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

In 31 dogs chronically beta blocked with oral propranolol (12 to 14 mg/kg/day), glucagon (20 micrograms/kg) and combined dopamine (10 micrograms/kg/min) and isoproterenol (0.2 micrograms/kg/min) were given intravenously and tested for hemodynamic efficacy. Dogs were divided into four groups. Basal hemodynamics were obtained In Group I (n = 8) without cardiopulmonary bypass. In Group II (n = 8), hemodynamics were studied after 15 minutes of global ischemia during cardiopulmonary bypass. In Group III (n = 8), hemodynamics were studied after regional ischemia produced by ligation of the proximal left anterior descending coronary artery. In Group IV (n = 7), myocardial oxygen consumption and left ventricular mechanics were studied before and after 1 hour of cardiopulmonary bypass. Our results indicate the following: (1) Dopamine-isoproterenol improves hemodynamics in basal, post-global ischemic, and post-regional ischemic states. Glucagon improves hemodynamics either insignificantly or to a lesser extent than dopamine-isoproterenol. Furthermore, glucagon produces a larger increase in heart rate, which is not desirable. (2) Both dopamine-isoproterenol and glucagon increase myocardial oxygen consumption in comparison with control.
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PMID:Pharmacologic antagonism of propranolol in dogs. III. Effects of dopamine-isoproterenol and glucagon on hemodynamics and myocardial oxygen consumption in ischemic hearts during chronic propranolol administration. 671 51

Dopamine, ethanol, and mannitol were investigated to determine if they could increase pulmonary blood flow and oxygen delivery without significantly increasing intrapulmonary shunt. These drugs were studied in adult patients with respiratory distress following trauma, operation, or sepsis. Intravascular pressure, cardiac output, oxygen consumption and delivery, and limb blood flow and peripheral oxygen delivery were measured in all patients. Hypotensive patients received dopamine in incremental doses of 2 mu g/kg/min until either mean arterial pressure increased 15 mm Hg or heart rate increased by more than 15 beats/min. Ethanol was given as 10% ethanol in 5% dextrose at 2 ml/kg/hr. Mannitol was given as 25 gm of a 25% solution in a single bolus followed by infusion of 8 to 25 gm of 20% solution (mean 10 +/- 2 gm) as a continuous intravenous drip over 1 hour. No drug produced a significant change in intrapulmonary shunt. Ethanol produced significant (p less than 0.05) increases in cardiac index, heart rate, oxygen consumption, and oxygen delivery. Dopamine significantly decreased pulmonary vascular resistance while increasing systemic blood pressure. Visceral blood flow apparently increased while the peripheral vascular response to ischemia remained intact. Mannitol increased oxygen delivery and consumption in both the total body and limb. Thus in patients with adult respiratory distress syndrome (ARDS), increases in pulmonary blood flow can be achieved with several distinct pharmacologic agents without significant increases in intrapulmonary shunt. These increases in flow are generally accompanied by increases in oxygen delivery without increased pulmonary vascular resistance.
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PMID:Effects of dopamine, ethanol, and mannitol on cardiopulmonary function in patients with adult respiratory distress syndrome. 678 9

Dopamine and norepinephrine fluorescence in the nucleus caudatus and putamen and cerebral cortex was markedly depleted along with rCBF reduction in symptomatic stroke-prone spontaneously hypertensive rats (SHRSP) with bilateral carotid artery ligation under light pentobarbital anesthesia. An accumulation of fluorescence at the intima of blood vessels, especially in the nucleus caudatus and putamen, was noted in some SHRSP under the same experimental conditions. These changes were hardly seen in deeply anesthetized SHRSP, as well as in normotensive Wistar-Kyoto (WK) rats. It may be possible, therefore, that released cerebral amines in acute brain ischemia accelerate the vasoconstriction and permeability of cerebral arteries, which further decreases the blood supply to these areas. Also, a barbiturate protective effect against the release of central dopamine and norepinephrine during acute brain ischemia was noted in deeply anesthetized SHRSP.
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PMID:Role of central aminergic fibers in experimental cerebral ischemia in stroke-prone SHR. Relation to anesthetic effect. 741 67

The effect of L-arginine, the precursor of nitric oxide, on ischemic dopamine release from the striatum was investigated in Mongolian gerbils subjected to bilateral carotid artery occlusion (15 min) alone or with reflow (2 h). Dopamine and its metabolites were measured in the striatal extracellular space dialysate after continuous perfusion (2 microliters/min) of artificial extracellular fluid in the presence or absence of 15 mmol/liter L- or D-arginine or 1 mmol/liter nitro-L-arginine. L-Arginine but not D-arginine increased the striatal content of dopamine in pre- and postischemia whereas it lowered the levels of dopamine and 3-methoxytyramine induced by ischemia. In contrast, nitro-L-arginine reduced the preischemic levels of dopamine and 3,4-dihydroxyphenyl-acetic acid, and had no effect on the ischemic release of dopamine. These findings indicate that L-arginine stereospecifically modified the ischemic release and metabolism of dopamine. The data also suggest that the basal level of nitric oxide is not involved in dopamine release during ischemia but may participate in regulating dopamine release under physiological conditions.
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PMID:Modulation of striatal dopamine release in cerebral ischemia by L-arginine. 765 86

