论文部分内容阅读
用脊髓 (T8)中间外侧柱 (IML)微透析方法结合高效液相色谱 (HPLC)技术 ,研究延髓头端腹外侧区(RVLM)微量注射血管紧张素Ⅱ (ANGⅡ ,10 0pmol,n =11)后脊髓IML氨基酸递质释放的变化。在RVLM区微量注射ANGⅡ ( 10 0pmol,n =11) ,能显著增加 (P <0 0 1)脊髓 (T8)内天门冬氨酸 (ASP ,从 4 75± 1 0 1升至 8 90± 2 2 8pmol/2 0 μl)和谷氨酸 (GLU ,从 18 99± 8 64升至 73 88± 2 9 2 6pmol/2 0 μl)的释放。在同一RVLM部位注射losartan( 10nmol,n =8)可以显著抑制注射ANGⅡ引起的GLU释放升高反应 (P <0 0 5 )。免疫荧光双标记结合共聚焦显微镜观察到RVLM内 62 %～ 91%的谷氨酸能神经元呈AT1受体免疫阳性。此结果提示ANGⅡ诱发的脊髓内谷氨酸释放可能来源于RVLM内AT1受体免疫阳性的谷氨酸能脊髓投射神经元。
Microinjection of angiotensin Ⅱ (ANGⅡ, 10 0 pmol, n = 11) into the rostral ventrolateral medulla (RVLM) was performed by microdialysis of the medial lateral column of spinal cord (T8) combined with high performance liquid chromatography Post-spinal cord IML amino acid transmitter release changes. Microinjection of ANGⅡ into the RVLM zone (10 0 pmol, n = 11) significantly increased (P <0.01) ASP in the spinal cord (T8) from 4 75 ± 1 0 1 to 8 90 ± 2 2 8 pmol / 2 μl) and glutamic acid (GLU, from 18 99 ± 8 64 to 73 88 ± 2962 pmol / 2 μl). Injection of losartan (10 nmol, n = 8) in the same RVLM site significantly inhibited the release of GLU induced by angiotensin Ⅱ (P <0 05). Immunofluorescence double labeling combined with confocal microscopy showed that 62% ~ 91% of glutamatergic neurons in RVLM were AT1 receptor immunopositive. The results suggest that ANG Ⅱ -induced glutamate release from the spinal cord may originate from the AT1 receptor-immunoreactive glutamatergic neurons in the RVLM.