To acquire more understanding about the myocardial cell membrane structural damageduring severe burns on the molecular level. Methods: In the in vivo burn model established in rats, alterations of the anion sites at h...To acquire more understanding about the myocardial cell membrane structural damageduring severe burns on the molecular level. Methods: In the in vivo burn model established in rats, alterations of the anion sites at hasal lamina of the myocardial cells was assessed with a PEI cationic probe. The membrane permeability of the myocardial cells was observed using colloidal lanthanum as a marker and the myocardial water content measured. Results: The anion sites of hasal lamina of the myocardial cells showed regular linear lattice arrangement (40 nm- 80nm). The PEI granules of the hasal lamina were decreased at the lst h and decreased significantly at the 6th h after burns. The lanthanum granules entered into the myocardial cells at the lst h and the myocardial water content was significantly increased (P<0. 01 ) at the 3rd h after burns. Conclusion: The damage of the hasal lamina and decrease of the anion sites on the myocardial cells might be a contributive factor causing the increase of membrane permeability, tissue edema and membrane protective barrier dysfunction after severe burns.展开更多
文摘To acquire more understanding about the myocardial cell membrane structural damageduring severe burns on the molecular level. Methods: In the in vivo burn model established in rats, alterations of the anion sites at hasal lamina of the myocardial cells was assessed with a PEI cationic probe. The membrane permeability of the myocardial cells was observed using colloidal lanthanum as a marker and the myocardial water content measured. Results: The anion sites of hasal lamina of the myocardial cells showed regular linear lattice arrangement (40 nm- 80nm). The PEI granules of the hasal lamina were decreased at the lst h and decreased significantly at the 6th h after burns. The lanthanum granules entered into the myocardial cells at the lst h and the myocardial water content was significantly increased (P<0. 01 ) at the 3rd h after burns. Conclusion: The damage of the hasal lamina and decrease of the anion sites on the myocardial cells might be a contributive factor causing the increase of membrane permeability, tissue edema and membrane protective barrier dysfunction after severe burns.
