Bums (1990) 16, (4) 249-253
249
Printed in Great Britain
Roles of thromboxane and its inhibitor in burn shock
anisodamine
Huang Yuesheng, Li Ao(Ngao) and Yang Zongcheng Bum Institute,
Southwestern
Hospital, Third Military Medical College of PLA, Chongqing,
Thromboxane (TXA,) and prostacyclin (PGI,) levels,circdatory platelet aggregate ratios (CPAR), CPK, LDH, GOT, platelet counts, blood viscosity, cortisol and urine epinephn’ne con&nts were determined in 42 burned patients who were divided into two groups: Group I control (n = 34) and Group II (n = 8) treated with T&4, synthesis inhibitor, anisodamine. It was found that in controls, both 7X4, and the DtA,/PGl, ratio increased significantly. There was no marked differolce in FGI, levels between the lwo groups. Platelet counts and CPAR decreased, while blood viscosity, CPK, LDH, GOT cortisol and epkephn’nein the controls were all significantly higher than those found in Group II patients. All these findings suggesfed that the changes of I%, and the TxA,/pGI, ratios pkzyed an imporfanf role in the haemodynamics and haemorrheology in burn shock. The TX/I, synthesis inhibitor, anisodamine, showed beneficial effects by restoring fhe haemodynamicand rheological disturbances towards normal by virtue of their ability to induce vascular constriction, platelet aggregation, cellular a%rucfion, destabilization of membranes and release of chemical mediafors (including enzymes). Furthermore, at 1-3 days postbum, fhe levels of CPK, LDH and at 12 h postbum, but GOT in controls were higher than those m-red this phenomenon was not marked in the treated group, suggesting that after resusciiation, reperfusion damage had occurred and 7X4, might be responsible for the damage. It is assumed that an&&amine could proteck tissues fram reperfusion damage. The findings also suggested that anisodamine couM quicken the restoration of neuroendocrine disturbance initiated by shock (stress)).
Introduction The treatment of shock is one of the crucial steps in the successful treatment of patients with major bums, but the precise mechanisms which induce burn shock are not yet fully understood. This ignorance may limit the optimal means of treating shocked burned patients. It is thus imperative to try to understand the mechanisms leading to microvascular changes postburn and to lessen or block this change with specific drugs. It has been reported by Alemayehu et aI. (1987), Bittennan et al. (1986) Carmona et aI. (1984) and Reines et aI. (1982) that an imbalance of thromboxane (TXA,) and prostacyclin (PGI,) levels plays an important role in haemorrhagic and septic shock. 0 1990 Butterworth-Heinema 0305-4179f90/040249-05
Ltd
China
In this study, we investigated the changes of TXA, and PGI, and some other relevant variables in burned patients in order to define the roles of TxA,/PGI, imbalance in bum shock and the therapeutic effects of TXA, synthesis inhibitor, anisodamine, in the antishock treatment.
Materials and methods Forty-two patients admitted to the Bum Institute of the Southwestern Hospital, Chongqing from February, 1987 to February, 1988, were studied. Twenty-seven patients were male and 15 were female. The average patient age was 28.9 & 10.0 years (16-58 years). The average percentage of total body burn was 53.5 f 17.8 per cent (30-85 per cent) and average percentage of deep body burn was 13.0 f 15.2 per cent. AI1 42 patients survived. The 42 patients were randomly divided into two groups. Group 1, the control group (n = 34), had an average age of 28.3 f 10.1 years, an average TBSA of 53.4 &18.7 per cent and an average area of full thickness skin loss of 12.4 f 15.6 per cent. AI1 patients in this group received conventional treatment in our Institute after admission. The volume of intravenous fluid replacement required was estimated according to the formula- developed in our Institute for adults (T&k I; Bum Research Unit, 1977). Blood and urine samples were collected and measured at 12 h, I, 2,3,5 and 7 days postbum. Group II patients (n = 8) had an average age of 31.5 f 9.7 years, and average TBSA of 53.9f 14.8 per cent and an average full thickness skin loss of 17.1 f 13.2 per cent. In addition to the conventional treatment, three doses (each of 0.5 mg/kg body weight diluted in 100 ml of 5 per cent dextrose) of TXA, synthesis inhibitor, anisodamine (Changzheng Pharmaceutical Factory, Suzhou), were infused intravenously within 48 h postbum with an interval of 8.4 f 5.9 h. Each infusion lasted about 30min. Measurements were made as in Group I patients. Radioimmunoassay techniques were adapted to measure TXB,, the stable degradation product of TXA, and 6-ketoPGF,,, the stable degradation product of PGI,, in plasma (RIA kits supplied by the General Hospital of PLA, Beijing) (Li et al., 1985). Circulatory platelet aggregate ratio (CPAR) was determined by the method of Wu and Hoak (1974). Blood viscosity was measured with a Model NZ-4 viscosity
BLlms(1990)vol.16iNo.4
250
2200 --L
a” $ 1300 z
:z.
