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

The effects of different dopamine (DA) D2 receptor agonists and the DA D2 receptor antagonist, emonapride, on body temperature were studied in male mice. The aim of the study was to test whether DA D2 receptor agonists ranging from full agonists to agonists with low efficacy could be differentiated by means of their effect on body temperature. Talipexole induced a marked hypothermia (maximum decrease of 6.5 degrees C). Apomorphine, quinelorane, (+)-4-propyl-9-hydroxy-naphtoxazine((+)-PHNO), and (-)-N-n-propylnorapomorphine ((-)-NPA) induced a maximum hypothermia of 3.5-4.1 degrees C. Quinpirole and (+)-3-(3-hydroxyphenyl)-N-n-propylpiperidine ((+)-3-PPP) induced a less pronounced hypothermia (1.7 and 1.5 degrees C), and preclamol ((-)-3-PPP), terguride and 3-(4-(4-phenyl-1,2,3,6-tetrahydropyridyl)-(1))-butyl)-indole (EMD 23448) had no or only a slight effect. Emonapride induced significant hyperthermia at high doses. Apomorphine-, quinelorane- and talipexole-induced hypothermia was reversed by terguride and preclamol, whereas EMD 23448 partially reversed the apomorphine-induced hypothermia. The alpha 2-adrenoceptor antagonist, idazoxan, partly reversed the effect of talipexole. Quinpirole had no effect on the hypothermic effect of the above-mentioned agonists. Pretreatment with the catecholamine synthesis inhibitor, alpha-methyl-m-tyrosine, increased significantly the hypothermic response to quinpirole, whereas the effect of quinelorane was unchanged. It is suggested that the effect of DA D2 agonists on body temperature in mice can be used to differentiate between agonists with different efficacies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects on body temperature in mice differentiate between dopamine D2 receptor agonists with high and low efficacies. 135 51

Injection of ibotenic acid (IA), a glutamate agonist, into the ventral medullary raphe (VMR; especially the nucleus raphe magnus) of the rat produced respiratory failure and death following a predictable course of events. The response to the IA injection was characterized initially by increased respiratory frequency and was followed by pulmonary arterial hypertension, systemic arterial hypoxemia, acidosis, and hypothermia. Within 90 min apnea occurred as a terminal event in all animals. Gravimetric, bronchoalveolar lavage protein, and histological analyses revealed no evidence of pulmonary edema. Intracerebral (VMR) pretreatment with PPP, a sigma receptor agonist, or scopolamine, a muscarinic cholinergic antagonist, prevented pulmonary failure and death even though postmortem histological analysis showed VMR cell loss and gliosis consequent to the cytotoxic IA injection. Based on the results of the study, it is suggested that the VMR has a role in regulation of pulmonary blood flow. Preliminary pharmacological studies suggested that a disruption of glutamatergic and cholinergic mechanisms mediates the lethal pulmonary phenomenon.
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PMID:Respiratory failure without pulmonary edema following injection of a glutamate agonist into the ventral medullary raphe of the rat. 137 23

The novel dopaminergic agents (+)- and (-)-3-PPP were evaluated for their effects upon thermoregulation in rats maintained at room temperature (approximately 22 degrees C). Although approximately 30 times less potent than apomorphine, (+)-3-PPP induced a clearcut, dose-dependent and haloperidol/pimozide-reversible hypothermia. In contrast, the (-)-enantiomer per se lacked a significant effect upon rat body temperature. However, (-)-3-PPP clearly attenuated apomorphine-induced hypothermia. Simultaneous biochemical investigations confirmed the presence of central dopamine (DA) agonist and antagonist properties for (+)- and (-)-3-PPP, respectively, at the doses employed. The results are compared to the agonist and antagonist effects of the 3-PPP enantiomers in various other central DA receptors systems. Particular reference is made to the recent hypothesis by Carlsson (J. Neural Transm. 57 (1983) 309, relating agonist intrinsic activity to the DA receptor responsiveness state, in turn determined by the endogenous tone. Based on the findings with (+)- and (-)-3-PPP it is suggested that DA receptors mediating hypothermia in the rat may be more akin to 'normosensitive' postsynaptic than to highly 'agonist-responsive' autoreceptors.
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PMID:Dopamine receptor-mediated hypothermia induced in rats by (+)-, but not by (-)-3-PPP. 397 30

Generation of pulsatile flow depends on an energy gradient. Surplus hemodynamic energy (SHE) is the extra hemodynamic energy generated by a pulsatile device when the adequate pulsatility is achieved. The objective of this study was to precisely quantify and compare pressure-flow waveforms in terms of surplus hemodynamic energy levels of six different pediatric heart-lung machines in a neonatal piglet model during cardiopulmonary bypass (CPB) procedures with deep hypothermic circulatory arrest (DHCA). Thirty-nine piglets (average weight, 3 kg) were subjected to CPB with a hydraulically driven physiologic pulsatile pump (PPP; n=7), Jostra-HL 20 pulsatile roller pump (Jostra-PR; n=6), Stockert Sill pulsatile roller pump (SIII-PR; n=6), Stockert Sill mast-mounted pulsatile roller pump with a miniature roller head (Mast-PR; n=7), Stockert Sill mast-mounted nonpulsatile roller pump (Mast-NP; n=7), or Stockert CAPS nonpulsatile roller pump (CAPS-NP, n=7). Once CPB was begun, each animal underwent 20 minutes of hypothermia, 60 minutes of DHCA, 10 minutes of cold reperfusion, and 40 minutes of rewarming. The pump flow rate was maintained at 150 ml x kg(-1) x min(-1) and the mean arterial pressure (MAP) at 45 mm Hg. In the pulsatile experiments, the pump rate was kept at 150 bpm and the stroke volume at 1 ml/kg. The SHE (ergs/cm3) = 1,332 ([(integral fpdt) / (integral fdt)] - MAP) was calculated at each experimental stage. During normothermic CPB (15 minutes on pump), the physiologic pulsatile pump generated the highest surplus hemodynamic energy (8563 +/- 1918 ergs/cm3, p < 0.001) compared with all other pumps. The Jostra HL-20 and Stockert Sill pulsatile roller pumps also produced adequate surplus hemodynamic energy. Nonpulsatile roller pumps and the Stockert Sill mast-mounted pulsatile roller pump did not generate any extra hemodynamic energy. During hypothermic CPB and after DHCA and rewarming, the results were extremely similar to those seen during normothermic CPB. The surplus hemodynamic energy formula is a novel method to precisely quantify different levels of pulsatility and nonpulsatility for direct and meaningful comparisons. The PPP produced the greatest surplus hemodynamic energy. Most of the pediatric pulsatile pumps (except Mast-PR) generated significant surplus hemodynamic energy. None of the nonpulsatile roller pumps generated adequate surplus hemodynamic energy.
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PMID:Precise quantification of pulsatility is a necessity for direct comparisons of six different pediatric heart-lung machines in a neonatal CPB model. 1632 24