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At least 181 records · Page 10Linked to original sources
PubMed1997

NO-mediated vasodilation in the rat liver. Role of hepatocytes and liver endothelial cells.

BACKGROUND/AIMS: Nitric oxide (NO) is a potent vasodilator. We investigated the mechanisms responsible for this effect in the liver. METHODS: Isolated perfused rat liver and cultures of endothelial sinusoidal cells and hepatocytes were used. RESULTS: L-arginine (10(-3) M) and NO donor Sin-1 (10(-5) M) respectively increased the liver flow by 52% (p<0.01) and 93% (p<0.01) vs controls. The NO synthase inhibitor Nw-nitro-L-arginine (10(-3) M) and the guanylate cyclase inhibitor methylene blue (10(-5) M) respectively decreased the basal liver flow by 26% and 16% (p<0.05) and inhibited the vasodilating effects of L-arginine. L-arginine (10(-3) M) increased nitrite concentration in hepatocyte culture (77.25+/-7.40 micromol x l(-1) vs 14.70+/-3.55 micromol x l(-1) in controls; p<0.01) and in liver endothelial cell culture (0.36+/-0.09 micromol x l(-1) vs 0.12+/-0.05 micromol x l(-1) in controls; p<0.05). Nw-nitro-L-arginine inhibited the basal production and abolished the L-arginine-induced production of nitrites both in hepatocyte and in liver endothelial cell cultures. The concentration of nitrites in the hepatocyte supernatant rose from 14.70+/-3.55 micromol x l(-1) to 150.50+/-45.55 micromol x l(-1) in the presence of a combination of interleukin-1beta, TNF alpha and interferon gamma. CONCLUSIONS: Under basal conditions, NO regulates the vascular tone of liver circulation. Both liver endothelial cells and hepatocytes can be implicated. NO production by hepatocytes may increase during inflammation.

Animals↗
PubMed1994

Hepatectomy with extracorporeal circulation for liver metastasis from colon carcinoma located at the confluence of the major hepatic vein: a case report.

Liver metastasis located at the confluence of the major hepatic veins developed after an operation for sigmoid colon carcinoma in a 63-year-old patient. Curative resection of the tumor was performed by in situ hypothermic perfusion of the liver and extracorporeal circulation. Intra-abdominal bleeding occurred on the first postoperative day, and ligation of the right inferior phrenic artery was performed via an emergency laparotomy. Only mild elevation of ALT and recovery of the arterial ketone body ratio to the "safety zone" was noted on the second postoperative day. Hepatic function gradually deteriorated after the 4th postoperative day with no distinct cause. Diffuse fatty liver was suspected as a cause of liver failure. The patient died on the 31st postoperative day. The problems encountered in this case are discussed in this paper.

Adenocarcinoma↗
PubMed2006

Optimal portal venous circulation for liver graft function after living-donor liver transplantation.

BACKGROUND: Previous studies have shown poor outcome after living-donor liver transplantation (LDLT) as a result of excessive portal venous pressure (PVP), excessive portal venous flow (PVF), or inadequate PVF. We investigated optimal portal venous circulation for liver graft function after LDLT in adult recipients retrospectively. METHODS: Between June 2003 and November 2004, 28 adult patients underwent LDLT in our institution. We modulated PVP under 20 mmHg in these 28 cases by performing a splenectomy (n=4) or splenorenal shunt (n=1). The PVF and PVP were measured at the end of the operation. Compliance was calculated by dividing PVF by PVP. RESULTS: PVF and compliance showed a significant inverse correlation with peak billirubin levels after LDLT (r = -0.63: r=-0.60, P<0.01), and with peak international normalized ratio after LDLT (r=-0.41: r=-0.51, P<0.05). Compliance was higher in right-lobe graft with middle hepatic vein cases (148+/-27 ml/min/mmHg), and lower in left-lobe graft cases (119+/-50 ml/min/mmHg). CONCLUSIONS: Liver graft function was better when PVF and graft compliance were higher and PVP was maintained under 20 mmHg.

Adult↗
PubMed2000

[Correction of lymph circulation in liver cirrhosis].

The approach to surgical correction of lymph circulation in hepatic cirrhosis is described. The main criteria in the choice of operations draining neck lymphatic duct were hyperkinetic central hemodynamics with high functional pressure in thoracic lymphatic duct and lymphovenous pressure gradient, central or mixed type of intrahepatic lymph flow. All the 26 patients underwent transvenous external-internal drainage of thoracic duct as a temporal measure for stabilization of patients state. Reinfusion of lymph after lymphosorption promoted detoxication in hepatic failure in patients with cirrhosis, complicated by resistant ascites. Low pressure indices of central lymphodynamics and mixed intrahepatic lymph flow are indications for anastomosis creation between right lumbar vein and right lymphatic duct. In this case it is possible to save the behind-hepatic portion of cava inferior in potential recipients of liver transplants.

Anastomosis, Surgical↗
PubMed1978

[Umbilical collateral circulation in liver cirrhosis - Cruveilhier-v. Baumgarten syndrome (author's transl)].

Embryonal development and anatomy of the liver are shortly discussed; they do explain collateral circulation in liver cirrhosis. A case report is given of a patient with umbilical collateral circulation (Cruveilhier-v. Baumgarten syndrome), exhibiting impressive clinical and radiological findings. Such an umbilical collateral circulation will develop in up to 21% of all patients with an intrahepatic block. This is only one variant - not prone to complications by the way - of a multitude of different portosystemic shunts in liver cirrhosis. Therefore it should not be talked about as an independent syndrome.

Collateral Circulation↗
PubMed1993

Effects of the liver on circulating adenosine in blood.

