Acute Portal Hypertension after Gastric Administration of Ethanol in the Pig

Elmér, Olle; Bengmark, S; Göransson, Göran; Sundqvist, Kaj; Söderström, Nils

doi:10.1159/000128302

Cited by 13 publications

(10 citation statements)

References 10 publications

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“…Mendeloff (10) reported an increase in splanchnic blood flow during intravenous administration of ethanol in healthy men, where Castenfors, Hultman and Josephson (11) reported no change. Elmer et al (12) failed to show a significant or sustained increase in hepatic blood flow in pigs given intragastric ethanol boluses. These discrepancies may be related in part to the dose of ethanol given.…”

Section: Resultsmentioning

confidence: 95%

The Effects of Ethanol Administration on Portal Pressure and Gastroesophageal Collateral Blood Flow in Patients With Alcoholic Cirrhosis

Ready¹,

Hossack

1990

Hepatology

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The pathogenesis of variceal hemorrhage is not well understood. Portal pressure and gastroesophageal collateral (azygous) blood flow are similar in patients with cirrhosis with or without a history of variceal bleeding. However, acute increases in these parameters in individual patients might predispose them to variceal rupture. Fifteen patients with alcoholic cirrhosis and portal hypertension were evaluated to test the hypothesis that ethanol intake acutely increases portal pressure or gastroesophageal blood flow and is a possible risk factor in variceal hemorrhage. A 10% solution of ethanol in 5% dextrose in water was infused intravenously at a rate sufficient to raise the blood-alcohol level to 100 mg/dl over 30 min. Eight patients received ethanol 5% dextrose in water; seven patients received a placebo (5% dextrose in water alone). Ethanol did not produce a significant change in wedged hepatic-vein pressure, free hepatic-vein pressure, azygous blood flow, mean arterial pressure or heart rate compared with the effects of 5% dextrose in water alone. Acute administration of ethanol does not increase portal pressure or gastroesophageal blood flow. It is unlikely that acute ethanol ingestion is a risk factor for variceal hemorrhage.

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Section: Resultsmentioning

confidence: 95%

The Effects of Ethanol Administration on Portal Pressure and Gastroesophageal Collateral Blood Flow in Patients With Alcoholic Cirrhosis

Ready¹,

Hossack

1990

Hepatology

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“…Acute ethanol effects on the liver caused alterations in liver morphology such as hepatocyte swelling and a decrease in sinusoidal fenestrae as seen by electron microscopy in pigs and rats [84,85] . Also, the hepatic microcirculation was acutely impaired.…”

Section: Acute Effects Of Ethanol On the Livermentioning

confidence: 97%

“…Also, the hepatic microcirculation was acutely impaired. Narrowed vessels and partially occluded sinusoids due to erythrocyte stasis led to decreased liver blood fl ow, thus disturbing the transport of plasma substances from the sinusoids to hepatocytes and impairing hepatic metabolic capacity [84][85][86][87] .…”

Section: Acute Effects Of Ethanol On the Livermentioning

confidence: 99%

Animal Models and Their Results in Gastrointestinal Alcohol Research

Siegmund

Haas

Singer

2005

Dig Dis

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Alcohol-induced diseases of the gastrointestinal tract play an important role in clinical gastroenterology. However, the precise pathophysiological mechanisms are still largely unknown. Alcohol research depends essentially on animal models due to the fact that controlled experimental studies of ethanol-induced diseases in humans are unethical. Animal models have already been successfully applied to disclose and analyze molecular mechanisms in alcohol-induced diseases, partially by using knockout technology. Because of a lack of transferability of some animal models to the human condition, results have to be interpreted cautiously. For some alcohol-related diseases like chronic alcoholic pancreatitis, the ideal animal model does not yet exist. Here we provide an overview of the most commonly used animal models in gastrointestinal alcohol research. We will also briefly discuss the findings based on animal models as well as the current concepts of pathophysiological mechanisms involved in acute and chronic alcoholic damage of the esophagus, stomach, small and large intestine, pancreas and liver.

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“…This was not confirmed by macroscopic observation or Hct values. Reports that alcohol increases hepatic vascular resistance, as demonstrated in pigs and dogs [8,12] causes reduced ve nous return of splanchnic blood, thereby ag gravating the traumatic shock. Alcohol also has a general negative inotropic effect on the heart [27] which may reduce the ability to restore circulation after trauma in intoxi cated animals.…”

Section: -I a K -Ibmentioning

confidence: 99%

“…Platelet func tion is also affected by soft tissue trauma, making the platelets more aggregable [20] and more susceptible to being filtered out in the pulmonary capillary bed, resulting in pul monary microvascular obstruction [24]. Platelet microaggregates are also formed after alcohol ingestion in pigs [12]. As pulmonary trapping of microaggregates seems to be one etiologic factor in the development of posttraumatic pulmonary insufficiency [5], alco hol-induced microaggregates might, when trapped in the lung, increase the susceptibil ity for development of this syndrome.…”

Section: Introductionmentioning

confidence: 99%

Acute Alcohol Intoxication and Traumatic Shock

Elmér¹,

Gustafsson²,

Göransson³

et al. 1983

Eur Surg Res

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The reaction to a standardized soft tissue trauma was investigated in pigs pre-treated with gastric administration of saline or 40% ethanol. Circulating microaggregates in vena cava, vena portae and aorta were determined with screen filtration pressure (SFP). Using Swan-Ganz thermistor catheters changes in central hemodynamics were recorded. 1 min after trauma, pulmonary capillary wedge pressure (PCW) increased over pretrauma values in alcohol-intoxicated pigs while cardiac output (CO) and mean arterial pressure (MAP) decreased. In control animals, CO and MAP were reduced. 30 min after trauma the control animals had restored their circulatory parameters while intoxicated animals had not. SFP increased in alcohol-intoxicated animals before trauma and more so after trauma except for in aorta. The standardized trauma was nonlethal to control animals while 6 out of 7 pigs, pretreated with alcohol, died within 65 min of the trauma. The data indicate that alcohol intoxication decreases survival after traumatic shock and that alcohol and trauma induced a significant increase in circulating microaggregates.

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Acute Portal Hypertension after Gastric Administration of Ethanol in the Pig

Cited by 13 publications

References 10 publications

The Effects of Ethanol Administration on Portal Pressure and Gastroesophageal Collateral Blood Flow in Patients With Alcoholic Cirrhosis

The Effects of Ethanol Administration on Portal Pressure and Gastroesophageal Collateral Blood Flow in Patients With Alcoholic Cirrhosis

Animal Models and Their Results in Gastrointestinal Alcohol Research

Acute Alcohol Intoxication and Traumatic Shock

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