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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood cardioplegia at 8 degrees C results in cardiac standstill whilst maintaining minimal metabolic functions of the cardiac cell. Reinjection every 20 minutes allows cellular reoxygenation, the delivery of essential elements (Tham, CPD), and the elimination of products of myocardial degradation accumulated during ischemia. Before declamping the aorta, a reperfusion with warm blood (34 degrees C) containing glutamate and GTN enables restocking of the energy reserves (Krebs' cycle) and a lowering of coronary and systemic resistances. This technique used systematically if even more effective when the ischemic time is prolonged as is the case in cardiac transplantation. The 50 transplants performed since January 1989 with this form of myocardial protection were compared with 50 procedures performed in 1988 with crystalloid cardioplegia. There was no significant difference in the duration of ischemia or of cardiopulmonary bypass between the two groups. Patients benefitting from blood cardioplegia defibrillated spontaneously more frequently, required lower doses of Dopamine for shorter periods and were extubated earlier.
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PMID:[Value of the association of blood cardioplegia and energetic warm reperfusion in cardiac transplantation]. 189 13

Dopamine frequently is used to improve cardiac performance after acute myocardial ischemia. Inotropic agents, however, increase myocardial oxygen demand and could potentially delay recovery from ischemic injury. To evaluate this problem, we studied eight chronically instrumented dogs in the conscious state and performed two 15-minute coronary occlusions 48 hours apart. After one of the occlusions, either dopamine (15 micrograms/kg/min) or saline placebo was administered intravenously from 1.0 to 1.5 hours of reperfusion. The alternative infusion was given during the second study. Preload recruitable work area, the area beneath the stroke work versus end-diastolic length relationship, was used to assess intrinsic myocardial performance. Ischemia decreased preload recruitable work area to 13% of control after both occlusions. After reperfusion, a 30-minute dopamine infusion acutely increased myocardial function nearly threefold as compared with placebo. Myocardial performance after dopamine administration, however, was significantly depressed compared with placebo throughout the remaining 24 hours of reperfusion (p less than 0.01). These data indicate that dopamine may impair functional recovery after ischemic myocardial injury and suggest that inotropic interventions should be used in this setting only when absolutely indicated.
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PMID:The effects of dopamine on myocardial functional recovery after reversible ischemic injury. 223 34

Hydroxylase cofactor, monoamine neurotransmitters and their metabolites were measured in ischemic rat brain produced by four-vessel occlusion for 30 and 60 min periods. Slight reduction of hydroxylase cofactor activity was observed in the ischemic cortex after 60 min. Dopamine increased in the brainstem, and its metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid, increased throughout the brain. Decrease in norepinephrine was observed in the whole brain. Decrease in serotonin and increase in 5-hydroxyindoleacetic acid, a metabolite of serotonin, was observed in the ischemic cerebral cortex. The present study has revealed that there appears to be no significant relationship between hydroxylase cofactor activity and monoamine levels in the ischemic brain. Thus, the hydroxylase cofactor does not play a main role in regulating monoamine synthesis in the acute phase of brain ischemia.
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PMID:Effect of ischemia on hydroxylase cofactor (tetrahydrobiopterin) and monoamine neurotransmitters in rat brain. 242 55

The effect of dopexamine hydrochloride on myocardial performance, and on the susceptibility of the myocardium to generation of arrhythmias during the development of myocardial infarction has been compared with dopamine and dobutamine in 2 experimental models of myocardial ischemia. All 3 agents improved cardiac function in the presence of a developing infarct. Dopamine and dobutamine increased myocardial contractility (left ventricular dP/dt and left ventricular dP/dt/P), which would be expected to increase oxygen consumption and thus further compromise the ischemic myocardium. Dopexamine hydrochloride, however, improved cardiac function mainly by reducing afterload. The infusion of dopamine and dobutamine resulted in a high (100%) incidence of ventricular arrhythmias compared with only 63% with dopexamine hydrochloride. The effects of these agents on early ischemic arrhythmias after coronary artery ligation in anesthetized rats were also studied. Dopexamine hydrochloride reduced the incidence and severity of arrhythmias in the early stages of ischemia: At a dose of 0.25 micrograms/kg/min, the total number of ectopic beats was reduced to 375 +/- 175, from 1,250 +/- 330 in control rats (p less than 0.05). Dopexamine hydrochloride also significantly reduced mortality from ventricular fibrillation and there was a slight reduction in the incidence and duration of ventricular tachycardia and fibrillation.
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PMID:Effect of dopexamine hydrochloride in the early stages of experimental myocardial infarction and comparison with dopamine and dobutamine. 245 4

