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1.
Chinese Journal of Cerebrovascular Diseases ; (12): 78-82, 2015.
Article in Chinese | WPRIM | ID: wpr-462043

ABSTRACT

Objective To investigate the effect of arterial and venous subarachnoid hemorrhage ( SAH)on voltage-dependent calcium channel( VDCC)currents of cerebral artery smooth muscle cells and the relationship between the concentration of oxyhemoglobin( OxyHb)in arterial and venous blood and cerebral blood flow. Methods Thirty-six clean grade rats were colleted. A rat SAH model was induced by injection of autologous arterial or venous blood in suprasellar cistern using assisted stereotaxic apparatus. The rats were divided into three groups:an arterial SAH( n=14 ),a venous SAH( n=13 ),and a sham operation( n=9 )group. The arterial and venous OxyHb concentrations were measured. Three days after SAH modeling,a patch clamp was used to detect the relative surface area of the cerebral artery smooth muscle cells,resting potential,and VDCC currents in rats. A fluorescent microsphere method was used to quantitatively analyze cerebral blood flow(CBF). Results (1)Arterial SAH OxyHb concentration (127 ± 4 g/L)was significantly higher than venous SAH OxyHb concentration(54 ± 6 g/L),and that of the sham operation group was 50 ± 5 g/L. The differences were statistically significant among the 3 groups( P<0. 01).(2)The maximum current of VDCC of the arterial SAH group(3. 22 ± 0. 31 pA)was significantly higher than that of the venous SAH group(2. 19 ± 0. 27 pA)and the sham operation group(2. 18 ± 0. 29 pA). The differences were statistically significant among the 3 groups( P<0. 01 ). The VDCC currents of the arterial SAH group were consisted of L- and R-currents,while the currents of the venous SAH group were only consisted of L-VDCC.(3)The cerebral blood flow of the arterial SAH group(0. 83 ± 0. 14 mL/[g·min])was significantly higher than that of the venous SAH group(1. 28 ± 0. 28 mL/[g·min])and the sham operation group(1. 35 ± 0. 19 mL/[g·min]). The differences were statistically significant(P<0. 01). Conclusions The changing effect of arterial SAH on the expression and function of the cerebral artery smooth muscle cells are greater than that of the venous SAH. This difference may be associated with the concentration and composition of vasospasm factors of OxyHb in arterial and venous blood.

2.
Chinese Journal of Neurology ; (12): 871-875, 2014.
Article in Chinese | WPRIM | ID: wpr-469046

ABSTRACT

Objective To study the effect of subarachnoid hemorrhage (SAH) on voltagedependent potassium channels (Kv) currents of smooth muscle cells,which is hypothesized to be different between cerebral pial arteries and penetrating arteries.Methods Smooth muscle cells from cerebral pial arteries and penetrating arteries in rats were enzymatically isolated 72 h after SAH,and patch clamp was used to test the relative cell size,resting potential and Kv currents.Results Resting potential of either pial ((45.63 ±1.18) mV) or penetrating artery ((41.55-± 1.19) mV) was shifted positively by SAH,even more significantly in latter (F =8.24,P < 0.05 ; F =9.36,P < 0.01) ; Resting potential of pial artery of control ((38.76 ± 1.03) mV),penetrating artery of control ((38.53 ± 0.67) mV),pial artery of SAH ((36.87 ± 1.49) mV) and penetrating artery of SAH((37.89 ± 1.24) mV) were shifted positively to the same level by 1 μmol/L 4-aminopyridine (4AP; F =3.08,P >0.05).Maximum Current Density (Imax) of either pial ((20.82 ±0.59) pA/pF) or penetrating artery ((15.15 ±0.37) pA/pF) was compromised by SAH,also more significantly in latter (F =6.22,P < 0.05) ; Imax of pial artery of control (9.15 ± 0.16),penetrating artery of control (9.04 ± 0.36),pial artery of SAH (8.77 ± 0.26) and penetrating artery of SAH (9.12 ± 0.17) were decreased to the same level by 1 μmol/L 4AP (F =2.96,P > 0.05).Conclusions SAH probably shares the similar pathway with Kv blocker (4AP) in Kv currents inhibition.Further,SAH differently inhibits smooth muscle cells Kv currents and resting potential of cerebral pial arteries and penetrating arteries,which may be related with their different sensitivity towards cerebral vasospasm following SAH.

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