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

Although acute perfusion of guinea pig hearts with ethanol does not affect cardiac protein synthesis, the latter is inhibited after prolonged ingestion of ethanol when tested in an in vitro system with the working right ventricle. This study reports on the added stress of ischemia on such hearts. Hearts were removed from maturing guinea pigs after 13-16 weeks of ingesting 10% ethanol and were perfused in vitro under conditions of relative ischemia (one-sixth of normal coronary flow) with maintenance of right ventricular load and outflow resistance identical to normal pre-ischemic levels. With this degree of ischemia, there was a 4-6 fold increase in lactate production, an 80% drop in ATP, and a 90% decrease in creatine phosphate after 150 min of the ischemia. Incorporation of both labeled lysine and phenylalanine into cardiac protein was also diminished to 35% of control in the left ventricle and 55% of control in the right. This diminution of protein synthesis was the same in hearts from ethanol-drinking and matched control animals. Thus, prior prolonged ingestion of ethanol did not worsen the inhibition of protein synthesis by oxygen deprivation. There were, however, two significant differences in hemodynamic response to the ischemia by the right ventricles of hearts from ethanol-drinking guinea pigs compared to their matched controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcohol Clin Exp Res
PMID:Prolonged feeding of ethanol to the young growing guinea pig. II. A model to study the effects of severe ischemia on cardiac protein synthesis. 642 90

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

After finding changes in the biochemical response to injury in patients who had consumed ethanol (27) we have examined the effect of acute ethanol intoxication on the outcome of injury using the bilateral hindlimb ischemia model in the rat. Technical difficulties were encountered but it was possible to devise an experiment in which realistic plasma ethanol levels and a lowered redox state were present during the response to a standard 4-hr period of bilateral hind-limb ischemia. Acute intoxication had little effect on the mortality rate or survival time. Extrapolating the findings to man it would seem that if ethanol intoxication increased the dangers associated with trauma its effect would be in increased risks of airway obstruction due to vomit, etc., rather than in altered biochemical responses.
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PMID:Interactions between ethanol and the responses to injury. 686 43

The circulatory responses to ethyl alcohol are quantitatively related to the route and rate of administration as well as to the dose and the time of physiological measurements. A variety of acute regional blood flow responses have been described in the basal state in animals without prior exposure to ethanol. Gastric mucosal blood flow is substantially increased by ethanol. Pancreatic blood flow, on the other hand, has been found to undergo a dose-dependent reduction. Hepatic blood flow has been found to increase in baboons without evidence of ischemia. Renal arteries appear to be unresponsive up to 3 g/kg. Similarly, the cerebral vasculature does not seem to be affected by ethanol except at high dose levels where increased flow occurs. Animal studies, however, have suggested that ethanol may interfere with autoregulation. In terms of limb blood flow, oral administration has been found to enhance flow to the skin but to diminish skeletal muscle blood flow. Vasodilatation of the coronary vasculature has been consistently reported to be significantly greater in animals than in humans. The major metabolite of ethanol, acetaldehyde, has significant effects on circulation. At blood levels achieved after feeding ethanol, there was a 60% rise of coronary blood flow but myocardial oxygen consumption was reduced, presumably representing a shunting effect in myocardium.
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PMID:Regional circulatory responses to alcohol and its congeners. 708 87

We have examined the effect of ethanol on muscle blood flow at rest and during electrically stimulated exercise in five normal dogs using the isolated gracilis muscle preparation. Under pentobarbital anesthesia and mechanical ventilation, ethanol (15% in 0.9% NaCl) infused at 4 mL/min for 2 hr produced an arterial blood concentration of 268 +/- 10 mg/dL (X +/- SEM). Resting muscle blood flow was 6.3 +/- 0.9 mL/min/100 gm in 8 dogs infused with saline alone. During stimulated contraction using supramaximal voltage at a rate of 5 stimuli/sec, respective mean flows for ETOH and saline dogs at 1, 5, 10, and 30 min were 35.5, 19.9, 27.7, 22.2, and 22.0, 20.0, 23.6, and 19.1 mL/min/100 gm. The 1-min flow rate for ethanol infused animals was significantly greater (P < 0.05) than that observed in saline infused animals. The remainder of the values were not significantly different. Potassium release from contracting muscle was normal. These observations do not support the theory that ethanol induces vasoconstriction in the vascular bed of skeletal muscle nor do they support the postulation that muscle cell ischemia plays a role in alcoholic myopathy.
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PMID:Normal resting and exercising muscle blood flow during acute ethanol infusion. 744 54

Intravital microscopy used with fluorescent vital stains provides the opportunity to measure the temporal and spatial extent of tissue injury following disease processes. However, this assumes that prolonged exposure to such dyes does not alter microvascular perfusion or cellular viability. To test this hypothesis, the extensor digitorum longus (EDL) muscle in 24 male Wistar rats, anesthetized with sodium pentobarbital (Somnotal, 65 mg/kg, ip), were prepared for microscopy. The EDL was either bathed continuously (n = 6) in Krebs solution containing bisbenzimide (5 micrograms/ml; labels nuclei of all cells) and ethidium bromide (5 micrograms/ml; labels nuclei of injured cells) or had dyes topically applied 1 hr (n = 4) and 4 hr (n = 4) following dissection of the muscle. Noxious stimuli (i.e., hypoxia:FiO2 of 8-10% (n = 3), 95% ethanol (n = 3), and 2 hr ischemia followed by 90 min reperfusion (n = 4) were used to test the ability of ethidium bromide, when used in conjunction with intravital microscopy, to differentiate injured tissue. Video recordings at the surface of the EDL muscle were made every 30 min for 5 hr from which the number of perfused capillaries was counted (NCper). The numbers of bisbenzimide- and ethidium bromide-labeled nuclei were counted at the surface of the muscle and at two to three additional locations within the muscle (to a maximum depth of approximately 120-160 microns). The average NCper (19.05 +/- 1.7) remained constant over 5 hr, while the number of nuclei stained by bisbenzimide increased linearly with time from an initial value of 1218 +/- 125.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Measurement of tissue viability using intravital microscopy and fluorescent nuclear dyes. 747 97