The effects of the liver on circulating adenosine in vivo were examined by monitoring plasma adenosine levels in hepatic afferent and efferent blood during intraportal venous (i.p.v.) and intravenous (i.v.) infusions of adenosine (0.04-1 mg.kg-1.min-1). Dilazep, a blocker of nucleoside uptake, was also used for studying the uptake of adenosine into the liver and extrahepatic sites. Basal levels of plasma adenosine in portal venous, arterial, and hepatic venous blood were similar. However, increased adenosine levels during infusions were significantly cleared by a single passage through the liver, suggesting that the liver is a potent organ for eliminating the increased adenosine in circulation. Dilazep inhibits extrahepatic elimination but does not affect hepatic extraction of circulating adenosine. Subtypes of nucleoside uptake are suggested to exist between the liver and other cell types, such as red blood cells.

Adenosine↗
PubMed1993

Persistence of systemic and splanchnic hyperkinetic circulation in liver transplant patients.

Portal pressure and portal-systemic collateral circulation after orthotopic liver transplantation have not been investigated. We studied systemic and splanchnic hemodynamics in 17 patients with cirrhosis before and 205 +/- 146 days after orthotopic liver transplantation. Among the 17 orthotopic liver transplantation patients, 12 had undergone hemodynamic study in the 6 mo before orthotopic liver transplantation. Controls were 50 patients with normal liver architecture. Cardiac index remained elevated in orthotopic liver transplantation patients compared with controls (3.6 +/- 0.9 vs 3.1 +/- 0.4 L/min.m2; p < 0.05). Azygos blood flow, which was elevated before orthotopic liver transplantation (585 +/- 402 ml/min), remained elevated after orthotopic liver transplantation (553 +/- 343 ml/min). In transplant patients, hepatic blood flow was higher than it was in controls (2.26 +/- 0.86 vs. 1.38 +/- 0.57 L/min; p < 0.05). Elevated hepatic blood flow correlated with cardiac index (r = 0.647, p < 0.025). In patients with normal graft function, hepatic venous pressure gradient was normal (2 +/- 1 mm Hg). In a patient with acute rejection, a sharp elevation in the hepatic venous pressure gradient was observed; it returned to normal 45 days after treatment. We conclude that despite normal portal pressure, portal-systemic collateral blood flow remains elevated after orthotopic liver transplantation. Possibly because of persistent collateral circulation, which may keep portal tributary blood flow elevated, hepatic blood flow is increased after orthotopic liver transplantation. Elevated splanchnic blood flow, in turn, contributes to the high cardiac index in liver recipients. Finally, a sharp elevation in portal pressure, which may be observed during acute rejection and subsides after treatment, merits further study.

Adult↗
PubMed2000

Changes in prostaglandin and nitric oxide levels in the hyperdynamic circulation following liver resection.

BACKGROUND AND AIMS: Significant changes in hepatic haemodynamics occur after major hepatectomy, but the pathogenesis of this phenomenon is unclear. This study investigates the serum profile of prostaglandin and nitric oxide in the hepatic and systemic circulation before and after hepatectomy and the temporal relationship of these to changes in the hepatic blood flow. METHODS: Blood samples were collected from the internal jugular, portal and hepatic veins of six Yorkshire pigs (17-25 kg) before, immediately after and 48 h after partial hepatectomy. RESULTS: Serum levels of prostacyclin I2 (PGI2) and prostaglandin E2 (PGE2) from the systemic circulation, the portal circulation and from the hepatic veins were found to differ considerably even before hepatectomy. After the hepatectomy was performed, there was a significant rise in PGI2 levels in the systemic circulation (P=0.027). Hepatic blood flow and cardiac output were measured before hepatectomy, 24 and 48 h after hepatectomy in another six pigs. A significant increase in hepatic blood flow (P=0.029) occurred after the hepatectomy and this was accompanied by a concomitant increase in the cardiac output (P=0.042). The increase in PGI2 concentration in the systemic circulation after hepatectomy appears to accompany the development of hyperdynamic hepatic and systemic circulations. No significant change was found in circulating PGE2 levels in the systemic, portal and hepatic veins at the three collection intervals (i.e. pre, post and 48 h after hepatectomy). The PGE2 levels in the hepatic vein, however, were significantly higher from than in the portal vein (P=0.028). No significant changes were observed in the level of nitric oxide. CONCLUSION: This study demonstrates an increase in the total hepatic blood flow after hepatectomy together with a threefold increase in prostacyclin in the systemic circulation. The liver was identified as the main source of circulatory prostaglandin.

Animals↗
PubMed1977

The circulation in liver tissue and experimental liver metastases before and after embolization of the liver artery.

Simultaneous measurement of cardiac output distribution with 86Rubidium and 57Cobalt-tagged microspheres in rats implanted with liver tumors by intraportal injection of sarcoma cells enables quantitation of arterial and portal tumor circulation. The portal circulation was found to be increased in small tumors as compared to the liver, but as the tumor grew there was a decrease in the portal tumor circulation. When the tumor growth became massive even the total liver circulation was reduced, as measured with 133Xenon wash-out. All the tumors had increased arterial circulation. This arterial hyperperfusion was changed into ischemia when the liver artery was occluded through embolization with degradable microspheres.

Animals↗
PubMedDate not supplied

[Enzyme activity of microsomal oxidation in ischemic and intact lobes of the rat liver after resumption of the liver blood circulation].

Forty-minute lobular ischemia of the rat liver produces no considerable changes in the activity of the enzymes of the hydroxylation system of the hepatocyte endoplasmic reticulum. After resumption of circulation in the microsomes of ischemized and intact lobes of the liver the activity of hydroxylases appreciably decreases, reaching the minimum level by the 72nd hour of the postischemic period. During this time lipid peroxidation increases.

Animals↗