Alcohol ingestion before burn injury decreases splanchnic blood flow and oxygen delivery

Abstract

. Alcohol ingestion before burn injury decreases splanchnic blood flow and oxygen delivery. Am J Physiol Heart Circ Physiol 288: H716 -H721, 2005. First published September 23, 2004; doi:10.1152/ajpheart.00797.2004.-Recent studies from our laboratory have shown that alcohol and burn injury impair intestinal barrier and immune functions. Although multiple factors can contribute to impaired intestinal barrier function, such an alteration could result from a decrease in intestinal blood flow (BF) and oxygen delivery (DO2). Therefore, in this study, we tested the hypothesis that alcohol ingestion before burn injury reduces splanchnic blood flow and oxygen delivery. Rats (250 g) were gavaged with alcohol to achieve a blood ethanol level in the range of 100 mg/dl before burn or sham injury (25% total body surface area). Day 1 after injury, animals were anesthetized with methoxyflurane. Blood pressure, cardiac output (CO), ϮdP/dt, organ BF (in ml ⅐ min Ϫ1 ⅐ 100 g Ϫ1 ), and DO2 (in mg ⅐ ml Ϫ1 ⅐ 100 g Ϫ1 ) were determined. CO and organ BF were determined using a radioactive microsphere technique. Our results indicate that blood pressure, CO, and ϩdP/dt were decreased in rats receiving a combined insult of alcohol and burn injury compared with rats receiving either burn injury or alcohol alone. This is accompanied by a decrease in BF and DO 2 to the liver and intestine. No significant change in BF to the coronary arteries (heart), brain, lung, skin, and muscles was observed after alcohol and burn injury. In conclusion, the results presented here suggest that alcohol ingestion before burn injury reduces splanchnic BF and DO 2. Such decreases in BF and DO2 may cause hypoxic insult to the intestine and liver. Although a hypoxic insult to the liver would result in a release of proinflammatory mediators, a similar insult to the intestine will likely perturb both intestinal immune cell and barrier functions, as observed in our previous study. hemodynamic; liver; intestine; shock; trauma; ethanol; cardiovascular response; thermal injury NEARLY 50% of burn and a similar percentage of trauma patients are found positive for alcohol at the time of hospital admission (6,21,25). Previous studies have suggested that the severity of injury is increased in patients who have consumed alcohol before injury compared with those who have not (for reviews, see Refs. 6,21,and 25). These studies have shown that intoxicated patients require frequent intubations, experience delayed wound healing, and unnecessary longer hospital stays (6,7,11,18,21,(23)(24)(25). As a consequence, enormous resources are consumed to treat trauma patients who are positive for blood alcohol compared with those who sustained injuries in the absence of alcohol. Furthermore, intoxicated patients are more susceptible to infection and are more likely to die than injured patients who are not intoxicated at the time of injury (6,18,21,(23)(24)(25). In contrast, some studies suggest that alcohol does not influence the severity of injury (7, 11), whereas others have suggested t...

Upregulation of cardiac NOS due to endotoxemia and vagal overactivity contributes to the hypotensive effect of chronic ethanol in female rats

“…This notion is supported by lack of changes in vascular NOS in ethanol fed rats (data not shown). On the other hand, reported studies including ours have established a role for reduced cardiac output, stroke volume, and myocardial contractility in the acute hypotensive effect of ethanol in female rats (El-Mas and Abdel-Rahman, 1999a, b; Choudhry et al, 2005); these findings conform with the reported depressant effect of ethanol on cardiac function (Kelbaek, 1990). Therefore, we tested the hypothesis that alterations in cardiac dynamics (myocardial contractility and autonomic activity) might underlie the hypotensive action of chronic ethanol in female rats.…”

Role of Myocardial Contractility and Autonomic Control in the Hypotensive Response to a Limited Access Ethanol Paradigm in SHRs

“…Based on this temporal relationship between BP and 1dP/dt max , it is conceivable to assume that the reduced myocardial contractility might be responsible, at least in part, for the hypotensive action of 5% ethanol. The present demonstration of reduced myocardial contractility in ethanol-fed SHRs is consistent with the reported depressant effect of ethanol on cardiac function (Child et al, 1979;Kelbaek et al, 1985), and the established role of reduced cardiac output and stroke volume associated with ethanol-evoked hypotension in other rat models (Choudhry et al, 2005;Abdel-Rahman, 1999a, 1999b). In contrast, modulation of myocardial contractility does not appear to contribute to the hypotensive effect of 2.5% ethanol as 1dP/dt max remained unaltered in these rats.…”

“…The radiotelemetry technique adopted in the present study allowed the computation of the maximum rate of pressure rise across the BP waveform (1dP/dt max ), which serves as an index of myocardial contractility (Mehta et al, 1998;van den Buuse, 2003). Reported findings concerning the effect of ethanol on myocardial contractility are quite variable and depend on the animal species, concentration, duration, and route of ethanol administration (Choudhry et al, 2005;Kettunen et al, 1992;Mehta et al, 1998). Our results showed that 1dP/dt max was significantly reduced by the 5% concentration of ethanol.…”

Exacerbation of myocardial dysfunction and autonomic imbalance contributes to the estrogen-dependent chronic hypotensive effect of ethanol in female rats

“…In this latter study, spectral analyses presented evidence that ethanol caused remarkable shifts in the cardiac sympathovagal balance towards parasympathetic dominance, which resulted in weakening of the cardiac contractile force and lowered BP (El-Mas et al, 2011). These observations complement those of acute studies (El-Mas and Abdel-Rahman, 1999a; Choudhry et al, 2005), which highlighted a key role for reduced cardiac output in the ethanol-evoked hypotension (El-Mas and Abdel-Rahman, 1999a, 1999b). …”