[Effect of hydroxyethyl starch on vascular reactivity of rat during hemorrhagic shock].
Zhibin Zhao, Ying Chen, Xinyue Gao, Zeng Yin-ming
Abstract
Zhibin Zhao, Ying Chen, Xinyue Gao, Zeng Yin-ming
Abstract
OBJECTIVE: To study the effect of hydroxyethyl starch (HES) on vascular reactivity of rat during hemorrhagic shock and its mechanism. METHODS: Forty SD rats were randomly divided into 5 groups: normal control group, shock group, sodium chloride (SC) group, HES 130/0.4 group and HES 200/0.5 group with 8 rats in each group. Rats were hemorrhaged and maintained mean arterial pressure (MAP) at 40 mm Hg (1 mm Hg=0.133 kPa) for 30 minutes, then rats were infused with fluids to restore and maintain MAP at 70 mm Hg for 60 minutes. The infusion volumes of each fluid to maintain MAP were recorded. The responses of MAP to norepinephrine (NE) were measured before shock, at 30, 60 and 90 minutes during hemorrhagic shock. Concentrations of nitric oxide (NO) and nitric oxide synthase (NOS) of plasma were measured at 90 minutes during hemorrhagic shock. RESULTS: The infusion volumes of each fluid to maintain MAP were significantly different (all P<0.01). HES 200/0.5 group<HES 130/0.4 group<SC group. In HES 130/0.4 group and HES 200/0.5 group at 90 minutes during hemorrhagic shock, the responses of MAP to NE were improved significantly compared with those of SC group (both P<0.05), plasma contents of NO and NOS were reduced markedly compared with those of SC group (P<0.05 or P<0.01). CONCLUSION: HES can improve vascular reactivity during hemorrhagic shock by inhibiting plasma contents of NO and NOS.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
OBJECTIVE: To study the effect of hydroxyethyl starch (HES) on vascular reactivity of rat during hemorrhagic shock and its mechanism. METHODS: Forty SD rats were randomly divided into 5 groups: normal control group, shock group, sodium chloride (SC) group, HES 130/0.4 group and HES 200/0.5 group with 8 rats in each group. Rats were hemorrhaged and maintained mean arterial pressure (MAP) at 40 mm Hg (1 mm Hg=0.133 kPa) for 30 minutes, then rats were infused with fluids to restore and maintain MAP at 70 mm Hg for 60 minutes. The infusion volumes of each fluid to maintain MAP were recorded. The responses of MAP to norepinephrine (NE) were measured before shock, at 30, 60 and 90 minutes during hemorrhagic shock. Concentrations of nitric oxide (NO) and nitric oxide synthase (NOS) of plasma were measured at 90 minutes during hemorrhagic shock. RESULTS: The infusion volumes of each fluid to maintain MAP were significantly different (all P<0.01). HES 200/0.5 group<HES 130/0.4 group<SC group. In HES 130/0.4 group and HES 200/0.5 group at 90 minutes during hemorrhagic shock, the responses of MAP to NE were improved significantly compared with those of SC group (both P<0.05), plasma contents of NO and NOS were reduced markedly compared with those of SC group (P<0.05 or P<0.01). CONCLUSION: HES can improve vascular reactivity during hemorrhagic shock by inhibiting plasma contents of NO and NOS.
Key concepts: Hydroxyethyl starch, Medicine, Shock (circulatory), Mean arterial pressure, Norepinephrine, Hemorrhagic shock, Nitric oxide synthase, Nitric oxide