CAJ | 학술논문

目的：观察自发性蛛网膜下隙出血（SAH）后血浆、脑脊液一氧化氮和一氧化氮合成酶（NOS）含量和颅内压的动态变化，以及尼莫地平治疗后对其的影响。方法收集68例自发性SAH 患者，根据其治疗方式分为常规治疗组（30例）和尼莫地平组（在常规治疗基础上加用尼莫地平1 mg／h 维持14 d，38例）。在发病后不同时点动态观察患者血浆和脑脊液的一氧化氮和 NOS 含量，同时观察颅内压的变化。结果自发性 SAH 后尼莫地平组和常规治疗组血浆和脑脊液中一氧化氮和NOS 均出现先下降后升高，但尼莫地平组较常规治疗组更早出现一氧化氮和 NOS 含量的升高（P ＜0.05），且尼莫地平组的颅内压在治疗后7～14日均低于对照组（P 均＜0.05）。结论一氧化氮在NOS 催化下生成并参与了自发性 SAH 后复杂的病理生理过程，尼莫地平能抑制一氧化氮的病理性减少，更早地降低颅内压，可能对减轻病情有积极作用。
목적：관찰자발성주망막하극출혈（SAH）후혈장、뇌척액일양화담화일양화담합성매（NOS）함량화로내압적동태변화，이급니막지평치료후대기적영향。방법수집68례자발성SAH 환자，근거기치료방식분위상규치료조（30례）화니막지평조（재상규치료기출상가용니막지평1 mg／h 유지14 d，38례）。재발병후불동시점동태관찰환자혈장화뇌척액적일양화담화 NOS 함량，동시관찰로내압적변화。결과자발성 SAH 후니막지평조화상규치료조혈장화뇌척액중일양화담화NOS 균출현선하강후승고，단니막지평조교상규치료조경조출현일양화담화 NOS 함량적승고（P ＜0.05），차니막지평조적로내압재치료후7～14일균저우대조조（P 균＜0.05）。결론일양화담재NOS 최화하생성병삼여료자발성 SAH 후복잡적병리생리과정，니막지평능억제일양화담적병이성감소，경조지강저로내압，가능대감경병정유적겁작용。
Objective To observe the effect of nimodipine on dynamic changes of nitric oxide (NO) and nitric oxide synthase (NOS)in plasma and cerebrospinal fluid (CSF),and the variation of intracranial pressure of the patients after spontaneous subarachnoid hemorrhage (SAH)and the variation of intracranial pressure,to evaluate the therapeutic effect of Nimodipine on their changes.Methods Sixty eight cases of the patients with SAH were randomly divided into two groups:routine treatment group (n =30)and nimodipine treatment group (n =38,routine therapy +1 mg/h nimodipine for 1 4 days).The NO and NOS levels in plasma and CSF on different time points,and the variation of intracranial pressure of the patients after SAH were ob-served.Results The NO and NOS levels in plasma and CSF of the patients in two groups are all decreased at the beginning,then increased.But the increase of the NO and NOS levels in plasma and CSF of the patients in nimodipine treatment group was earlier than those of the patients in the routine treatment group.The difference is significant (P <0.05).Conclusions NO is generated under catalysis of NOS and NO and participates in the complex pathologic process of SAH.Nimodipine can exert important therapeutic effects including relieving cerebral angio spasm,down-regulating intracranial pressure at early stage to reduce the risk of delayed cerebral infarction by inhibiting the pathological decrease of NO.