To investigate the mechanisms of splanchnic hyperdynamics in portal hypertension (PHT), angiotensin Ⅱ(A-Ⅱ) receptor maximal binding capacity (Bmax) and dissociation constants (Kd) of splanchnic blood vessels in rats with prehepatic PHT were studied by radioligand binding analysis. The results showed that the A-Ⅱ receptor Bmax in the superior mesenteric artery and portal vein of PHT animals (206.9±39.3 fmol/mg protein and 31.5±9.2 fmol/mg protein respectively) was all significantly lower than that of the controls (297.2±44.7 fmol/mg protein and 53.4±12.1 fmol/mg protein respectively, Ｐ＜0.01). The A-Ⅱ receptor Kd in the superior mesenteric artery was markedly increased in PHT animals (1.03±0.11 nmol/L) compared with that in controls (0.88±0.08 nmol/L, Ｐ＜0.05). In the portal vein, the A-Ⅱ receptor Kd in PHT animals was slightly higher than in controls, but no significant difference was observed between the two groups. These results suggest that the vascular hyporesponsiveness to A-Ⅱ in PHT is caused partially by a reduction in number and a decrease in affinity of vascular A-Ⅱ receptors, and these changes may possibly lead to the formation of hyperdynamic circulation.
The synthesis and secretion of inflammatory cytokines in the monocytes of 68 cases of multiple system organ failure (MSOF) patients was investigated by the method of MTT stained in cytokines dependent defferential cell strain. The data showed that the serum levels of tumor necrosis factor, interleukine 1 and interleukine 6 were increased (Ｐ＜0.01) in the monocytes of MSOF patients. The synthesis and secretion of these inflammatory cytokines gradually increased in the monocytes after onset of MSOF. After 5 days of treatment with antibiotics and electrolytes intravenous infusion, the secretion of TNF, IL-1 and IL-6 were decreased respectively. These results suggested that the TNF, IL-1 and IL-6 are integrated into system inflammatory responese and caused the injury to the tissues and organs. The production levels of these cytokines can be regarded as the index of MSOF and its severity.