Cocaine can cause myocardial ischemia or infarction. The incidence of these events, and the influence of specific dosing routes or regimens on their occurrence is not established. In the current study, we obtained frequent 12-lead electrocardiograms (ECGs) and continuous 2 or 3 channel ECGs from 20 subjects participating in a behavioral study of smoked cocaine. Subjects received 10 or 11 doses of cocaine 0.4 mg/kg per dose, or 10 doses of 35 mg per dose at 30 min intervals (range 233-408 mg total dose per session). ECGs were also recorded on control days on which subjects received no cocaine. The mean peak plasma cocaine concentration on cocaine days was 640 +/- 262 ng/ml. There were no changes in digitized ST segment amplitude on 12-lead ECGs obtained during cocaine administration (P = 0.098). Of 17 subjects who had technically satisfactory continuous ECGs, four had significant ST segment depression (> 1 mm below the PR segment); two on cocaine days and two on control days (P > 0.5). One subject had frequent premature beats on both cocaine and control days. One subject had an asymptomatic run of 4 ventricular beats 30 s after cocaine administration that could have been due to cocaine. All episodes of ST depression or premature beats were asymptomatic. No evidence of either symptomatic or subclinical cardiac ischemia related to cocaine administration was found. Thus no clinically important adverse events were found as a result of smoked cocaine administered by this dosing regimen to healthy males with a history of heavy cocaine use. Additional study with larger numbers of subjects will be helpful in further assessing the safety of administering smoked cocaine to research subjects.
Drug Alcohol Depend 1994 Apr
PMID:12-lead and continuous ECG recordings of subjects during inpatient administration of smoked cocaine. 751 76

Blood flow plays an important role in protection of normal gastric mucosa and in the protection and healing of damaged mucosa. Blood flow contributes to protection by supplying the mucosa with oxygen and HCO3-, and by removing H+ and toxic agents diffusing from the lumen into the mucosa. Low mucosal blood flow predisposes to injury, whereas high blood flow protects against injurious agents. Superficial mucosal damage is followed by increased blood flow which supports the healing process and prevents superficial lesions from developing into deep ones. The hypermic response increases the supply of HCO3- to the mucosa and increases the resistance of the injured mucosa against back diffusing H+ and aggressive drugs such as ethanol (adaptive protection). Mucosal ischemia contributes to gastric ulceration in various clinical conditions such as hemorrhagic shock, stress, aorta aneurysm and after proximal gastric vagotomy. Blood vessels are damaged in gastric ulcers. During ulcer healing blood flow returns to normal. Stimulated or inhibited angiogenesis in the granulation tissue effects the healing of a gastric ulcer.
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PMID:The role of blood flow in gastric mucosal defence, damage and healing. 753 77

The aim of the present study was to determine whether calcium channel antagonists attenuated hypoxia/hypoglycemia- or glutamate-induced reduction in 2-deoxyglucose (2-DG) uptake of hippocampal slices obtained from ethanol withdrawal rats. Ethanol withdrawal significantly potentiated the hypoxia/hypoglycemia- and glutamate-induced reductions in 2-DG uptake of hippocampal slices. Both nifedipine and flunarizine exhibited attenuating effects on ethanol withdrawal-induced potentiation of impairment of 2-DG uptake caused by hypoxia/hypoglycemia or glutamate. Hypoxia/hypoglycemia-induced deficit of 2-DG uptake was prevented by ethanol, but chronic consumption of ethanol resulted in the development of tolerance to neuroprotective effect. These findings suggest that the increased sensitivity of neurons to ischemic damage by ischemia may involve in the increased activity of calcium channels in the hippocampus.
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PMID:Calcium channel blockers improve hypoxia/hypoglycemia-induced impairment of rat hippocampal 2-deoxyglucose uptake in vitro after ethanol withdrawal. 760 47

We have previously shown that administration of Escherichia coli to a rat induces cardiac dysfunction, but also prevents the myocardium from being further damaged by total ischemia. We have also previously shown that induction of sepsis in a rat that has consumed alcohol as 36% of its caloric intake for 8-10 weeks, results in a potentiation of the cardiac depression resulting from sepsis. In this study, we determined if administration of Gram-negative bacteria to a chronically alcoholic rat would still protect the heart from ischemia-reperfusion injury. We tested the protective effect of sepsis using an in vitro, isovolumically contracting heart preparation. Global ischemia was maintained for 35 min, followed by 25-min reperfusion. In the present experiments, sepsis produced a 40% decrease in cardiac performance, but was also protective of hearts made ischemic the next day. Hearts from septic and alcoholic septic rats recovered 100% of preischemic ventricular function after 35-min ischemia, whereas hearts from the control and alcohol groups recovered only 80% of preischemic left ventricular performance. Whereas preischemic function was significantly decreased in the septic groups compared with the two nonseptic groups, postischemic function was no longer significantly different in the four groups. Thus, sepsis resulted in development of protection of the hearts from ischemia-reperfusion injury, even in hearts that were severely compromised by the combination of chronic alcoholism and Gram-negative sepsis.
Alcohol Clin Exp Res 1994 Dec
PMID:Sepsis protects the heart of alcoholic rats from ischemia-reperfusion injury. 769 39


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