400 0[
h 0.5
1
--_i---i-___*___
7
2
3
;,,;+ 5
7
Days postburn
Days postburn
Figure 1. Changes in TXB,, 6-keto-PGF,, and TXES,/6-ketoAnisodamine-treated group (n = 8); -.-‘-.-, PGF,, ratio. -, control group (n= 34).+P
249
Printed in Great Britain
Roles of thromboxane and its inhibitor in burn shock
anisodamine
Huang Yuesheng, Li Ao(Ngao) and Yang Zongcheng Bum Institute,
Southwestern
Hospital, Third Military Medical College of PLA, Chongqing,
Thromboxane (TXA,) and prostacyclin (PGI,) levels,circdatory platelet aggregate ratios (CPAR), CPK, LDH, GOT, platelet counts, blood viscosity, cortisol and urine epinephn’ne con&nts were determined in 42 burned patients who were divided into two groups: Group I control (n = 34) and Group II (n = 8) treated with T&4, synthesis inhibitor, anisodamine. It was found that in controls, both 7X4, and the DtA,/PGl, ratio increased significantly. There was no marked differolce in FGI, levels between the lwo groups. Platelet counts and CPAR decreased, while blood viscosity, CPK, LDH, GOT cortisol and epkephn’nein the controls were all significantly higher than those found in Group II patients. All these findings suggesfed that the changes of I%, and the TxA,/pGI, ratios pkzyed an imporfanf role in the haemodynamics and haemorrheology in burn shock. The TX/I, synthesis inhibitor, anisodamine, showed beneficial effects by restoring fhe haemodynamicand rheological disturbances towards normal by virtue of their ability to induce vascular constriction, platelet aggregation, cellular a%rucfion, destabilization of membranes and release of chemical mediafors (including enzymes). Furthermore, at 1-3 days postbum, fhe levels of CPK, LDH and at 12 h postbum, but GOT in controls were higher than those m-red this phenomenon was not marked in the treated group, suggesting that after resusciiation, reperfusion damage had occurred and 7X4, might be responsible for the damage. It is assumed that an&&amine could proteck tissues fram reperfusion damage. The findings also suggested that anisodamine couM quicken the restoration of neuroendocrine disturbance initiated by shock (stress)).
Introduction The treatment of shock is one of the crucial steps in the successful treatment of patients with major bums, but the precise mechanisms which induce burn shock are not yet fully understood. This ignorance may limit the optimal means of treating shocked burned patients. It is thus imperative to try to understand the mechanisms leading to microvascular changes postburn and to lessen or block this change with specific drugs. It has been reported by Alemayehu et aI. (1987), Bittennan et al. (1986) Carmona et aI. (1984) and Reines et aI. (1982) that an imbalance of thromboxane (TXA,) and prostacyclin (PGI,) levels plays an important role in haemorrhagic and septic shock. 0 1990 Butterworth-Heinema 0305-4179f90/040249-05
Ltd
China
In this study, we investigated the changes of TXA, and PGI, and some other relevant variables in burned patients in order to define the roles of TxA,/PGI, imbalance in bum shock and the therapeutic effects of TXA, synthesis inhibitor, anisodamine, in the antishock treatment.
Materials and methods Forty-two patients admitted to the Bum Institute of the Southwestern Hospital, Chongqing from February, 1987 to February, 1988, were studied. Twenty-seven patients were male and 15 were female. The average patient age was 28.9 & 10.0 years (16-58 years). The average percentage of total body burn was 53.5 f 17.8 per cent (30-85 per cent) and average percentage of deep body burn was 13.0 f 15.2 per cent. AI1 42 patients survived. The 42 patients were randomly divided into two groups. Group 1, the control group (n = 34), had an average age of 28.3 f 10.1 years, an average TBSA of 53.4 &18.7 per cent and an average area of full thickness skin loss of 12.4 f 15.6 per cent. AI1 patients in this group received conventional treatment in our Institute after admission. The volume of intravenous fluid replacement required was estimated according to the formula- developed in our Institute for adults (T&k I; Bum Research Unit, 1977). Blood and urine samples were collected and measured at 12 h, I, 2,3,5 and 7 days postbum. Group II patients (n = 8) had an average age of 31.5 f 9.7 years, and average TBSA of 53.9f 14.8 per cent and an average full thickness skin loss of 17.1 f 13.2 per cent. In addition to the conventional treatment, three doses (each of 0.5 mg/kg body weight diluted in 100 ml of 5 per cent dextrose) of TXA, synthesis inhibitor, anisodamine (Changzheng Pharmaceutical Factory, Suzhou), were infused intravenously within 48 h postbum with an interval of 8.4 f 5.9 h. Each infusion lasted about 30min. Measurements were made as in Group I patients. Radioimmunoassay techniques were adapted to measure TXB,, the stable degradation product of TXA, and 6-ketoPGF,,, the stable degradation product of PGI,, in plasma (RIA kits supplied by the General Hospital of PLA, Beijing) (Li et al., 1985). Circulatory platelet aggregate ratio (CPAR) was determined by the method of Wu and Hoak (1974). Blood viscosity was measured with a Model NZ-4 viscosity
BLlms(1990)vol.16iNo.4
250
2200 --L
a” $ 1300 z
:z.
400 0[
h 0.5
1
--_i---i-___*___
7
2
3
;,,;+ 5
7
Days postburn
Days postburn
Figure 1. Changes in TXB,, 6-keto-PGF,, and TXES,/6-ketoAnisodamine-treated group (n = 8); -.-‘-.-, PGF,, ratio. -, control group (n= 34).+P
