Twelfth rib resection as an approach for portal vein cannulation in sheep.
A surgical technique involving resection of the twelfth rib was used to insert silastic cannulas into the portal veins of three sheep to study amino acid metabolism. Good exposure to the vein was achieved by this method although it required positive ventilation due to the penetration of the thoracic cavity. All cannulas were buried subcutaneously and exteriorized near the dorsal midline. This facilitated continuous infusion into the portal cannula without disturbing cannula placement. (+info)
Casts of hepatic blood vessels: a comparison of the microcirculation of the penguin, Pygoscelis adeliae, with some common laboratory animals.
Latex casts of the hepatic blood vessels of the penguin, Pygoscelis adeliae, and of some common laboratory animals were compared. There was general similarity between the different species, but the portal venous and hepatic arterial systems of the penguin were simpler than those of other species. Measurements were made of the volume and length of portal veins and it appears that the portal venous system is capable of being a more efficient blood reservoir in the penguin than in other species studied. The peribiliary plexus was especially well formed in the penguin and was drained by long veins which usually joined portal venous branches. Some of the long veins drained directly into the hepatic venous tree: these translobular veins were more prominent than in mammals. Anastomoses between hepatic artery and portal vein were not present in penguins, and the supply to the sinusoids appeared to be separate. The morphology of small hepatic veins of all the species appeared to be similar. (+info)
Pulsed Doppler ultrasonographic evaluation of portal blood flow in dogs with experimental portal vein branch ligation.
Portal blood flow was measured using pulsed Doppler ultrasound in 6 dogs before and after left portal vein branch ligation. Mean portal vein blood flow velocity and mean portal vein blood flow were significantly reduced after ligation and the congestion index was increased (p < 0.01). Pulsed Doppler ultrasound studies provide valuable physiological information which may assist the clinician with the diagnosis of canine hepatic circulatory disorders. (+info)
Identification, cloning and expression of rabbit vascular smooth muscle Kv1.5 and comparison with native delayed rectifier K+ current.
1. The molecular basis of voltage-gated, delayed rectifier K+ (KDR) channels in vascular smooth muscle cells is poorly defined. In this study we employed (i) an antibody against Kv1.5 and (ii) a cDNA clone encoding Kv1.5 derived from rabbit portal vein (RPV) to demonstrate Kv1.5 expression in RPV and to compare the properties of RPVKv1.5 expressed in mammalian cells with those of native RPV KDR current. 2. Expression of Kv1.5 channel protein in RPV was demonstrated by (i) immunocytolocalization of an antibody raised against a C-terminal epitope of mouse cardiac Kv1.5 in permeabilized, freshly isolated RPV smooth muscle cells and (ii) isolation of a cDNA clone encoding RPVKv1.5 by reverse transcription-polymerase chain reaction (RT-PCR) using mRNA derived from endothelium-denuded and adventitia-free RPV. 3. RPVKv1.5 cDNA was expressed in mammalian L cells and human embryonic kidney (HEK293) cells and the properties of the expressed channels compared with those of native KDR channels of freshly dispersed myocytes under identical conditions. 4. The kinetics and voltage dependence of activation of L cell-expressed RPVKv1.5 and native KDR current were identical, as were the kinetics of recovery from inactivation and single channel conductance. In contrast, there was little similarity between HEK293 cell-expressed RPVKv1.5 and native KDR current. 5. Inactivation occurred with the same voltage for half-maximal availability, but the kinetics and slope constant for the voltage dependence of inactivation for L cell-expressed RPVKv1.5 and the native current were different: slow time constants were 6.5 +/- 0.6 and 3.5 +/- 0.4 s and slope factors were 4.7 +/- 0.2 and 7.0 +/- 0.8 mV, respectively. 6. This study provides immunofluorescence and functional evidence that Kv1.5 alpha-subunits are a component of native KDR channels of vascular smooth muscle cells of RPV. However, the differences in kinetics and voltage sensitivity of inactivation between L cell- and HEK293 cell-expressed channels and native KDR channels provide functional evidence that vascular KDR current is not due to homomultimers of RPV Kv1.5 alone. The channel structure may be more complex, involving heteromultimers and modulatory Kvbeta-subunits, and/or native KDR current may have other components involving Kvalpha-subunits of other families. (+info)
Factors mediating the hemodynamic effects of tumor necrosis factor-alpha in portal hypertensive rats.
Nitric oxide, prostacyclin, and glucagon have been implicated in promoting the hyperdynamic circulatory state of portal hypertension. Recent evidence also indicates that increased tumor necrosis factor-alpha (TNF-alpha) production is involved in the pathogenesis of this hemodynamic abnormality. This study was aimed at investigating in rats with portal vein stenosis (PVS) the effects on splanchnic hemodynamics of blocking circulating TNF-alpha and the factors mediating the vascular action of this cytokine in this setting. Anti-TNF-alpha polyclonal antibodies or placebo was injected into rats (n = 96) before and 4 days after PVS (short-term inhibition) and at 24 h and 4, 7, 10 days after PVS (long-term inhibition). Short-term TNF-alpha inhibition reduced portal venous inflow and cardiac index and increased splanchnic and systemic resistance. Portal pressure was unchanged, but portal-systemic shunting was decreased. After long-term TNF-alpha inhibition, portal venous inflow and portal pressure were unchanged, but arterial pressure and systemic resistance rose significantly. Anti-TNF-alpha PVS rats exhibited lower increments of systemic resistance after Nomega-nitro-L-arginine methyl ester and indomethacin administration and lower serum levels of TNF-alpha, nitrates-nitrites, and 6-keto-PGF1alpha, both over the short and the long term. Serum glucagon levels rose after long-term inhibition. In conclusion, the specific role played by TNF-alpha in the development of the hyperdynamic state of portal hypertension appears to be mainly mediated through an increased release of nitric oxide and prostacyclin. Maintenance of the splanchnic hyperemia after long-term TNF-alpha inhibition could be due to a compensatory release of glucagon. (+info)
Lobar decrease in 99mTc-GSA accumulation in hilar cholangiocarcinoma.
