A homemade regulator and transformer apparatus was used to reproduce the model of
electric burn (0.5 cm×0.5 cm in size) with depth from full-thickness to full-thickness skin plus muscle and bone on the middle of the inside of right hind limb in 60 Wistar rats. The open
wounds were covered with 20 g/L
sulfadiazine silver paste immediately after injury. The
wound condition was observed every day. The injured rats were divided into group
LMWH and control group (C) according to the random number table, with 30 rats in each group. Rats in group
LMWH were given
subcutaneous injection of
LMWH (1 U/g) in abdominal wall, 2 times a day. No other treatment was given in rats in group C. On post
burn day (PBD) 3, 5, and 10, 10 rats respectively of two groups were sacrificed. The damaged tissue of
wound and that around the
wound (1.0 cm×0.5 cm in size) were excised, and heart blood was obtained. The pathological changes and
thrombosis in damaged tissue were observed with HE, Masson, and
aldehyde fuchsin staining, and the
thrombosis rate was calculated. Serum contents of TNF-α and
endothelin-1 were determined with ELISA. The
mRNA expression of TNF-α in damaged tissue was detected with RT-PCR. Data were processed with Levene homogeneity test, analysis of variance of factorial design,
LSD- t test, SNK- q test, and Friedman M nonparametric test.
RESULTS: (1) The injured limb of rats was obviously swollen after
electric burn, which reached deeply to the muscle and bone. Compared with those of group C, the swelling of rats subsided slightly faster and the inflammatory response was lighter in group
LMWH at each time point. (2) The
necrosis of damaged tissue and profuse infiltration of inflammatory cells were observed. Dilatation of blood vessels, congestion and
thrombosis, and swelling,
necrosis, and desquamation of vascular endothelial cells were observed in the damaged tissue. Damaged blood vessel wall, ruptured elastic fiber, loss of internal elastic membrane, and other pathological changes were observed in the damaged tissue of rats in the two groups. Above lesions were improved gradually along with the passage of time, and the improvement was more obvious in rats of group
LMWH compared with that of group C on PBD 5 and 10. (3) The
thrombosis rates of rats in group
LMWH were obviously lower than those of rats in group C (F = 4.921, P < 0.05). The
thrombosis rates of rats in group
LMWH on PBD 3 and 10 were respectively (0.07 ± 0.11)% and (0.03 ± 0.05)%, which were significantly lower than those of rats in group C [(0.16 ± 0.15)% and (0.13 ± 0.18)%, with t values respectively 2.17 and 2.07, P values below 0.05]. In group
LMWH, the
thrombosis rate of rats on PBD 10 was obviously lower than that on PBD 3 (t = 3.61, P < 0.05). (4) The serum contents of TNF-α and
endothelin-1 of rats in group
LMWH were significantly lower than those of rats in group C (F = 47.161, χ(2) = 81.46, P values below 0.01). In group
LMWH, TNF-α contents were respectively (71 ± 24), (74 ± 14), (72 ± 20) pg/mL, and
endothelin-1 contents were respectively (20.9 ± 3.2), (19.8 ± 5.2), (18.6 ± 1.1) ng/mL on PBD 3, 5, and 10, and they were significantly lower than those of rats in group C [(195 ± 148), (96 ± 20), (159 ± 46) pg/mL and (38.8 ± 15.4), (27.9 ± 3.6), (25.6 ± 7.6) ng/mL, with t values from 3.81 to 8.05, q values from 4.41 to 7.85, P < 0.05 or P < 0.01]. (5) The
mRNA expression levels of TNF-α in damaged tissue of rats in group
LMWH were significantly lower than those of rats in group C (F = 199.113, P < 0.01). The
mRNA expression levels of TNF-α of rats in group
LMWH were respectively 0.93 ± 0.10, 1.15 ± 0.12, 1.21 ± 0.11 on PBD 3, 5, and 10, and they were significantly lower than those of group C (1.68 ± 0.15, 1.43 ± 0.12, 1.50 ± 0.13, with t values from 3.75 to 6.12, P < 0.05 or P < 0.01). In group
LMWH, the
mRNA expression level of TNF-α of rats on PBD 10 was obviously higher than that on PBD 3 (t = 3.61, P < 0.05).
CONCLUSIONS: