老年脑梗死患者血浆神经肽Y、降钙素基因相关肽水平的动态变化

Dynamic changes of levels of neuropeptide Y and calcitonin gene-related peptide in plasma of elderly patients with cerebral infarction

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.

AIM: To observe the changes and dynamic changes of plasma levels of neuropeptide Y and calcitonin gene-related peptide(CGTP) in elderly patients with cerebral infarction(CI), and investigate the pathophysiological mechanism and clinical significance of neuropeptide Y and CGRP in elderly CI. METHODS: Forty-two elderly CI patients were involved in the study. They were divided into mild CI group(n=12), moderate CI group(n=18) and severe CI group(n=12) according to their severities of CI; into large focal size group(n=22) and small focal size group(n=20) according to their focal size; into ≤24 hours group(n=19), 1 to 3 days group(n=22), 4 to 7 days group (n=27), 8 to 15 days group(n=21) and >15 days group(n=18) according to their disease course; into < 6 group(n=25) and ≥6 group(n=17) according to their episode score; into hypertension history group(n=18) and non-hypertension group(n=24) according to whether they had the history of hypertension or not. Another 30 healthy elderly subjects were taken as the controls. The plasma levels of neuropeptide Y and CGRP were measured by radioimmunoassay. RESULTS: The plasma level of neuropeptide Y in the elderly CI group [(590.66±305.45) ng/L]was significantly higher than that in the control group [(114.76±65.92) ng/L] (t=5.284 6, P< 0.000 1).It started to increase significantly during the 24 hours [(439.13±237.80) ng/L], and reached the peak value at 1 to 3 days [(668.54±261.44) ng/L], and it began to decrease at 8 to 15 days [(528.59±215.67)] ng/L, and was still higher after 15 days [(372.80±200.96) ng/L]. The plasma levels of neuropeptide Y in the severe CI group[(698.96±206.85) ng/L ]and large focal size group [(769.61±296.48) ng/L] were significantly higher than those in the mild CI group [(488.60±201.75) ng/L] and small focal size group[(483.40±312.31) ng/L](P< 0.01); It was higher in the≥6 scores groups[(631.28±286.86) ng/L] than in the < 6 scores group [(573.35±337.64) ng/L](t=2.968 7, P< 0.01), higher in the hypertension group [(697.37±310.33) ng/L] than in the normal blood pressure group [(457.24±239.91) ng/L](t=3.612 5, P< 0.01). The plasma level of CGRP in the elderly CI group [(170.16±95.48) ng/L] was significantly lower than that in the control group [(335.70±198.38) ng/L](t=4.120 9, P< 0.000 1); It started to decrease significantly during the 24 hours after episode [(86.58±22.74) ng/L] and decreased further at 1 to 3 days [(42.66±20.01) ng/L] and 4 to 7 days [(79.01±29.44) ng/L], it began to increase 8 to 15at days [(211.37±115.98) ng/L], and increased to the normal level after 15 days[(319.67±152.35) ng/L]. The plasma levels of CGRP in the severe CI group [(44.79±23..43) ng/L] and large focal size group [(98.66±68.16) ng/L] were significantly lower than those in the mild CI group [(356.86±209.61) ng/L] and small focal size group [(241.19±124.48) ng/L] (P< 0.001); It was lower in the ≥6 scores group [(80.41±48.26) ng/L] than in the < 6 scores group [(246.57±126.37) ng/L](t=3.549 1, P< 0.001); lower in the hypertension group [(163.36±79.09) ng/L]than in the normal blood pressure group [(91.41±47.46) ng/L](t=3.967 1, P< 0.01). CONCLUSION: The abnormal secretion of neuropeptide Y and CGRP play a major role in the pathophysiological mechanisms of elderly cerebral infarction.