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目的:观察老年脑梗死患者神经肽Y、降钙素基因相关肽(calcitoningene-relatedpeptide,CGRP)水平改变及其动态变化,探讨神经肽Y、CGRP参与老年脑梗死的病理生理机制及其临床意义。方法:选择老年脑梗死患者42例,依病情轻重分为轻型12例,中型18例,重型12例。依病灶大小分为大灶组22例,小灶组20例。按病程分为≤24h组19例,1～3d组22例、4～7d组27例、8～15d组21例及>15d组18例。按伴发病积分分为<6分组25例与≥6分组17例。按有无高血压史分为有高血压史组18例与无高血压史组24例。选择30例健康老人查体者作为对照组。用放免法检测血浆神经肽Y与CGRP浓度。结果:神经肽Y的变化:老年脑梗死组神经肽Y水平犤(590.66±305.45)ng/L犦显著高于对照组犤(114.76±65.92)ng/L犦(t=5.2846,P<0.0001),于发病后24h内犤(439.13±237.80)ng/L犦显著升高,1～3d犤(668.54±261.44)ng/L犦达高峰,8～15d犤(528.59±215.67)ng/L犦开始下降,15d犤(372.80±200.96)ng/L犦后仍在较高水平;重型犤(698.96±206.85)ng/L犦与大灶组犤(769.61±296.48)ng/L犦显著高于轻型犤(488.60±201.75)ng/L犦与小灶组犤(483.40±312.31)ng/L犦(P<0.01),发病积分≥6分组犤(631.28±286.86)ng/L犦显著高于<6分组犤(573.35±337.64)ng/L犦(t=2.9687,P<0.
OBJECTIVE: To observe the changes of neuropeptide Y and calcitonin gene-related peptide (CGRP) levels and their dynamic changes in elderly patients with cerebral infarction and to explore the pathophysiological mechanism of neuropeptide Y and CGRP involved in senile cerebral infarction and its clinical significance. Methods: Forty-two elderly patients with cerebral infarction were selected according to the severity of their illness. They were divided into 12 cases of light, 18 cases of medium and 12 cases of heavy. Divided according to the size of the lesion into a large group of 22 cases, small group of 20 cases. According to the course of disease, there were 19 cases in ≤24h group, 22 cases in 1-3 days group, 27 cases in 4-7 days group, 21 cases in 8-15 days group and 18 cases in> 15 days group. According to the disease points were divided into <6 group of 25 cases and> 6 group of 17 cases. According to whether the history of hypertension is divided into 18 cases of history of hypertension and no history of hypertension in 24 cases. Thirty healthy people were selected as the control group. Radioimmunoassay was used to detect plasma neuropeptide Y and CGRP concentrations. Results: The changes of neuropeptide Y: The level of neuropeptide Y in elderly cerebral infarction group (590.66 ± 305.45 ng / L) was significantly higher than that in control group (114.76 ± 65.92) ng / L 犦 (t = 5.2846, P <0.0001) (439.13 ± 237.80) ng / L 犦 increased significantly at 24h after onset, peaked at 1 ~ 3d 犤 (668.54 ± 261.44) ng / L, reached the peak, and reached peak at 8 ~ 15d 犤 (528.59 ± 215.67) ng / L 犦(372.80 ± 200.96) ng / L 仍, but the levels of heavy 犤 (698.96 ± 206.85) ng / L 犦 and 灶 组 犤 (769.61 ± 296.48) ng / L 犦 were significantly higher than those of the light 犤(483.40 ± 312.31) ng / L 犦 (P <0.01), and the incidence of disease score≥6 group 犤 (631.28 ± 286.86) ng / L 犦 was significantly higher than that of <6 group 48 (488.60 ± 201.75) ng / 573.35 ± 337.64) ng / L 犦 (t = 2.9687, P <0.