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)

Prostacyclin (PGI2) administered icv into the lateral rat brain ventricle in a dose of 1 and 10 micrograms caused hypothermia and catalepsy. Joint administration of PGI2 and chlorpromazine produced a greater cataleptic effect than that observed after the neuroleptic alone. Cimetidine (CMT) 2 g/kg po administered 60 min before PGI2 icv injection inhibited hypothermic and cataleptogenic action of PGI2. CMT blocked the cataleptogenic effect of chlorpromazine as well as combination of it with PGI2. CMT inhibited cataleptogenic effect of haloperidol, but it did not block the catalepsy induced by joint administration of haloperidol and PGI2. PGI2 did not change concentration of noradrenaline and dopamine in different brain areas. The results indicate that H2 receptors take part in some central pharmacological effects of PGI2 in rats.
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PMID:Influence of H2 receptors blockade upon some central effects of prostacyclin in rats. 287 Apr 86

The antithrombotic effects of prostacyclin infusion on myocardial platelet deposition were studied in a canine model during and after global ischemia. Eleven isolated heart preparations were subjected to 1 hour of cardioplegic arrest under moderate hypothermia (27 degrees to 28 degrees C), including a control group (n = 7) and a prostacyclin-treated group (n = 4). The hearts of four other dogs were continuously perfused for 180 minutes. Platelet deposition was measured at 15 minute intervals throughout the 3 hour study. Serial full-thickness myocardial biopsy specimens were analyzed for activity of 111In-labeled platelets with 99mTc-labeled erythrocyte correction for tissue blood content. The pattern of platelet distribution was determined by scintiscans of each heart, taken with a gamma camera at the end of the 60 minute reperfusion period. Substantial myocardial platelet deposition was found in the control hearts after ischemia but not in the prostacyclin-treated group (p less than 0.05). Furthermore, prostacyclin infusion had a significant disaggregatory effect on intracoronary platelet deposits when the precardioplegic and postcardioplegic biopsy specimens were analyzed (p less than 0.05). Three hours of continuous perfusion did not increase tissue 111In-labeled platelet activity. Ex vivo images showed platelet deposition to be a diffuse patchy process with significantly more 111In activity in the endocardium than in the epicardium after global ischemia (p less than 0.05). These data show the potent antithrombotic properties of prostacyclin in preventing and disaggregating ischemia-induced intracoronary platelet deposition during and after cardioplegic arrest.
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PMID:Prevention of ischemia-induced myocardial platelet deposition by exogenous prostacyclin. 301 30

Cerebral blood flow and metabolism of oxygen, glucose, and lactate were studied in 43 patients undergoing aortocoronary bypass. Twenty-five patients received prostacyclin infusion, 50 ng per kilogram of body weight per minute, during cardiopulmonary bypass (CPB), and 18 patients served as a control group. Regional cerebral blood flow (CBF) was studied by intraarterially injected xenon 133 and a single scintillation detector. Oxygen tension, carbon dioxide tension, oxygen saturation, glucose, and lactate were measured in arterial and cerebral venous blood. Mean arterial blood pressure decreased during hypothermia and prostacyclin infusion to less than 30 mm Hg. The regional CBF was, on average, 22 (standard deviation [SD] 4) ml/100 gm/min before CPB. It increased in the control group during hypothermia to 34 (SD 12) ml/100 gm/min, but decreased in the prostacyclin group to 15 (SD 5) ml/100 gm/min. It increased during rewarming in the prostacyclin group. After CPB, regional CBF was about 40 ml/100 gm/min in both groups. The cerebral arteriovenous oxygen pressure difference decreased more in the control group than in the prostacyclin group during hypothermia. The cerebral metabolic rate of oxygen decreased in both groups from approximately 2 ml/100 gm/min to about 1 ml/100 gm/min during hypothermia, increased again during rewarming, and after CPB was at the levels measured before bypass in both groups. There was no difference between the groups in regard to glucose and lactate metabolism.
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PMID:Cerebral blood flow and metabolism during cardiopulmonary bypass with special reference to effects of hypotension induced by prostacyclin. 308 93