Dopamine (DA) is released in large quantities from the striatum during cerebral ischemia. Along with excitatory neurotransmitters, DA plays a role in cellular neuronal ischemic injury. In this study we examined the role of nitric oxide (NO) in the ischemia-induced release of DA. A microdialysis probe was stereotactically placed into the corpus striatum of 16 Sprague-Dawley rats for DA, 3,4-dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA) level determinations. After probe stabilization, the animals received either NG-nitro-L-arginine-methyl ester (L-NAME), a NO synthase inhibitor, or vehicle through the microdialysis probe. Temporary global forebrain ischemia was induced using bilateral carotid artery ligature tightening and controlled hemorrhagic hypotension for 15 min. L-NAME administration caused a reduction in ischemic estimated extraneuronal DA concentration by 60% (P < 0.005) compared with control. There was an increase in both DOPAC and HVA concentrations during the recovery period compared to baseline values in the control group (P < 0.05). L-NAME also caused a reduction in HVA concentration compared to vehicle administration during the latter part of recovery (P < 0.05). These data support the concept that ischemic dopamine release may be mediated by NO. This NO-modulated DA release may contribute to the previously reported deleterious neurotoxic effects of NO during ischemia.
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PMID:Nitric oxide modulates dopamine release during global temporary cerebral ischemia. 776 37

Neurotransmitter release during cerebral ischemia has been extensively studied and is thought to play a key role in excitotoxic neuronal death. The changes in neurotransmitter release and its metabolism may reflect changes in cellular metabolism during ischemia. The purpose of this study is to assess alterations in extracellular dopamine and serotonin and their metabolites under varied degrees of ischemia in rat striatum to elucidate the pathophysiology of cerebral ischemia. Twenty rats were used to induce varied forebrain ischemia by means of bilateral common carotid artery occlusion along with hemorrhagic hypotension. Cerebral blood flow (CBF) in the striatum was measured every 40 minutes by methods of hydrogen clearance and maintained within certain ranges for 6 hours. Dopamine, serotonin, and their metabolites were measured every 20 minutes by in vivo microdialysis. Varying degrees of ischemia were obtained, ranging from 9.4 to 81.3% of control CBF. The animals were divided into three groups according to CBF levels measured 20 minutes after the induction of ischemia. In the mild ischemia group (n = 5), CBF ranged from 65 to 88% of baseline levels and resulted in only a slight increase of dopamine. In the moderate ischemia group (n = 10), CBF ranged from 21 to 48% of baseline levels and resulted in transient increases of dopamine (24-fold) and serotonin (5-fold). In the severe ischemia group (n = 5), CBF was below 14% of baseline levels and resulted in marked increases in dopamine (462-fold) and serotonin (225-fold). These alterations remained elevated for 3 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of monoaminergic neurotransmitters in the rat striatum during varied global cerebral ischemia. 796 35

Dopamine (DA) is released in large quantities into the corpus striatum during cerebral ischemia and may exacerbate tissue damage. Using cerebral microdialysis, we studied the effect of etomidate on in vivo ischemia-induced DA release in rat corpus striatum. Reversible cerebral ischemia was induced by using carotid ligatures and hypovolemic hypotension, and monitored with laser Doppler flowmetry. After baseline measurements, 20 normothermic, anesthetized rats were subjected to three separate periods of cerebral ischemia, interrupted by 45- to 75-min periods of reperfusion. The rats were randomized into two groups. All rats received 400 mg/kg of intraperitoneal chloral hydrate for induction of anesthesia. In Group I (n = 10) anesthesia was maintained using additional intraperitoneal chloral hydrate 100 mg/kg every 2 h. Group II received etomidate 0.6 mg/kg 10 min before the first episode of cerebral ischemia, followed by an infusion of 60 micrograms.kg-1 x min-1. Before each subsequent period of induced ischemia, an additional dose of etomidate (0.6 mg/kg) was administered. DA levels were approximately 350 times above baseline in Group I during the three ischemic episodes (IS1, IS2, and IS3). In Group II, ischemia-induced DA release was significantly attenuated (by 79%) during IS1, IS2, and IS3 compared to Group I (P < 0.01). DA levels did not significantly change in magnitude during the three ischemic episodes in either group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of etomidate on in vivo ischemia-induced dopamine release in the corpus striatum of the rat: a study using cerebral microdialysis. 826 84

