CAJ | 학술논문

目的:比较吲达帕胺和缬沙坦治疗对高血压病患者外周血中细胞因子单核细胞趋化因子-1(MCP-1)、巨噬细胞炎性蛋白1α(MIP-1α)、可溶性P选择素(sP-selectin)、非对称二甲基精氨酸(ADMA)、血管紧张素Ⅱ(AngⅡ)和6-酮-PGF1α(6-keto-PGF1α)的影响. 方法:选取我院门诊健康体检者20例和41例原发性高血压患者,将41例高血压患者随机分为吲哒啪胺组(20例)和缬沙坦组(21例),分别予吲哒啪胺(商品名钠催离)1.5mg/d和缬沙坦(商品名代文)80mg/d治疗4周,治疗前和治疗4周后抽血检测MCP-1, MIP-1α, sP-selectin, ADMA, AngⅡ和6-keto-PGF1α含量.结果:同正常血压组相比,高血压病患者外周血中MCP-1, MIP-1α, sP-selectin,ADMA浓度显著增加.吲哒啪胺组治疗前后MCP-1, MIP-1α和sP-selectin浓度无明显变化;而缬沙坦治疗4周后,MCP-1, MIP-1α和sP-selectin浓度与治疗前相比均显著下降[分别为(19.16±3.11)pg/mL vs (16.08±2.67)pg/mL, P＜0.05; (27.74±8.36)pg/mL vs (17.64±7.59)pg/mL, P＜0.05; (2.67±3.18)pg/mL vs (6.15±2.94)pg/mL, P＜0.01].吲达帕胺和缬沙坦治疗后,ADMA浓度均下降[分别为(1.35±0.74)μmol/L vs (0.98±0.56) μmol/L, P＜0.05; (1.31±0.68)μmol/L vs (0.71±0.52)μmol/L, P＜0.01],而6-keto-PGF1α浓度增加,但在缬沙坦组增高更加显著[分别为(61.96±20.81)pg/mL vs (96.72±25.89)pg/mL, P＜0.05; (63.25±16.92)pg/mL vs (143.22±43.45)pg/mL, P＜0.01].两组治疗前后AngⅡ无显著变化. 结论:轻中度高血压病患者外周血中细胞因子MCP-1,MIP-1α,sP-selectin和ADMA的浓度增加;缬沙坦和吲哒啪胺具有相似的降压疗效,同时还可降低上述细胞因子水平.
목적:비교신체파알화힐사탄치료대고혈압병환자외주혈중세포인자단핵세포추화인자-1(MCP-1)、거서세포염성단백1α(MIP-1α)、가용성P선택소(sP-selectin)、비대칭이갑기정안산(ADMA)、혈관긴장소Ⅱ(AngⅡ)화6-동-PGF1α(6-keto-PGF1α)적영향. 방법:선취아원문진건강체검자20례화41례원발성고혈압환자,장41례고혈압환자수궤분위신달박알조(20례)화힐사탄조(21례),분별여신달박알(상품명납최리)1.5mg/d화힐사탄(상품명대문)80mg/d치료4주,치료전화치료4주후추혈검측MCP-1, MIP-1α, sP-selectin, ADMA, AngⅡ화6-keto-PGF1α함량.결과:동정상혈압조상비,고혈압병환자외주혈중MCP-1, MIP-1α, sP-selectin,ADMA농도현저증가.신달박알조치료전후MCP-1, MIP-1α화sP-selectin농도무명현변화;이힐사탄치료4주후,MCP-1, MIP-1α화sP-selectin농도여치료전상비균현저하강[분별위(19.16±3.11)pg/mL vs (16.08±2.67)pg/mL, P＜0.05; (27.74±8.36)pg/mL vs (17.64±7.59)pg/mL, P＜0.05; (2.67±3.18)pg/mL vs (6.15±2.94)pg/mL, P＜0.01].신체파알화힐사탄치료후,ADMA농도균하강[분별위(1.35±0.74)μmol/L vs (0.98±0.56) μmol/L, P＜0.05; (1.31±0.68)μmol/L vs (0.71±0.52)μmol/L, P＜0.01],이6-keto-PGF1α농도증가,단재힐사탄조증고경가현저[분별위(61.96±20.81)pg/mL vs (96.72±25.89)pg/mL, P＜0.05; (63.25±16.92)pg/mL vs (143.22±43.45)pg/mL, P＜0.01].량조치료전후AngⅡ무현저변화. 결론:경중도고혈압병환자외주혈중세포인자MCP-1,MIP-1α,sP-selectin화ADMA적농도증가;힐사탄화신달박알구유상사적강압료효,동시환가강저상술세포인자수평.
Objective To investigate and compare the effect of valsartan and indapamide on inflammatory cytokines in hypertension. Methods Forty-one untreated patients with mild to moderate hypertension and 20 age- and sex-matched normotensives were enrolled in this study. Hypertensives were treated with indapamide 1.5 mg/d (n=20) or valsartan 80 mg/d (n=21) for 4 weeks, and blood samples for determining monocyte chemotactic protein-1 (MCP-1), macrophage inflammatory protein-1 (MIP-1α), sP-selectin, asymmetric dimethylarginin (ADMA), angiotensin Ⅱ (AngⅡ), and 6-keto-PGF1α were collected before the treatment and 4 weeks after the treatment. Results Hypertensives exhibited significantly higher blood pressure, as well as elevated plasma levels of MCP-1, MIP-1α, sP-selectin and serum level of ADMA compared with the normotensives. Nevertheless, there was no significant difference in serum 6-keto-PGF1α and AngⅡ between the hypertensives and the normotensives. After the treatment with indapamide or valsartan for 4 weeks, both the systolic and diastolic blood pressures, though still higher than those of the normotensives, decreased markedly. After the treatment with indapamide for 4 weeks, MCP-1, MIP-1α and sP-selectin slightly decreased, but not statistically significant (P＞0.05). Those cytokines decreased significantly after being treated with valsartan for 4 weeks [(19.16±3.11) pg/mL vs (16.08±2.67) pg/mL, P＜0.05; (27.74±8.36) pg/mL vs (17.64±7.59) pg/mL, P＜0.05; (2.67±3.18) pg/mL vs (6.15±2.94) pg/mL, P＜0.01]. In the 2 treatment groups, 6-keto-PGF1α markedly increased [(61.96±20.81) pg/mL vs (96.72±25.89) pg/mL, P＜0.05; (63.25±16.92) pg/mL vs (143.22±43.45) pg/mL, P＜0.01]; ADMA decreased significantly [(1.35±0.74) pg/mL vs (0.98±0.56) μmol/L, P＜0.05; (1.31±0.68) pg/mL vs (0.71±0.52) μmol/L, P＜0.01]. Though AngⅡ slightly increased, no statistical significance was found (P＞0.05). Conclusion The levels of MCP-1, MIP-1α, sP-selectin and ADMA were elevated in mild to moderate hypertensives. Valsartan and indapamide have similar blood pressure lowering effect. Valasartan exerts more significant effect on cytokines than indapamide does.