2006PubMedRequires access

[Dipyridamole preconditioning protects against ischemia/reperfusion injury of rat liver].

Yong Hong, Wensheng Liao, Rui-xiang Mo

Open publisher page 5 citations

Abstract

OBJECTIVE: To investigate the protective mechanism of dipyridamole preconditioning against hepatic ischemia/reperfusion injury. METHODS: Thirty SD rats were randomly divided into normal control group, ischemia/reperfusion group, and dipyridamole group, with 10 rats in each group. Using 45-minute ischemia/reperfusion rat model at normal temperature, 10 mg/kg of dipyridamole normal saline were injected into portal vein before ischemia. Only normal saline was injected in the ischemia/reperfusion group. An hour later, blood was obtained from the portal vein to determine the enzyme levels, including alanine aminotransferase (ALT) , lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-alpha), and endothelin-1 (ET-1). The alteration in pathological morphology of the ischemia lobe was observed. The content of adenosine phosphates in the liver was determined. RESULTS: The ALT and LDH activity, TNF-alpha, ET-1 levels were significantly higher in the ischemia/reperfusion group than those in the control group (all P<0.01). The levels of these variables were much lower in the dipyridamole group than those of the ischemia/reperfusion group (P<0.01), but little higher than those of the control group (P>0.05). The adenosine phosphates levels of ischemia/reperfusion group were significantly lower than those of the control group (P<0.01). They were much higher in the dipyridamole group than those of the ischemia/reperfusion group (P<0.01), but little higher than those of the control group (P>0.05). The control group had obvious alteration in pathological morphology, but only slight alteration was found in dipyridamole group, compared with control group. CONCLUSION: Dipyridamole preconditioning protects against ischemia/reperfusion injury of the liver.

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OBJECTIVE: To investigate the protective mechanism of dipyridamole preconditioning against hepatic ischemia/reperfusion injury. METHODS: Thirty SD rats were randomly divided into normal control group, ischemia/reperfusion group, and dipyridamole group, with 10 rats in each group. Using 45-minute ischemia/reperfusion rat model at normal temperature, 10 mg/kg of dipyridamole normal saline were injected into portal vein before ischemia. Only normal saline was injected in the ischemia/reperfusion group. An hour later, blood was obtained from the portal vein to determine the enzyme levels, including alanine aminotransferase (ALT) , lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-alpha), and endothelin-1 (ET-1). The alteration in pathological morphology of the ischemia lobe was observed. The content of adenosine phosphates in the liver was determined. RESULTS: The ALT and LDH activity, TNF-alpha, ET-1 levels were significantly higher in the ischemia/reperfusion group than those in the control group (all P<0.01). The levels of these variables were much lower in the dipyridamole group than those of the ischemia/reperfusion group (P<0.01), but little higher than those of the control group (P>0.05). The adenosine phosphates levels of ischemia/reperfusion group were significantly lower than those of the control group (P<0.01). They were much higher in the dipyridamole group than those of the ischemia/reperfusion group (P<0.01), but little higher than those of the control group (P>0.05). The control group had obvious alteration in pathological morphology, but only slight alteration was found in dipyridamole group, compared with control group. CONCLUSION: Dipyridamole preconditioning protects against ischemia/reperfusion injury of the liver.

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Available abstract

OBJECTIVE: To investigate the protective mechanism of dipyridamole preconditioning against hepatic ischemia/reperfusion injury. METHODS: Thirty SD rats were randomly divided into normal control group, ischemia/reperfusion group, and dipyridamole group, with 10 rats in each group. Using 45-minute ischemia/reperfusion rat model at normal temperature, 10 mg/kg of dipyridamole normal saline were injected into portal vein before ischemia. Only normal saline was injected in the ischemia/reperfusion group. An hour later, blood was obtained from the portal vein to determine the enzyme levels, including alanine aminotransferase (ALT) , lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-alpha), and endothelin-1 (ET-1). The alteration in pathological morphology of the ischemia lobe was observed. The content of adenosine phosphates in the liver was determined. RESULTS: The ALT and LDH activity, TNF-alpha, ET-1 levels were significantly higher in the ischemia/reperfusion group than those in the control group (all P<0.01). The levels of these variables were much lower in the dipyridamole group than those of the ischemia/reperfusion group (P<0.01), but little higher than those of the control group (P>0.05). The adenosine phosphates levels of ischemia/reperfusion group were significantly lower than those of the control group (P<0.01). They were much higher in the dipyridamole group than those of the ischemia/reperfusion group (P<0.01), but little higher than those of the control group (P>0.05). The control group had obvious alteration in pathological morphology, but only slight alteration was found in dipyridamole group, compared with control group. CONCLUSION: Dipyridamole preconditioning protects against ischemia/reperfusion injury of the liver.

Key concepts: Medicine, Ischemia, Dipyridamole, Reperfusion injury, Lactate dehydrogenase, Adenosine, Saline, Internal medicine

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