Effect of Alcohol Intoxication on the Respiratory Exchange and Mortality Rate Associated with Acute Hemorrhage in Anesthetized Dogs

Gettler, Dean T.; Allbritten, Frank F.

doi:10.1097/00000658-196308000-00001

Cited by 35 publications

(7 citation statements)

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“…Previous studies conducted in HS models without TBI indicate that EtOH intoxication may lead to exaggerated early hypotension, impaired myocardial contractility, and an impaired ventilatory response to the metabolic acidosis induced by hemorrhage. 2,20,26,52,70,74 In our study, the fact that cardiac output was reduced in the TBI/HS/EtOH group, but postinjury SVR was not, supports the idea that hemodynamic changes were caused by reduced myocardial contractility and not EtOH-induced peripheral vasodilation.…”

Section: Possible Mechanisms For Etoh Potentiation Of Secondary Brainsupporting

confidence: 69%

Acute ethanol intoxication in a model of traumatic brain injury with hemorrhagic shock: effects on early physiological response

Zink¹,

Sheinberg²,

Wang³

et al. 1998

Journal of Neurosurgery

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Section: Possible Mechanisms For Etoh Potentiation Of Secondary Brainsupporting

confidence: 69%

Acute ethanol intoxication in a model of traumatic brain injury with hemorrhagic shock: effects on early physiological response

Zink¹,

Sheinberg²,

Wang³

et al. 1998

Journal of Neurosurgery

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“…Consequently we could not determine if the potentiating process occurs equally across all body regions, nor could we ascertain if differences are attributable to a greater number of injuries among alcϩ patients as opposed to greater severity of similar injuries. Animal studies have shown a potentiation of alcohol on the physiologic effects of injury (Desiderio, 1988;Flamm et al, 1977;Garrison et al, 1984;Gettler and Allbritten, 1963;Liedtke and DeMuth, 1975;Moss et al,1959;Webb et al, 1966;Zink et al, 1988a,b;Zink et al, 1998a,b;Zink et al, 1999). However, using WRTS as a parameter of physiologic injury severity, we found no statistically significant potentiating effect.…”

Section: Discussioncontrasting

confidence: 48%

Alcohol Effects on Motor Vehicle Crash Injury

Waller

Hill

Maio

et al. 2003

Alcoholism Clin & Exp Res

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“…Ethanol also causes myocardial depression, exaggerated hypotension and increased mortality in various animal models of haemorrhagic shock (Gettler & Allbritten 1963;Reves & Newman 1972;Zink et al 1988;Horton 1992). Hypoxia due to decreased oxygen delivery via blood perfusion may have been the cause of the increase in ethanol toxicity in these studies.…”

Section: Discussionmentioning

confidence: 89%

Influence of Hypoxia and Hyperoxia on the Cardiovascular and Lethal Effects of Ethanol

Strubelt¹,

Younes²

1999

Pharmacology & Toxicology

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Abstract:The mutual potentiation of the hepatotoxic effects of ethanol and hypoxia raised the question of whether such an interaction also occurs in the cardiovascular system. Therefore, anaesthetized rats were infused intravenously with ethanol (25 mgikgxmin.) over 90 min. to reach blood ethanol concentrations between 2.2 and 2.6 g/l and were ventilated artificially either with room air, 10% 0,190'%1 N2 or 100'%, 02. Under normoxic conditions, ethanol produced a slow decrease of mean arterial blood pressure from 130 to 100 mmHg due to the decline in cardiac output and stroke volume (-20%) while heart rate and peripheral resistance remained unchanged. Hypoxia (arterial oxygen tension 35-38 mmHg) without ethanol produced immediate hypotension (-60 mmHg) without decreasing the cardiac output, i.e. by reducing peripheral resistance. In combination with ethanol, hypoxia produced an even stronger hypotension (-90 mmHg) due to reduction in both cardiac output and peripheral resistance. On the other hand, respiration with loo'%) O2 (arterial oxygen tension about 500 mmHg) elevated peripheral resistance, attenuated ethanol-induced cardiodepression and prevented ethanol-induced hypotension. The lethal doses of ethanol evaluated by infusing 75 mgikgxmin. ethanol until death amounted to 4.1 gikg with lo'% 02, to 5.5 gikg with 20% O2 (room air) and to 6.9 gikg with loo'%, 02. Thus decrease in vascular contractility induced by hypoxia combined with ethanol-induced cardiodepression may result in lethal cardiovascular failure. Hyperoxia, on the other hand, counteracts ethanol-induced cardiodepression and its acute toxicity by raising the vascular contractility.Mutual potentiation of the hepatotoxic effects of ethanol and hypoxia were observed in rats in vivo (French er 01.1984), in isolated perfused rat liver (Younes & Strubelt 1987;Younes et al. 1989) and in hepatocytes (Khan & O'Brien 1995). These results raised the question of whether such an interaction also occurs in other organs. Particularly in the cardiovascular system, the depressive effects of ethanol and hypoxia (see Discussion) might combine and enhance the cardiovascular toxicity of both ethanol and hypoxia and to our knowledge, this question has not been evaluated experimentally before. Following our findings with hypoxia we decided to investigate the influence of hyperoxia on the cardiovascular effects of ethanol. Materials and MethodsAniniuls. Male Wistar rats weighing between 340 and 370 g (conventional animals from Winkelmann, Borchen, Germany) were used in this study. The animals were housed at 23" and fed with Altromin@ pellets ud libitum until use.Experiniental design. The rats were anaesthetized by intraperitoneal injection of 60 mgikg pentobarbital and placed on an operating table. Body temperature was kept at 36.5k0.5" by using a rectal thermocouple, a YSI telethermometer model 73 (Yellow Springs Instrument Co., Yellow Springs, O H , USA), and a heated operating table. Artificial ventilation was performed via a tracheal cannula using a StarAuthor for c...

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Effect of Alcohol Intoxication on the Respiratory Exchange and Mortality Rate Associated with Acute Hemorrhage in Anesthetized Dogs

Cited by 35 publications

References 1 publication

Acute ethanol intoxication in a model of traumatic brain injury with hemorrhagic shock: effects on early physiological response

Acute ethanol intoxication in a model of traumatic brain injury with hemorrhagic shock: effects on early physiological response

Alcohol Effects on Motor Vehicle Crash Injury

Influence of Hypoxia and Hyperoxia on the Cardiovascular and Lethal Effects of Ethanol

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