[Changes of platelet rheological behavior and the interventional effects of ulinastatin in rats with high-voltage electrical burns].

Objective: To explore the influence of high-voltage electrical burns on the number of platelet aggregation, β-thromboglobulin (β-TG) and platelet factor 4 (PF-4) and the interventional effects of ulinastatin in rats with high-voltage electrical burns. Methods: A total of 240 Sprague-Dawley rats were divided into sham injury (SI) group, simple electrical burn (SEB) group, normal saline (NS) group, and ulinastatin (UTI) group according to the random number table, with 60 rats in each group. The electrical current was applied to the outside proximal part of left forelimb of rats and exited from the outside proximal part of right hind limb of rats. Rats in groups SEB, NS, and UTI were inflicted with high-voltage electrical burn wounds of 1 cm×1 cm at current entrances and exits, with the voltage regulator and experimental transformer. Rats in group SI were sham injured through connecting the same equipments without electricity. At 2 min post injury, rats in group NS were intraperitoneally injected with 2 mL/kg NS, and rats in group UTI were intraperitoneally injected with 2×10(4) U/kg UTI of 10 g/L. At 15 min before injury and 5 min, 1 h, 2 h, 4 h, 8 h post injury, 10 rats in each group were selected to collect 5-7 mL blood of heart respectively. Blood of 0.05 mL were collected to make fresh blood smear for observing the number of platelet aggregation, and serum were separated from the remaining blood to determine content of β-TG and PF-4 with enzyme-linked immunosorbent assay. Data were processed with analysis of factorial design of variance, student-Newman-Keuls test, Kruskal-Wallis H test, Wilcoxon rank sum test, and Bonferroni correction. Results: (1) At 15 min before injury, the numbers of platelet aggregation of rats were close among groups SI, SEB, NS and UTI (5.9±1.2, 5.8±1.2, 5.9±1.3, 5.9±1.1, respectively, with P values above 0.05). At 5 min, 1 h, 2 h, 4 h, 8 h post injury, the numbers of platelet aggregation of rats in group SEB were 57.2±16.3, 59.1±16.9, 60.8±20.6, 83.6±24.9, and 83.4±30.3, respectively, obviously more than those in group SI (6.0±1.3, 6.0±1.4, 5.9±1.4, 5.7±1.1, and 5.8±1.3, respectively, with P values below 0.001); the numbers of platelet aggregation of rats in group UTI were 29.6±7.4, 31.9±10.1, 35.0±14.2, 43.0±13.6, and 35.2±11.1, respectively, obviously more than those in group NS (58.3±16.1, 63.9±18.0, 60.8±17.7, 74.2±23.0, and 82.3±21.9, respectively, with P values below 0.001). There was no significantly statistical difference in the number of platelet aggregation of rats in group SI between each two time points within the same group (with P values above 0.05), but the number of platelet aggregation of rats in the other 3 groups at each time point post injury was significantly more than that of the same group at 15 min before injury (with P values below 0.001). (2) At 2, 4, and 8 h post injury, β-TG content of serum of rats in group SEB was significantly higher than that in group SI (with Z values from -3.780 to -3.477, P values below 0.05). At 5 min and 4 h post injury, β-TG content of serum of rats in group UTI was significantly lower than that in group NS (with Z values respectively -3.477 and -3.780, P values below 0.05). There was no significantly statistical difference in β-TG content of serum of rats in group SI at all time points of the same group ( χ (2)=0.130, P >0.05). At 2, 4, and 8 h post injury, β-TG content of serum of rats in group SEB was significantly higher than that of the same group at 15 min before injury (with Z values from -3.780 to -3.553, P values below 0.05). At 5 min, 1 h, and 4 h post injury, β-TG content of serum of rats in group NS was significantly higher than that of the same group at 15 min before injury (with Z values from -3.780 to -3.477, P values below 0.05). At 1 and 4 h post injury, β-TG content of serum of rats in group UTI was significantly higher than that of the same group at 15 min before injury (with Z values respectively -3.250 and -3.780, P values below 0.05). (3) At 2 and 8 h post injury, PF-4 content of serum of rats in group SEB was significantly higher than that in group SI (with P values below 0.05). At 2 h post injury, PF-4 content of serum of rats in group UTI was significantly higher than that in group NS ( P <0.05), and at 4 and 8 h post injury, PF-4 content of serum of rats in group UTI was significantly lower than that in group NS (with P values below 0.05). At all time points, PF-4 content of serum of rats in group SI was close (with P values above 0.05). At 2 and 8 h post injury, PF-4 content of serum of rats in group SEB was significantly higher than that of the same group at 15 min before injury (with P values below 0.05). At 1, 4, and 8 h post injury, PF-4 content of serum of rats in group NS was significantly higher than that of the same group at 15 min before injury (with P values below 0.05). There were significantly statistical differences in PF-4 content of serum of rats between all time points except for 5 min post injury and 15 min before injury (with P values below 0.05). Conclusions: Increasing number of platelet aggregation and abnormal secretion of β-TG and PF-4 of rats with high-voltage electrical burns can lead to microcirculation disturbance. UTI can alleviate microcirculation disturbance caused by high-voltage electrical burns by reducing the number of platelet aggregation and inhibiting secretion of β-TG and PF-4.