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 effect of prostaglandin I2 (PGI2) on the postischemic recovery of the heart orthotopically transplanted under deep hypothermia was evaluated using puppies. Twenty-four pairs of dogs were divided into 4 groups according to the usage of PGI2 and preservation of the donor heart (in Euro-Collins' solution at 4 degrees C for 4 hours), namely Group I (non PGI2, no preservation), Group II (PGI2-treated, no preservation), Group III (non PGI2, 4 hours preservation), Group IV (PGI2-treated, 4 hours preservation). PGI2 was added into the donor's cardioplegic solution (500 ng/ml) and also was given intravenously to the recipient during cooling and rewarming periods (1 microgram/kg/min), and left ventricular pressure, max dp/dt, cardiac output were continuously monitored, and postmortem studies on myocardium were performed. Results were as follows: PGI2 yielded significantly better recovery of cardiac output and left ventricular pressure after transplanted of the heart, [Group I vs Group II (p less than 0.05), Group III vs Group IV (p less than 0.01)]. This effect was especially remarkable in the preserved heart groups. Microscopically, the contraction band formation in the myocardium was more prominent in Group III than in Group IV. It is concluded that PGI2 is of great use for the postischemic recovery of the transplanted heart not only by ameliorating the myocardial ischemic recovery of the transplanted heart, but also by reducing the afterload of the recipient during the recovery period from deep hypothermia.
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PMID:[The effect of prostaglandin I2 on the postischemic recovery of the transplanted heart under deep hypothermia]. 202 15

Beraprost sodium (sodium (+/-)-(1R*,2R*,3aS*,8bS*)-2,3,3a,8b-tetrahydro-2- hydroxy-1-[(E)-(3S*)-3-hydroxy-4-methyl-1-octen-6-ynyl]-1H- cyclopenta[b]benzofuran-5-butyrate, TRK-100) is an orally active epoprostenol (prostaglandin I2, PGI2) analogue. Its effect on the central nervous system (CNS) was studied. 1. When orally administered in mice, beraprost sodium at 0.3 mg/kg caused a flush of skin, a suppression of spontaneous motility, and a fall of body temperature. At 1 mg/kg and more, it showed obvious sedation, prolongation of hexobarbital hypnosis, and analgesic action in acetic acid-induced writhing test. However, even at 3 mg/kg beraprost sodium neither induced ataxia nor had anticonvulsant activity. Hypothermia was also observed in rabbits at 1 mg/kg (p.o. and i.v.). 2. When intravenously administered, beraprost sodium exerted long-lasting action on the CNS, while its pharmacological effects resembled those of PGI2. 3. Oral administration of beraprost sodium did not inhibit aggregation toxicity induced by methamphetamine (20 mg/kg i.p.) in mice. Beraprost sodium at doses higher than 1 mg/kg enhanced aggregation toxicity induced by methamphetamine (5 mg/kg i.p.), while intracerebral ventricular administration of beraprost sodium failed to enhance it. 4. In rat spinal reflex, intravenous administration of beraprost sodium (0.1 mg/kg) slightly enhanced monosynaptic reflex and at a high dose (1 mg/kg) suppressed polysynaptic reflex. 5. In the rabbit EEG, intravenous administration of beraprost sodium at a high dose (1 mg/kg) showed some effects such as the continuous pattern of wakefulness and a fall in power of the EEG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:General pharmacology of beraprost sodium. 1st communication: effect on the central nervous system. 251 Jul 42

Mitochondrial function of the liver is one of the limiting factors in liver preservation. Nowadays, prostaglandin I2 (PGI2) is used as a cytoprotective agent in liver preservation without full understanding its mechanism involved. It is the objective of the present study to evaluate the protective effect of PGI2 on mitochondrial function of the rat liver during hypothermic preservation. Collins' solution was used as a preservation solution and PGI2 was added to it in some experimental groups. Both ischemic and non-ischemic livers were perfused with the preservation solution and preserved under simple hypothermia for 8 hr. Parameters of the mitochondrial function such as respiratory control, oxygen consumption rate in state 3 respiration, ADP/O ratio and the rate of ATP synthesis were decreased significantly after 8 hr hypothermic preservation, even if ischemic injury was not induced prior to preservation. ADP/O ratio, which represents the efficiency of oxidative phosphorylation in mitochondria, was improved significantly (p less than 0.01) when PGI2 was used as a cytoprotective agent. The rate of ATP synthesis, a parameter of energy producing reaction, showed a tendency to be increased by PGI2, but was not significant. It was concluded that hypothermic preservation of the rat liver is associated with the deterioration of the mitochondrial function and PGI2 has a favorable effect on the impaired ADP/O ratio of oxidative phosphorylation in mitochondria.
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PMID:Protective effect of prostaglandin I2 on hepatic mitochondrial function of the preserved rat liver. 355 Nov 89