosis, diarrhea, weight loss, and hypothermia in butorphanol-dependent rats undergoing withdrawal. Furthermore, kappa-opioid receptors become desensitized to agonists (in the cortex and striatum), down-regulated (in the cortex), and supersensitive to antagonists in butorphanol-dependent rats.
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PMID:Effects of nor-binaltorphimine on butorphanol dependence. 822 88

A mouse bioassay, validated for the quantification of ciguatoxin in up to 20 mg of ether extract from fish flesh, revealed that 63 +/- 14% of spiked ciguatoxin was recovered using a standard extraction procedure. Except for extracts from the least toxic of ciguateric fish (0.1-0.5 nmol ciguatoxin-1/kg fish), signs in mice of intoxication by ciguatoxin (hypothermia to below 33 degrees C as well as at least severe diarrhoea or lachrymation or hypersalivation) could be distinguished from the toxic reaction that follows administration of ciguatoxin-free ether extracts. Ciguatoxin recovery was similar for four variants of the ether-water partition, with the 2 M NaC1/ether partition extracting half the contaminants. The method described is selective for ciguatoxin and could be used to quantify natural levels ciguatoxin in the flesh of fish in the absence of a validated in vitro test.
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PMID:Recovery of ciguatoxin from fish flesh. 830 28


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