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[L-arginine pretreatment lowers cerebral metabolism for cerebral protection during deep hypothermic circulatory arrest].

Yong Gao, Xiao-Ming Zou, Wujun Wang

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Abstract

OBJECTIVE: To evaluate the effect of L-arginine pretreatment on cerebral metabolism for cerebral protection during deep hypothermic circulatory arrest (DHCA). METHODS: Fifteen healthy adult canines of either sex weighing 14.7-/+2.4 kg were randomly divided into 3 groups (n=5), namely the normal saline group, L-arginine pretreatment group (pretreated with 100 mg/kg L-arginine 60 min before DHCA), and L-arginine combined with 7- nitroindazole treatment group (pretreated with 100 mg/kg L-arginine and 25 mg/kg7-Ni 60 min before DHCA). For all the canines, extracorporeal circulation was established routinely to allow nasopharyngeal temperature reduction to 18 degrees celsius;, at which point DHCA commenced followed 90 min later by reperfusion. At 30 min before DHCA and 0, 45 and 90 min after DHCA as well as at 60 min after reperfusion initiation, blood samples were collected from the jugular vein and arterial to measure the plasma lactic acid, and the cerebral cortex of the parietal lobe was sampled determine the activity of Na(+)-K(+)ATPase. The cerebral water content was also determined after execution of the canines. RESULTS: In the two pretreatment groups, the level of lactic acid production (shown by the difference in lactic acid levels between the jugular venous and arterial blood) and the cerebral ATP consumption were similar (P>0.05), but both were significantly lower than those of the control group (P<0.05). The cerebral water content was the lowest in the combined treatment group, followed by exclusive L-arginine group, and the highest in the control group (P<0.05), with significant difference between the 3 groups (P<0.05). CONCLUSION: L-arginine pretreatment can lower cerebral metabolism during DHCA to offer protective effect on the brain.

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OBJECTIVE: To evaluate the effect of L-arginine pretreatment on cerebral metabolism for cerebral protection during deep hypothermic circulatory arrest (DHCA). METHODS: Fifteen healthy adult canines of either sex weighing 14.7-/+2.4 kg were randomly divided into 3 groups (n=5), namely the normal saline group, L-arginine pretreatment group (pretreated with 100 mg/kg L-arginine 60 min before DHCA), and L-arginine combined with 7- nitroindazole treatment group (pretreated with 100 mg/kg L-arginine and 25 mg/kg7-Ni 60 min before DHCA). For all the canines, extracorporeal circulation was established routinely to allow nasopharyngeal temperature reduction to 18 degrees celsius;, at which point DHCA commenced followed 90 min later by reperfusion. At 30 min before DHCA and 0, 45 and 90 min after DHCA as well as at 60 min after reperfusion initiation, blood samples were collected from the jugular vein and arterial to measure the plasma lactic acid, and the cerebral cortex of the parietal lobe was sampled determine the activity of Na(+)-K(+)ATPase. The cerebral water content was also determined after execution of the canines. RESULTS: In the two pretreatment groups, the level of lactic acid production (shown by the difference in lactic acid levels between the jugular venous and arterial blood) and the cerebral ATP consumption were similar (P>0.05), but both were significantly lower than those of the control group (P<0.05). The cerebral water content was the lowest in the combined treatment group, followed by exclusive L-arginine group, and the highest in the control group (P<0.05), with significant difference between the 3 groups (P<0.05). CONCLUSION: L-arginine pretreatment can lower cerebral metabolism during DHCA to offer protective effect on the brain.

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Available abstract

OBJECTIVE: To evaluate the effect of L-arginine pretreatment on cerebral metabolism for cerebral protection during deep hypothermic circulatory arrest (DHCA). METHODS: Fifteen healthy adult canines of either sex weighing 14.7-/+2.4 kg were randomly divided into 3 groups (n=5), namely the normal saline group, L-arginine pretreatment group (pretreated with 100 mg/kg L-arginine 60 min before DHCA), and L-arginine combined with 7- nitroindazole treatment group (pretreated with 100 mg/kg L-arginine and 25 mg/kg7-Ni 60 min before DHCA). For all the canines, extracorporeal circulation was established routinely to allow nasopharyngeal temperature reduction to 18 degrees celsius;, at which point DHCA commenced followed 90 min later by reperfusion. At 30 min before DHCA and 0, 45 and 90 min after DHCA as well as at 60 min after reperfusion initiation, blood samples were collected from the jugular vein and arterial to measure the plasma lactic acid, and the cerebral cortex of the parietal lobe was sampled determine the activity of Na(+)-K(+)ATPase. The cerebral water content was also determined after execution of the canines. RESULTS: In the two pretreatment groups, the level of lactic acid production (shown by the difference in lactic acid levels between the jugular venous and arterial blood) and the cerebral ATP consumption were similar (P>0.05), but both were significantly lower than those of the control group (P<0.05). The cerebral water content was the lowest in the combined treatment group, followed by exclusive L-arginine group, and the highest in the control group (P<0.05), with significant difference between the 3 groups (P<0.05). CONCLUSION: L-arginine pretreatment can lower cerebral metabolism during DHCA to offer protective effect on the brain.

Key concepts: Deep hypothermic circulatory arrest, Extracorporeal circulation, Anesthesia, Lactic acid, Arginine, Jugular vein, Circulatory system, Medicine

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