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  • Title: Inhibition of glucagon improves splanchnic hyporesponse to terlipressin in cirrhotic rats with blood retention in the gastric lumen.
    Author: Yang YY, Lin HC, Huang YT, Hou MC, Lee FY, Chang FY, Lee SD.
    Journal: J Hepatol; 2005 May; 42(5):652-8. PubMed ID: 15826713.
    Abstract:
    BACKGROUND/AIMS: Portal hypotensive effect of terlipressin is less effective when given during hemorrhage than in stable state. Blood retention in the stomach can induce splanchnic hyperemia which is mainly a consequence of an increased glucagon release. This study was undertaken to evaluate whether gastric blood retention contributes to the splanchnic hyporesponse to terlipressin. METHODS: Plasma glucagon determination was performed under basal conditions and after intragastric blood gavage in sham-operated and cirrhotic rats. Additionally, splanchnic hemodynamic effects to terlipressin were measured in blood-gavaged cirrhotic rats with or without glucagon antiserum or octreotide infusion. Another set of air-gavaged cirrhotic rats was included for comparison. RESULTS: Plasma glucagon level increased in both sham-operated and cirrhotic rats following blood gavage. Compared to air-gavaged cirrhotic rats, splanchnic hyporesponse to terlipressin was observed in cirrhotic rats receiving intragastric blood gavage. However, this splanchnic hyporesponse to terlipressin in blood-gavaged cirrhotic rats was overcome by glucagon antiserum or octreotide infusion. CONCLUSIONS: Intragastric blood gavage induced an elevation of plasma glucagon level and led to a splanchnic hyporesponse to terlipressin. Glucagon antiserum or octreotide administration overcame this hyporesponse. Excessive release of circulating glucagon may be an important factor for splanchnic hyporesponse to terlipressin in cirrhotic portal hypertension during hemorrhage.
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