Pancreas · 2008
Cardiovascular homeostasis in hypotension associated with initial stages of severe acute pancreatitis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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García Mónica, Hernández-Barbáchano Ernesto, Hernández Lorenzo Maria Pilar, Calvo José Julián, López Novoa José M, San Román José Ignacio
Аннотация
OBJECTIVES: To identify the mechanisms underlying hypotension during the early phase of severe acute pancreatitis (SAP) by analyzing whether an impaired response to vasoactive substances occurs in this pathological process.
METHODS: Experimental SAP was induced by infusing 5% sodium taurocholate through the main pancreatic duct in rats. Once mean arterial pressure (MAP) in animals with pancreatitis was reduced, different vasoactive substances and inhibitors were administered.
RESULTS: Administration of the nonspecific nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester caused a similar increase in MAP in rats with pancreatitis and control rats, whereas inducible nitric oxide synthase inhibition did not cause changes in MAP. Moreover, the hypertensive response to endothelin and angiotensin II was lower in pancreatitis. Inhibition of angiotensin II synthesis by the angiotensin-converting enzyme inhibitor perindopril in animals with pancreatitis caused severe hypotension, causing death in 40% of them. Finally, pressor hyporesponsiveness to angiotensin II in animals with pancreatitis was avoided by previous administration of perindopril and N omega-nitro-L-arginine methyl ester.
CONCLUSIONS: The SAP-induced hypotension is associated with a deficient pressor responsiveness to angiotensin II and endothelin-1. The renin-angiotensin system plays an important role in the control of MAP in animals with pancreatitis.
METHODS: Experimental SAP was induced by infusing 5% sodium taurocholate through the main pancreatic duct in rats. Once mean arterial pressure (MAP) in animals with pancreatitis was reduced, different vasoactive substances and inhibitors were administered.
RESULTS: Administration of the nonspecific nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester caused a similar increase in MAP in rats with pancreatitis and control rats, whereas inducible nitric oxide synthase inhibition did not cause changes in MAP. Moreover, the hypertensive response to endothelin and angiotensin II was lower in pancreatitis. Inhibition of angiotensin II synthesis by the angiotensin-converting enzyme inhibitor perindopril in animals with pancreatitis caused severe hypotension, causing death in 40% of them. Finally, pressor hyporesponsiveness to angiotensin II in animals with pancreatitis was avoided by previous administration of perindopril and N omega-nitro-L-arginine methyl ester.
CONCLUSIONS: The SAP-induced hypotension is associated with a deficient pressor responsiveness to angiotensin II and endothelin-1. The renin-angiotensin system plays an important role in the control of MAP in animals with pancreatitis.