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

Puppies 6-12 kg underwent cardiopulmonary bypass with profound hypothermia. Thirteen animals received 200 ng kg-1 min-1 of PGI2 during bypass whilst 11 control animals received equivalent volumes of glycine buffer (placebo) over a similar period. Results indicated preservation of platelets, leukocytes and fibrinogen levels, together with shortened activated partial thromboplastin times and fewer fibrinogen degradation products post-bypass in PGI2-treated animals. There was an initial fall in blood pressure and systemic vascular resistance in PGI2 treated animals, but pulmonary pressures and resistances, cardiac outputs, and heart rates showed no significant differences from controls. Higher and more satisfactory end of bypass and post-bypass blood pressure levels, together with a lesser fall-off in mean total pulmonary compliance, and shortened bypass times were achieved in treated animals. PGI2 appeared to afford some protection against lung damage as observed by histological studies. All beneficial effects appeared to be significantly greater amongst smaller animals. The results indicate possible benefits from the use of PGI2 in infant open heart surgery.
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PMID:The effects of prostacyclin (PGI2) on haematological and haemodynamic parameters, and lung histology in puppies undergoing cardiopulmonary bypass surgery with profound hypothermia. 388 67

To determine whether prostacyclin (PGI2) plays a beneficial role in the blood-perfused heart undergoing global ischemia, 20 isolated canine hearts were studied after sustaining one hour of cardioplegic arrest under moderate hypothermia (27 degrees to 28 degrees C). Left ventricular function (peak systolic pressure, rate of rise of left ventricular pressure [dP/dt], and compliance change in left ventricular volume), myocardial edema, coronary blood flow, and oxygen content were measured during the preischemic period and at 15 and 30 minutes during reperfusion. Results showed an improved hemodynamic recovery (peak systolic pressure, p = 0.018 at 30 minutes; dP/dt, p = 0.020 at 15 minutes) in the group of hearts treated with PGI2 infusion compared with controls. There was no difference in ventricular compliance or myocardial edema between the two groups. This benefit was attributed to a significant increase in myocardial blood flow (p = 0.028 at 15 minutes) and oxygen delivery (p = 0.021 at 15 minutes) during the reperfusion period with PGI2. These data suggest a potential clinical role for PGI2 when applied to the globally ischemic heart in the improvement of myocardial resuscitation during the early reperfusion period.
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PMID:Does prostacyclin (PGI2) cardioplegic infusion improve myocardial protection after ischemic arrest? 390 45

Somatosensory evoked potentials and cerebral metabolism were studied during cardiopulmonary bypass in 41 patients undergoing coronary bypass. Twenty-two patients received prostacyclin 50 ng/kg/min during cardiopulmonary bypass for platelet protection and 19 patients served as controls. Mean arterial blood pressure in the prostacyclin group was below 30 mm Hg during the first 30 minutes of bypass, but it remained above 50 mm Hg in the control group. Central conduction time, a measure of the electrical conduction time in the central nervous system, was prolonged in both groups during bypass up to 30 minutes of rewarming. The prolongation was greater in the control group early during bypass. At 20 minutes of cardiopulmonary bypass, central conduction time was increased by 81% (standard deviation 38) of the prebypass value in the control group and by 44% (standard deviation 17) in the prostacyclin group (p less than 0.001). Arteriovenous oxygen difference across the brain was greater in the prostacyclin group early during bypass. It was 36 ml/L (standard deviation 9) in the control group and 60 ml/L (standard deviation 18) in the prostacyclin group (p less than 0.001) at 10 minutes of bypass. There was no difference between the groups in regard to glucose and lactate. We conclude that cardiopulmonary bypass with hypothermia prolongs central conduction time. The hypotension induced by prostacyclin (50 ng/kg/min) did not further impair conduction in the central nervous system.
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PMID:Somatosensory evoked potentials and cerebral metabolism during cardiopulmonary bypass with special reference to hypotension induced by prostacyclin infusion. 392 43

