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Titolo:
Alterations in intrahepatic hemodynamics of the harvested porcine liver
Autore:
Ricciardi, R; Foley, DP; Quarfordt, SH; Kim, RD; Donohue, SE; Wheeler, SM; Chari, RS; Callery, MP; Meyers, MC;
Indirizzi:
Univ Massachusetts, Sch Med, Dept Surg, Worcester, MA 01655 USA Univ Massachusetts Worcester MA USA 01655 t Surg, Worcester, MA 01655 USA
Titolo Testata:
JOURNAL OF GASTROINTESTINAL SURGERY
fascicolo: 5, volume: 5, anno: 2001,
pagine: 490 - 498
SICI:
1091-255X(200109/10)5:5<490:AIIHOT>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE; REPERFUSION INJURY; HYALURONIC-ACID; VENOUS-PRESSURE; GRAFT FUNCTION; RAT-LIVER; TRANSPLANTATION; DONOR; ENDOTHELIN; RESISTANCE;
Keywords:
ischemia-reperfusion; compliance; resistance; nitric oxide; norepinephrine; hemodynamics;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Ricciardi, R Univ Massachusetts, Sch Med, Dept Surg, 55 Lake Ave N, Worcester, MA 01655USA Univ Massachusetts 55 Lake Ave N Worcester MA USA 01655 55USA
Citazione:
R. Ricciardi et al., "Alterations in intrahepatic hemodynamics of the harvested porcine liver", J GASTRO S, 5(5), 2001, pp. 490-498

Abstract

Hemodynamic properties of a donor liver, during initial reperfusion, are associated with the degree of graft preservation injury and have been proposed to correlate with subsequent markers of liver function. In the present study, hepatic hemodynamics, that is, portal venous pressure, hepatic vascular resistance, and compliance (vascular distensibility), were characterized(1) in situ before porcine livers were manipulated, (2) after these same livers were isolated and perfused within a bypass circuit, and (3) on reperfusion after 2 hours of cold ischemia. Hepatic vascular resistance was determined in each of these three states from the portal vein pressure response to differing hepatic blood flows. In addition, the response of the same livers to norepinephrine and nitroprusside was evaluated in each condition. Inthe in situ and isolated perfused liver, portal venous pressure increased only modestly despite doubling of hepatic flows. After cold ischemia, the pressure response to higher flows was significantly greater and much less ofa reduction in hepatic vascular resistance was noted than in studies priorto cold ischemia. Unlike livers prior to cold ischemia, the pressure response to norepinephrine was attenuated following cold ischemia. The response to nitroprusside, however, remained intact reducing the portal pressure to that of in situ livers. Therefore the portal hypertension that follows coldischemia appears to be largely provoked by the preservation injury and notby surgical manipulation or the by, pass circuit. This increment in portalpressure is responsive to a nitric oxide donor.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 15:07:46