Roles of thromboxane and its inhibitor anisodamine in burn shock

Abstract

Thromboxane (TXA 2) and prostacyclin (PGI 2) levels, circulatory platelet aggregate ratios (CPAR), CPK, LDH, GOT, platelet counts, blood viscosity, cortisol and urine epinephrine contents were determined in 42 burned patients who were divided into two groups: Group I control ( n = 34) and Group II ( n = 8) treated with TXA 2 synthesis inhibitor, anisodamine. It was found that in controls, both TXA 2 and the TXA 2/PGI 2 ratio increased significantly. There was no marked difference in PGI 2 levels between the two groups. Platelet counts and CPAR decreased, while blood viscosity, CPK, LDH, GOT, cortisol and epinephrine in the controls were all significantly higher than those found in Group II patients. All these findings suggested that the changes of TXA 2 and the TXA 2/PGI 2 ratios played an important role in the haemodynamics and haemorrheology in burn shock. The TXA 2 synthesis inhibitor, anisodamine, showed beneficial effects by restoring the haemodynamic and rheological disturbances towards normal by virtue of their ability to induce vascular constriction, platelet aggregation, cellular destruction, destabilization of membranes and release of chemical mediators (including enzymes). Furthermore, at 1–3 days postburn, the levels of CPK, LDH and GOT in controls were higher than those measured at 12 h postburn, but this phenomenon was not marked in the treated group, suggesting that after resuscitation, reperfusion damage had occurred and TXA 2 might be responsible for the damage. It is assumed that anisodamine could protect tissues from reperfusion damage. The findings also suggested that anisodamine could quicken the restoration of neuroendocrine disturbance initiated by shock (stress).