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Biomedical subjects

F Moriyasu

Publications and source records attributed to F Moriyasu.

At least 109 records · Page 6Linked to original sources

Measurement of portal vascular resistance in patients with portal hypertension.

Portal vascular resistance was measured percutaneously in 60 patients with chronic liver disease and in 5 control subjects. The portal vascular resistance (PVR) was calculated, using the following equation, from the portal blood flow (QPV), portal venous pressure (PPV), and hepatic venous pressure (PHV): PVR = (PPV - PHV)/QPV. The portal blood flow was measured using an ultrasonic Doppler duplex system, and the portal venous and hepatic venous pressures were measured using percutaneous transhepatic catheterization and venous catheterization, respectively. The wedged hepatic venous pressure was measured by occluding the hepatic venous branch using a balloon catheter. The portal vascular resistance was 0.25 +/- 0.13 mmHg X ml-1 X min X kg body weight (mean +/- SD, n = 5) in the control group, 0.64 +/- 0.29 mmHg X ml-1 X min X kg body wt (n = 13) in the chronic active hepatitis group, 1.34 +/- 0.79 mmHg X ml-1 X min X kg body wt (n = 30) in the cirrhosis group, and 0.85 +/- 0.69 mmHg X ml-1 X min X kg body wt (n = 13) in the idiopathic portal hypertension group.

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Portal hemodynamics in patients with hepatocellular carcinoma.

The protal blood flow was assessed in 46 patients with hepatocellular carcinoma, 81 with cirrhosis, and 110 control subjects using an ultrasonic B-mode pulsed Doppler duplex system. The cross-sectional area of the portal vein was increased, and the velocity of portal blood flow was decreased in hepatocellular carcinoma and cirrhosis, whereas the blood flow volume was not significantly different. A significant decrease in portal blood flow was found in hepatocellular carcinoma only when at least three of the four major branches of the portal vein were occluded. The change in portal hemodynamics before and after transcatheter arterial embolization (TAE) was investigated. Immediately after TAE, neither portal venous pressure nor portal blood flow showed any constant trend. The portal blood flow reached a peak 1 week after TAE and then returned to its former value after 3-4 weeks, while all cases with poor prognoses showed a drop in portal blood flow after TAE.

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"Congestion index" of the portal vein.

The "congestion index" is used to mean the ratio between the cross-sectional area (cm2) and the blood flow velocity (cm/sec) of the portal vein, as determined by a duplex Doppler system. The indices as determined in normal subjects and patients with liver disease were as follows: normal subjects (n = 85), 0.070 +/- 0.029 cm X sec; acute hepatitis (n = 11), 0.071 +/- 0.014 cm X sec; chronic active hepatitis (n = 42) 0.119 +/- 0.084 cm X sec; cirrhosis (n = 72), 0.171 +/- 0.075 cm X sec; and idiopathic portal hypertension (n = 11), 0.180 +/- 0.107 cm X sec. There was a statistically significant difference between the congestion indices from the normal subject group and indices obtained from patients with chronic hepatitis, cirrhosis, and idiopathic portal hypertension. A weak positive correlation was obtained between the congestion index and the portal venous pressure, measured simultaneously through a percutaneously placed catheter (n = 64, r = 0.45, p less than 0.01). It is suggested that the congestion index reflects the pathophysiological hemodynamics of the portal venous system in portal hypertension.

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