AIM: To investigate the therapeutic effects of recombinant human growth hormone (rhGH) on rat septic shock with intraabdominal infection by E. coli and its possible mechanism. METHODS: 76 SD rats were divided into 3 g...AIM: To investigate the therapeutic effects of recombinant human growth hormone (rhGH) on rat septic shock with intraabdominal infection by E. coli and its possible mechanism. METHODS: 76 SD rats were divided into 3 groups randomly:control group (group C, n=16) without any special treatnent,of E. coli(1×1010 cfu@ L-1,15 ml@kg-1, ip), treated group (group by rhGH injection (2.25 U@kg-1@d-1, im). Group S and group T were further divided into 1d and 3d subgroups, respectively (n=15 each). Mean arterial pressure (MAP), levels of plasma TNFα and endotoxin and leukocyte count were determined on 1st day and 3rd day after E. coli injection. Another 39 SD rats were divided into groups C, S and T (n=13 each) just for observing survival rate within 1 week.RESULTS: (1) On 1st and 3rd day, MAP in group S decreased markedly, and MAP on 1st day lowered more than that of 3rd day (P＜0.01), while MAP in group T just decreased slightly. The survival rate within 1 week was much higher in group T (84.6 %) than in group S (46.2 %) (P＜0.01). (2)On 1st day, plasma TNFα and endotoxin elevated significantly in group S and group T (P＜0.05), and endotoxin in group S had more increase (P＜0.01). On 3rd day, TNFα in group S returned to the level of group C (P＞0.05),while TNFα in group T went down below the level of group C(P＜0.01). On 3rd day, endotoxin in group S declined, but was still higher than that of group C (P＜0.01), endotoxin in group T returned to the level of group C (P＞0.05). (3) On 1st day, neutrophil ratio in total leukocyte count in both group S and group T increased significantly (P＜0.05 vs group C).CONCLUSION: rhGH showed beneficial effects on rat septic shock. The possible mechanisms may involve the attenuation of bacteria/endotoxin translocation and decreased systemic endotoxin level; inhibition of the production and release of TNFα; improved circulatory function; improved systemic host defenses and maintenance of intestinal mucosa barrier.展开更多
文摘AIM: To investigate the therapeutic effects of recombinant human growth hormone (rhGH) on rat septic shock with intraabdominal infection by E. coli and its possible mechanism. METHODS: 76 SD rats were divided into 3 groups randomly:control group (group C, n=16) without any special treatnent,of E. coli(1×1010 cfu@ L-1,15 ml@kg-1, ip), treated group (group by rhGH injection (2.25 U@kg-1@d-1, im). Group S and group T were further divided into 1d and 3d subgroups, respectively (n=15 each). Mean arterial pressure (MAP), levels of plasma TNFα and endotoxin and leukocyte count were determined on 1st day and 3rd day after E. coli injection. Another 39 SD rats were divided into groups C, S and T (n=13 each) just for observing survival rate within 1 week.RESULTS: (1) On 1st and 3rd day, MAP in group S decreased markedly, and MAP on 1st day lowered more than that of 3rd day (P＜0.01), while MAP in group T just decreased slightly. The survival rate within 1 week was much higher in group T (84.6 %) than in group S (46.2 %) (P＜0.01). (2)On 1st day, plasma TNFα and endotoxin elevated significantly in group S and group T (P＜0.05), and endotoxin in group S had more increase (P＜0.01). On 3rd day, TNFα in group S returned to the level of group C (P＞0.05),while TNFα in group T went down below the level of group C(P＜0.01). On 3rd day, endotoxin in group S declined, but was still higher than that of group C (P＜0.01), endotoxin in group T returned to the level of group C (P＞0.05). (3) On 1st day, neutrophil ratio in total leukocyte count in both group S and group T increased significantly (P＜0.05 vs group C).CONCLUSION: rhGH showed beneficial effects on rat septic shock. The possible mechanisms may involve the attenuation of bacteria/endotoxin translocation and decreased systemic endotoxin level; inhibition of the production and release of TNFα; improved circulatory function; improved systemic host defenses and maintenance of intestinal mucosa barrier.
