and his associates are to be commended upon pursuing an original research idea in the field of portal hypertension. The commonest cause of portal hypertension is an increased resistance to portal blood flow. Another important cause results from an increased blood flow secondary to arteriovenous fistulae in the splanchnic bed. The authors' study relates to the question of whether an increased portal flow (secondary to an arterioportal fistula) results in a significant rise in portal pressure. They also examined the hepatic effects of increasing the normal portal flow. Their results indicate that, on doubling the normal portal blood flow, no significant rise in portal pressure was encountered. Furthermore, they did not observe any deleterious effects of arterialization on the liver.
In this research effort, the experimental treatment relocated the right renal artery to the portal vein by way of an end-to-side anastomosis. Based on the Vorobioff et al. article (reference 4 in the authors' study), they assumed the procedure doubled the portal flow. On scrutinizing that paper,* we found portal and renal blood flow values of 1.67 k 0.15 and 3.31 f 0.19 ml/min/gm, respectively. The authors probably confused the issue, stating that the renal tissue supplied by the renal artery and the hepatic tissue