[Abstract] [Full Text PDF] (in Japanese / 8459KB) [Members Only And Two Factor Auth.]

J.Jpn. Surg. Soc.. 87(1): 29-43, 1986


Original article

ETIOPATHOGENESIS OF HEMORRHAGIC GASTRITIS AFTER ESOPHAGEAL TRANSECTION WITH EXTENDED DEVASCULARIZATION FOR VARICEAL PATIENTS

First Department of Surgery, Kurume University School of Medicine, Kurume, Japan

Hirotoshi Satani

Postoperative hemorrhagic gastritis is often observed in cirrhotic patients with esophageal varices. We studied gastric and systemic hemodynamics including oxygen demand and supply before and after surgery to demonstrate the etiology of this entity.
Ten cirrhotic patients with esophageal varices were examined in this study. In hemodynamic studies, gastric blood flow and tissue oxgen tension (PtO2) of cardia portion were measured by hydrogen gas clearance method and PtO2 sensor. And systemic hemodynamics were measured by Swan-Ganz catheter including O2 availability, O2 extraction rate, O, consumption, A-VCDO2, and shunt rate. Moreover blood temperature, pH, Hb, P50, and 2, 3-DPG, and oxygenic dissociation curve, were also monitored.
Gastric blood flow showed moderate reduction immediately after surgery and returned to the previous value by the 7th postoperative day. But the value of PtO2 dropped gradually for 7 days after surgery. Marked systemic hyperdynamic circuration was observed before surgery and it was accelerated after surgery. In oxygen demand and supply, moderate to marked reduction was seen postoperatively. Oxygen dissociation curve was sifted to the left after surgery due to significant decrease in P50 and 2, 3-DPG.
These results suggest extended devascularization causes severe damage of system oxygenic demand and supply, and progressive gastric tissue hypoxia without reduction of blood flows may result in hemorrhagic gastritis.


<< To previous pageTo next page >>

To read the PDF file you will need Adobe Reader installed on your computer.