Dopamine D1 and D2 receptors and uptake sites were studied in the gerbil striatum and frontal cortex 1 h to 7 days after 10 min of cerebral ischemia caused by occlusion of the bilateral common carotid arteries. [3H]SCH23390 ([N-methyl-3H]R[+]-8-chloro-2, 3,4,5-tetrahydro-3-methyl-5-phenyl-7-ol-benzazepine), [3H]nemonapride and [3H]mazindol were used as markers of dopamine D1 receptors, D2 receptors and uptake sites, respectively. A significant reduction in [3H] SCH23390 binding was found in the striatum from 48 h after ischemia. In contrast, during the recirculation periods, [3H]nemonapride and [3H]mazindol binding was mostly unaffected in this region which was the most vulnerable to ischemia. The frontal cortex, where ischemic neuronal damage was mild, also showed no significant changes in [3H]SCH23390, [3H]nemonapride and [3H]mazindol binding after ischemia. Thus, cerebral ischemia that was associated with cell loss in the striatum resulted in a selective reduction of dopamine D1 receptors and not D2 receptors. No changes in dopamine D1 or D2 receptors were observed in frontal cortex. If massive dopamine release occurs with cerebral ischemia, it is not reflected by modification in the number of uptake sites located on dopamine terminals.
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PMID:Effects of cerebral ischemia on dopamine receptors in the gerbil striatum. 881 17

Injury to the brain, whether by ischemia or trauma, results in the uncontrolled release of many neurotransmitters, including glutamate and dopamine. Both of these neurotransmitters are neurotoxic in high concentrations, and the oxidative stress caused by reactive oxygen species generation has been implicated in the mechanism of neurotoxicity. In this study, we used cultured rat forebrain neurons to characterize cell death caused by exposure to dopamine and/or glutamate and to investigate potential acute mechanisms of toxicity. Dopamine exposure (250 microM for 2 h) reduced cell viability to 34. 3 +/- 5.5% of untreated control 20 h later and increased the number of neurons with apoptotic morphology. The antioxidant N-acetylcysteine (100 microM) inhibited dopamine-induced toxicity and prevented the covalent binding of dopamine quinones to protein. In contrast, glutamate toxicity lacked the hallmark characteristics of apoptosis. When neurons were exposed successively to sublethal concentrations of dopamine and glutamate, cell viability at 20 h was reduced to 62.3 +/- 5.2% of untreated control. Apoptosis was not evident, and N-acetylcysteine blocked the potentiating effect of dopamine on glutamate-induced toxicity. We used single-cell fluorescence assays to measure changes in intraneuronal glutathione, intraneuronal Ca2+, mitochondrial membrane potential, and DNA integrity as potential acute inducers of neuronal injury. While changes in these parameters could be demonstrated, none were identified as the sole acute inducer of cell death caused by dopamine. In summary, we have characterized a number of neuronal responses to lethal dopamine injury. Also, we have demonstrated that dopamine and glutamate can interact in vitro to potentiate cell death and that the potentiation appears to be induced by oxidative stress.
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PMID:Mechanisms of dopamine-induced cell death in cultured rat forebrain neurons: interactions with and differences from glutamate-induced cell death. 905 89

Neurons in the dorsal neostriatum are highly vulnerable to transient cerebral ischemia. It has been suggested that excessive dopamine release during ischemia may play an important role in the pathogenesis of postischemic cell death in the neostriatum. However, it remains controversial whether depletion of dopamine protects neurons in the neostriatum against ischemic insult. In the present study, transient forebrain ischemia was induced using the four-vessel occlusion method. Ischemic depolarization was used as an indication of completed ischemia. Under our experimental conditions, ischemia that produces approximately 21 min ischemic depolarization caused more than 90% of cell death in the dorsolateral neostriatum. Using such ischemia as a standard insult, the effect of dopamine depletion on neostriatal neurons after ischemia was investigated. Dopamine depletion was produced by unilateral injection of 6-OHDA into the substantia nigra. No difference was found between the number of surviving neurons in the left and the right neostriatum after depletion of dopamine on the left side. In contrast, surviving neurons dramatically increased in the right neostriatum after depletion of dopamine on the right side. These results clearly demonstrate an asymmetrical protection of neostriatal neurons against ischemia after dopamine depletion. The mechanisms of this asymmetrical protection may clarify dopamine action on neuronal injury following cerebral ischemia.
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PMID:Asymmetrical protection of neostriatal neurons against transient forebrain ischemia by unilateral dopamine depletion. 922 58


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