[Effect of intensive insulin treatment on cardiac myocytes of severely scalded rats].

OBJECTIVE

To study the protective effect of intensive insulin treatment on cardiac myocytes of severely scalded rats.

METHODS

Eighteen model Sprague-Dawley (SD) rats were subjected to 30% total body surface area (TBSA) full thickness injury, and they were divided into three groups with 6 rats in each group. The right jugular vein was cannulated for fluid resuscitation and administration of drugs. The rats in burn group were injected with normal saline, the intensive insulin group with injection of insulin to maintain plasma glucose content in normal range, and the sham burn group received physiologic dose of saline without burn injury. Plasma glucose was monitored after burn injury. Rats were sacrificed at 6 hours postburn to examine plasma myocardial enzymes spectrum as well as histological and ultrastructure changes in cardiac tissue. The expression of p-Akt was detected by western blotting.

RESULTS

Plasma glucose level was significantly elevated in burn group within postburn 6 hours as compared with the sham burn group, and lowered in intensive insulin group (4.5 approximately 5.2 mmol/L vs. 7.6 approximately 8.4 mmol/L, P<0.05 or P<0.01). And the intensive insulin therapy could effectively inhibit the release of cardiac enzymes [lactate dehydrogenase (LDH): (2 369.3+/- 178.9) U/L vs. (2 684.1+/-335.0) U/L, P<0.05; alpha-hydroxybutyrate dehydrogenase (alpha-HBD): (576.7+/-219.2) U/L vs. (1 002.0+/-347.1) U/L, P<0.01; creatine kinase (CK): (1 041.9+/-623.2) U/L vs. (2 447.1+/-1 183.7) U/L, P<0.01]. The expression of p-Akt was significantly strengthened in the intensive insulin group (1.18+/-0.43 vs. 0.24+/-0.11, P<0.01). Light microscopic and electron microscopic examinations showed that intensive insulin therapy could alleviate the injury to myocardial cells and structural changes.

CONCLUSION

Intensive insulin treatment possesses protective effect on cardiomyocytes after a severe burn, and it is related to its up-regulation of phosphorylation level of Akt in cardiomyocyte, thus inhibiting the damage to myocytes.