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Biomedical subjects

H Kameda

Publications and source records attributed to H Kameda.

At least 127 records · Page 7Linked to original sources
PubMed1981

Anatomical basis of hepatic venographic alterations in idiopathic portal hypertension.

Hepatic venograms made in 40 authentic cases of idiopathic portal hypertension (Banti's syndrome) were compared with 13 normal venograms and venograms obtained in 88 cases of cirrhosis, and analyzed in the light of the pathological changes seen in 16 postmortem liver specimens. There were frequent anastomoses between hepatic vein radicles, approximation of middle-size branches to the liver surface, reduction in the angles between the main hepatic vein and its tributaries, and difficulty in opacifying portal vein branches in wedged retrograde portography. These angiographic alterations were corroborated by gross pathological findings which comprised displacement of middle-size hepatic vein branches closer to the liver surface and their approximation among themselves, and seem to be accounted for by the disappearance of liver parenchyma secondary to the peripheral portal circulatory failure.

Hepatic Veins↗
PubMed1981

Hepatic venography in noncirrhotic idiopathic portal hypertension. Comparison with cirrhosis of the liver.

Free and wedged hepatic venography were carried out in 37 patients with idiopathic portal hypertension (IPH) and the findings compared with those in 88 patients with cirrhosis of the liver. Characteristic changes in IPH included frequent vein-to-vein anastomoses, narrower angles between large veins and their tributaries, smooth and wavy middle-sized to large branches (giving a general "weeping willow" appearance), homogeneous sinusoidal filling, and minimal to absent filling of the portal venous system on wedged retrograde portography. In cirrhosis, by contrast, changes included rare vein-to-vein anastomoses, wide angles between veins and tributaries, irregular stenoses of large veins and branches at various levels, spotty sinusoidal filling, and frequent retrograde flow in the portal venous system. Hepatic venography is helpful in differentiating IPH from cirrhosis.

Adult↗
PubMed1980

Portographic liver changes in idiopathic noncirrhotic portal hypertension.

Intraoperative and transhepatic portograms in patients with noncirrhotic portal hypertension, or idiopathic portal hypertension, were compared with portograms of patients with liver cirrhosis. Although the portograms in idiopathic portal hypertension varied from case to case, they were distinctly different from those in cirrhosis. The most common features of the former included a paucity of medium-sized portal branches, irregular and often obtuse-angled division of the peripheral branches, occasional abrupt interruptions of them, an avascular area beneath the liver surface, nonopacification of some of the large intrahepatic portal branches and of their periphery, and increase of very fine vasculature around large intrahepatic portal branches. These findings are compatible with occlusion of intrahepatic portal vessels at various levels.

Adult↗
PubMed1980

[Effects of labetalol on the circulatory system (author's transl)].

Effects of labetalol on the cardiovascular system were studied in dogs, guinea pigs, rats, rabbits, and bullfrogs. In dogs anesthetized with pentobarbital, labetalol decreased heart rate, arterial blood pressure, and myocardial contractile force, and inhibited carotid sinus reflex, without affecting pO2 and pH of circulating blood, urine volume, and urinary excretion of sodium and potassium. Alpha- and beta-adrenergic blocking action of labetalol was demonstrated in dog hearts, arterial preparations of guinea pigs and rats, isolated rabbit hearts, and bullfrog hind limb and rabbit ear preparations. In bullfrog hind limb and rabbit ear preparations, labetalol dilated blood vessels in concentrations larger than those which produced alpha- and beta-adrenergic blockade. The dilatation of blood vessels was observed only when labetalol was added to the perfusate, whereas alpha- and beta-adrenergic blockade continued even after removal of labetalol from the perfusate. It is concluded that labetalol blocks alpha- and beta-adrenergic receptors in the heart and blood vessels of the species used herein, and that this compound inhibits carotid sinus reflex in dogs. In addition, the dilatation of the blood vessels of the bullfrog hind limb and rabbit ear as evoked by labetalol probably involves a mechanism different from that of adrenergic blockade.

Adrenergic alpha-Antagonists↗