Changes in cerebral monoamine metabolism were investigated in gerbils following a 5-min ischemia. During ischemia, monoamines were not changed, and 3-methoxy tyramine increased remarkably. After re-circulation, noradrenaline and serotonin decreased, and 5-hydroxyindole-3-acetic acid increased. Dopamine was not significantly changed, but its metabolites were elevated. At 1, 3 and 7 days after the ischemia, monoamine metabolism did not change. We discussed the possibility that these monoamine metabolism changes in the early period of reflow might be related to the delayed neuronal damage.
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PMID:Changes in monoamine contents in the brains of Mongolian gerbils following a 5-min occlusion of the bilateral carotid arteries. 247 87

The management of the pulseless, nonbreathing pediatric patient continues to be a frustrating experience because mortality and morbidity are high. Improvement in outcome awaits a better understanding of the pathophysiology of organ ischemia and reperfusion injury. In the interim, early recognition and therapy of respiratory and circulatory failure are the only effective means to affect outcome. The approach to the pediatric cardiac arrest victim differs from the adult, because dysrhythmias rarely are the etiology of pediatric arrest. Instead, attention to securing the airway and provision of adequate ventilation are keys. Epinephrine is the most effective drug in this setting, and may be administered through an endotracheal tube as well as intravenously or intraosseously. The latter route provides a useful means of rapid vascular access in the pediatric victim less than 3 years of age. Sodium bicarbonate use has been discouraged and there are few indications for calcium, greatly simplifying the pharmacologic approach to the pediatric cardiac arrest patient. In those patients in whom a rhythm and pulse are restored, support of the circulation often is required. Dopamine or epinephrine are the catecholamines of choice in this setting. Ventricular arrhythmias are treated with defibrillation or cardioversion as appropriate. Infrequently, lidocaine or bretylium may be needed. Once the patient has been stabilized, further care is best delivered at a tertiary care center with a pediatric intensive care unit.
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PMID:Cardiopulmonary resuscitation in children. 332 42

Ischemic brain injury affects the content and metabolism of brain monomines. Our aim was to know the time course of changes in regional cerebral catecholamines during focal cerebral ischemia, and whether focal cerebral ischemia may affect the metabolism of catecholamines in distant area of the brain. Methods Fifty-five rats were subjected to occlusion of the middle cerebral artery (MCA) on the olfactory tract, under halothane anesthesia. Fourteen animals were sham-operated group. Animals were decapitated at 1/2, 1,2,3,6,12 and 24 hours post-occlusion (PO), respectively. The brains were removed, and the brain structures dissected out include bilateral corpus striatum, cerebral cortex (MCA territory) and cerebellar hemisphere. Catecholamines were extracted by alumina procedure, and determined by high-performance liquid chromatography with electrochemical detection. Results Dopamine (DA) contents, in ipsilateral corpus striatum and cerebral cortex to the ischemia, decreased at 1 hour PO, and reached, at 6 hours PO, to 40% of control value in corpus striatum and 30% in cerebral cortex, respectively. After 6 hours PO, DA remained low. Norepinephrine (NE) content in the ipsilateral corpus striatum gradually reduced and reached to 60% of control value at 24 hours PO. NE in the ipsilateral cerebral cortex decreased to 50% of control at 1 hour PO, and thereafter remained reduced. In the contralateral corpus striatum and cerebral cortex, either DA or NE showed no significant changes, except 1/2 hour PO. NE contents in bilateral cerebral cortex showed a transient increase at 1/2 hour PO. Cerebellar NE content, bilaterally, reduced slowly to 70% of control at 24 hours PO.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in regional cerebral catecholamines following middle cerebral artery occlusion in the rat]. 407 79

