ArticleInternational journal of clinical and experimental medicine2015
Effect of subarachnoid hemorrhage on voltage-dependence calcium channel current in cerebral artery smooth muscle cells.
Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 authors at 1 institution in 1 country.
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Abstract
objectiveTo investigate the effect of subarachnoid hemorrhage (SAH) on voltage-dependent calcium channel (VDCC) current in cerebral artery smooth muscle cells (SMCs), oxyhemoglobins (OxyHb) concentration and vasospasm.
methodThirty-six clean SD rats were used to establish SAH model by injecting autologous arterial blood into suprasellar cistern with the aid of stereotaxic instrument. They were divided into arterial SAH group (14 rats), venous SAH group (13 rats) and sham operation group (9 rats), and OxyHb concentrations were measured in the first two groups. Relative membrane surface area of cerebral artery SMCs, resting potential and VDCC current were measured using a patch clamp at day 3 after modeling; cerebral blood flow (CBF) was measured by using fluorescent microsphere-based lateral flow assay.
resultsOxyHb concentration of arterial SAH group (127±4 g/L) was higher than that of venous SAH group (54±6 g/L) and sham operation group (50±5 g/L), with significant difference (P<0.05); The maximum VDCC current (3.22±0.31 pA/pF) of the arterial SAH group was obviously higher than that of venous SAH group (2.19±0.27 pA/pF) and sham operation group (2.18±0.29 pA/pF), also showing a significant difference (P<0.05). For arterial SAH group, VDCC current consisted of L- and R-type calcium current, and for venous SAH group the VDCC current consisted of L-type calcium current; CBF of arterial SAH group (0.83±0.14 ml/g/min) was significantly higher than that of venous SAH group (1.28±0.28 ml/g/min) and sham operation group (1.35±0.19 ml/g/min) (P<0.05).
conclusionThe effect of arterial SAH was greater on the expression and function of VDCCs in cerebral artery SMCs than venous SAH. This may be explained by the differences in the concentration and composition of pathogenic agents for vasospasm in the arterial and venous blood, such as OxyHb.
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26550294PMC4612979W2150750992What OpenQuestion holds
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