Experimental studies to this point have not identified a selective neonatal pulmonary vasodilator. They have indicated that the neonatal pulmonary circulation is a complex, active vascular bed that has a number of endogenous vasodilatory mechanisms which oppose vasoconstriction under normal circumstances. It seems likely that a better understanding of how those mechanisms become deranged in various disease states will be required before we can substantially improve our drug therapy in pulmonary hypertensive infants. The data we have outlined above indicate that firm recommendations for drugs and their doses cannot be made. Nonetheless, several principles of therapy can be outlined. Because of the marginal benefits, which have resulted from current drug therapy [9, 24, 34, 79, 84, 100, 107], it seems clear that, at the moment, the most prudent initial course in neonates with pulmonary vasospasm should be nonpharmacologic: restoration of normal blood gases, use of high concentrations of inspired oxygen with hyperventilation to pH 7.6 if cyanosis persists [22, 79], avoidance of agitation and hypothermia [22], and correction of any metabolic derangements [92]. Decreased cardiac output should be identified and treated with blood volume expanders and/or cardiotonic agents as necessary. Finally, if physiologic efforts to lower pulmonary vascular resistance fail, drug therapy sometimes is helpful in effecting salvage. Treated infants should be carefully monitored, not only for signs of improved oxygenation, but also for changes in right-to-left ductal shunting and cardiac output. If a given agent does not produce beneficial effects at a range of doses by 60 min, it is unlikely that prolonged therapy will result in late improvement. In such circumstances, a change in drug therapy is probably indicated. Finally, it would seem wise to use multiple agents with extreme cautions, being careful to pair a direct vasodilator (e.g., nitroprusside, tolazoline, or prostacyclin) with a cardiotonic agent (e.g., isoproterenol or dopamine), or simultaneously administered volume expanders as the individual clinical situation dictates. Further animal experimentation will undoubtedly identify new and promising agents and provide an increasing understanding of the cellular physiology of the newborn pulmonary circulation. However, only careful clinical and experimental studies into the cause(s) of the vasoconstriction in newborns will allow the development of a truly rational approach to specific therapy in the human species.
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PMID:Neonatal 'pulmonary vasodilator' drugs. Current status. 642 57

The cause of endothelial injury during vein harvesting and preservation is complex. Hypothermia is thought necessary to preserve cell viability but has been implicated in morphologic injury to the endothelium. This study explored the effect of temperature on preserving endothelial function using prostacyclin production as a metabolic marker. Canine veins were atraumatically excised and matched segments were stored at three temperatures using either nutrient medium or heparinized saline. After storage, endogenous production of prostacyclin by the luminal surface of each vein was collected in a closed perfusion system at 37 degrees C and assayed by radioimmunoassay. Optimal prostacyclin production was observed in veins stored in tissue culture medium at normothermia. Preservation of normal endothelial function may require revision of traditional vein graft-harvesting techniques.
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PMID:Functional injury of vein graft endothelium. Role of hypothermia and distention. 654 26

Factors influencing survival of neurons during ischemia and neuronal revival after ischemia are reviewed. During ischemia, biochemical and electro-physiological changes depend on residual blood flow rate: below 30 to 40 ml/100 g/min EEG amplitude decreases, below 18 ml/100 g/min spontaneous neuronal activity ceases, and below 10 ml/100 g/min cell membranes depolarize. Attempts to improve blood flow after middle cerebral artery occlusion with vasoactive drugs were not successful but there was an indication that the calcium antagonist nimodipine reduced ischemia-induced disturbances of ion homeostasis. Revival after ischemia depends mainly on post-ischemic hemodynamic factors, such as the no-reflow phenomenon or delayed post-ischemic hypoperfusion. No-reflow was successfully treated by induced hypertension, anticoagulation, and osmotherapy. Delayed post-ischemic hypoperfusion and the associated metabolic disturbances could not be ameliorated by either vasoactive drugs including prostacyclin, nor by metabolic inhibition with barbiturates and hypothermia. The disturbance of metabolic regulation of blood flow during post-ischemic hypoperfusion, therefore, remains one of the main problems of post-ischemic resuscitation.
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PMID:Neuronal survival and revival during and after cerebral ischemia. 668 Jun 20


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