Hilar cholangiocarcinoma can obstruct hepatic ducts and involve the portal veins. Both biliary stasis and decrease in portal venous flow are known to reduce 99mTc-diethylenetriamine pentaacetic acid-galactosyl human serum albumin (GSA) accumulation. The specific relationship between these pathological conditions due to hilar cholangiocarcinomas and 99mTc-GSA accumulation has never been clarified. METHODS: Sixteen patients with hilar cholangiocarcinomas who underwent 99mTc-GSA liver scintigraphy were reviewed. The relationship between significant decrease in 99mTc-GSA accumulation and lobar biliary stasis, or decrease in the portal venous flow, was evaluated. Average counts of region of interest placed in both right and left lobes were compared in the same transaxial SPECT section. Count ratios of right and left lobes were calculated. RESULTS: Significant lobar decrease in 99mTc-GSA accumulation was observed in 6 of the 16 patients. Ipsilateral portal venous stenosis or obstruction was seen in all these 6 patients, whereas ipsilateral portal venous stenosis or obstruction was seen in only 1 of the other 10 patients. Symmetric bile duct dilatation was seen in 13 patients, and asymmetric bile duct dilatation was seen in 3. Lobar decrease in 99mTc-GSA accumulation correlated well with decrease in ipsilateral portal venous flow (P < 0.0005). The count ratio was significantly reduced when unilateral portal venous flow decreased (P < 0.05). CONCLUSION: Using 99mTc-GSA liver scintigraphy, we can predict lobar decrease in ipsilateral portal venous flow and monitor hepatic functional lateralities in patients with hilar cholangiocarcinomas. (+info)
Modulation of the decay of Ca2+-activated Cl- currents in rabbit portal vein smooth muscle cells by external anions.
1. The effects of external anions on the decay kinetics of Ca2+-activated Cl- currents (ICl(Ca)) were studied in smooth muscle cells isolated from rabbit portal vein using the perforated patch whole-cell voltage clamp technique. 2. In normal NaCl-containing external solution the decay of spontaneous Ca2+-activated Cl- currents (STICs) and Ca2+-activated Cl- 'tail' currents (Itail) was described by a single exponential with a time constant (tau) that was prolonged by external anions which are more permeable than Cl- (Br-, I- and SCN-) and accelerated by less permeant anions. However, intracellular I- did not affect the tau of STICs and Itail. 3. There was a positive correlation between the ability of an external anion to affect the decay tau of ICl(Ca) and its permeability relative to Cl-. 4. The voltage dependence of STIC and Itail decay was not affected by external or internal anions. 5. External permeating anions were not obligatory for activation of ICl(Ca) and STIC tau was not altered in Cl--free external solution. 6. Modulation of tau by mole fractions of SCN- and Cl- ions was fitted by a logistic curve, suggesting competition between SCN- and Cl- ions for a binding site. 7. In conclusion, external anions affect the decay of ICl(Ca) by a mechanism compatible with an interaction with a binding site which modulates Cl- channel kinetics. (+info)
Specific galpha11beta3gamma5 protein involvement in endothelin receptor-induced phosphatidylinositol hydrolysis and Ca2+ release in rat portal vein myocytes.
In this study, we identified the receptor subtype activated by endothelin-1 (ET-1) and the subunit composition of the G protein coupling this receptor to increase in cytosolic Ca2+ concentration in rat portal vein myocytes. We used intranuclear antisense oligonucleotide injection to selectively inhibit the expression of G protein subunits. We show here that the endothelin receptor subtype A (ETA)-mediated increase in cytosolic Ca2+ concentration was mainly dependent on Ca2+ release from the intracellular store. ETA receptor-mediated Ca2+ release was selectively inhibited by antisense oligonucleotides that inhibited the expression of alpha11, beta3, and gamma5 subunits, as checked by immunocytochemistry. Intracellular dialysis of a carboxyl terminal anti-betacom antibody and a peptide corresponding to the Gbetagamma binding region of the beta-adrenergic receptor kinase-1 had no effect on the ETA receptor-mediated Ca2+ release. In contrast, a synthetic peptide corresponding to the carboxyl terminus of the alphaq/alpha11 subunit, heparin (an inhibitor of inositol 1,4,5-trisphosphate receptors), and U73122 (an inhibitor of phosphatidylinositol-phospholipase C) inhibited, in a concentration-dependent manner, the ETA receptor-mediated Ca2+ responses. Accumulation of [3H]inositol trisphosphate evoked by norepinephrine peaked at approximately 15 s, whereas that evoked by ET-1 progressively increased within 2 min. In myocytes injected with anti-alphaq antisense oligonucleotides, both amplitude and time course of the norepinephrine-induced Ca2+ release became similar to those of the ET-1-induced Ca2+ response. We conclude that the ETA receptor-mediated Ca2+ release is selectively transduced by the heterotrimeric G11 protein composed of alpha11, beta3, and gamma5 subunits, and that a delayed stimulation of phospholipase C occurs via the alpha11 subunit. (+info)