Interrelationship between splenic and superior mesenteric venous circulation manifested by transient splenic arterial occlusion using a balloon catheter
Article first published online: 5 DEC 2005
Copyright © 1987 American Association for the Study of Liver Diseases
Volume 7, Issue 3, pages 442–446, May/June 1987
How to Cite
Nishida, O., Moriyasu, F., Nakamura, T., Ban, N., Miura, K., Sakai, M., Uchino, H. and Miyake, T. (1987), Interrelationship between splenic and superior mesenteric venous circulation manifested by transient splenic arterial occlusion using a balloon catheter. Hepatology, 7: 442–446. doi: 10.1002/hep.1840070305
- Issue published online: 5 DEC 2005
- Article first published online: 5 DEC 2005
- Manuscript Accepted: 25 NOV 1986
- Manuscript Received: 14 JUL 1986
- Intractable Disease Division
- Public Health Bureau
- Ministry of Health and Welfare
We examined the hemodynamic changes induced by transient splenic arterial occlusion using a balloon catheter to investigate the hemodynamic effect of transcatheter splenic arterial embolization—a procedure that has been used since its introduction in 1973 as therapy for hypersplenism and more recently for portal hypertension. The blood flow volume was measured in 20 patients with liver disease using an ultrasonic duplex system (Toshiba SAL50A/SDL-01A). The portal venous pressure was also measured via a 3F catheter using a transducer. The catheter was placed in position by substituting it for a 25-gauge needle that had been inserted into the portal vein under ultrasonic guidance percutaneously and transhepatically.
Splenic arterial occlusion caused a drop in splenic venous blood flow from 708 ± 487 to 241 ± 155 ml per min, in portal venous blood flow from 993 ± 439 to 807 ± 419 ml per min and in portal venous pressure from 17.4 ± 7.2 to 14.4 ± 6.1 mm Hg. The latter two reductions were less than expected from the decrease in the splenic venous blood flow volume. This phenomenon was caused by an increase in the mesenteric venous blood flow from 475 ± 126 to 630 ± 270 mm per min.
This increase may be due to a compensatory mechanism under the control of a regulatory loop in the liver or portal vein, and there seems to be a relationship between splenic and intestinal circulation in portal hypertension that maintains hepatic circulation.