Infusion of ATP-MgCl2 following hepatic ischemia significantly improves the survival of animals. To determine the subcellular effects of infused ATP-MgCl2 and whether such effects are mediated through vasodilatation, global hepatic ischemia in rats was produced for 90 min followed by reperfusion. The rats then received iv 0.5 ml of saline, dopamine, papaverine, or ATP-MgCl2. At various intervals following reflow, hepatic mitochondria were isolated. ADP-to-O ratio and respiratory control ratio (RCR) were significantly lower 1 h following reflow, and there was a further decrease in these parameters 3 h after reflow in mitochondria from saline-treated rats. Dopamine and papaverine treatment did not improve RCR, however, ATP-MgCl2 treatment resulted in a progressive and significantly higher ADP/O and RCR following reflow. Hepatic ATP levels in saline, dopamine, and papaverine-treated rats were found to be 50% lower 3 h following reflow, however, treatment with ATP-MgCl2 resulted in significantly higher ATP levels and energy charge. Hepatic blood flow was markedly depressed 1 h following reflow in the saline-treated rats but was significantly higher in the ATP-MgCl2 group. Three hours following reflow, hepatic blood flow decreased further in the saline-treated rats, whereas in the ATP-MgCl2-treated rats there was a progressive increase in flow. Dopamine treatment resulted in an initial restoration in flow, however, this effect was not sustained. Hepatic ultrastructure deteriorated progressively following reflow in the saline-treated rats, however, it was normal in the ATP-MgCl2-treated rats 1 h as well as 20 h following reflow. These results lead us to conclude that infused ATP-MgCl2 improves mitochondrial and cellular functions either directly or by way of long-term improvement in microcirculation but not through vasodilatation.
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PMID:Studies on the mechanism of beneficial effects of ATP-MgCl2 following hepatic ischemia. 660 16

The purpose of this study was to determine whether myocardium salvaged by reperfusion following coronary occlusion could respond to inotropic stimulation by dopamine. Mongrel dogs underwent a 2-hour occlusion of the proximal left anterior descending coronary artery, followed by reperfusion for 5 or 28 hours. Dopamine (5 to 10 micrograms/kg/min) or dextrose was administered 1 hour or 24 hours after the onset of reperfusion. Serial, computer-assisted, two-dimensional echocardiographic determination of percentage of systolic wall thickening (%SWT) and cross-sectional ejection fraction (% delta area) were used to evaluate the response to treatment. Myocardium in the region of central ischemia contracted poorly after 1 hour of reperfusion (mean %SWT = 1.3 +/- 13.3% [mean +/- SD] compared to preocclusion value of 43.6 +/- 18.5%, p less than 0.001) and tended to thin at 24 hours of reperfusion (mean %SWT = -6.0 +/- 12.3%, p less than 0.001). After 1 hour of reperfusion, dopamine produced a greater than fourfold improvement in %SWT within the reperfused zone (to 15.3 +/- 7.3%, p less than 0.05). After 24 hours of reperfusion, dopamine again produced an improvement in %SWT (to 5.8 +/- 12.5%, p less than 0.05). There were no significant changes in %SWT with dextrose infusion. Thus, dopamine stimulates the reperfusion-salvaged but noncontracting (stunned) myocardium to contract as early as 1 hour after reperfusion.
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PMID:Response of reperfusion-salvaged, stunned myocardium to inotropic stimulation. 669 Dec 20

Interaction of sulpiride - both 1- and d- isomers as well as racemic- - with Dopamine (DA, subpressor dosage 0.1 microgram X kg -1 X min -1), on the renal hemodynamic, was studied in DOCA-pretreated men during hypotonic polyuria. P.A.H. and creatinine clearance and renal vascular resistances were determined. In the presence of d-Sulpiride, DA - induced renal vasodilation is carried out gradually and finally reaches similar levels as in the absence of d-Sulpiride. However no glomerular filtration rate increase is produced by DA. In the presence of 1-Sulpiride, DA vasodilating effect is suppressed. On the contrary a trend toward ischemia and a reduction in glomerular filtration rate becomes finally apparent. Stronger binding of 1- than d-Sulpiride with vascular DA receptors in suggested. When both isomers are simultaneously administered (at the nearly total dosage) much less inhibitory effect on DA vasodilator action is observed: it seems that each isomer decreases the affinity on the other isomer for vascular DA receptors.
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PMID:[Sulpiride (stereoisomers, racemic) and dopamine: actions and interactions on renal circulation]. 670 43


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