目的观察贝那普利及缬沙坦对大鼠残肾修复过程中Pax-2^+细胞的影响,探讨血管紧张素转化酶抑制剂(ACEI)及血管紧张素1型受体阻断剂(ARB1)非血液动力学肾保护作用的可能机制。方法5/6肾切除术制作SD大鼠残肾模型,术后分别以NS(模型组)、...目的观察贝那普利及缬沙坦对大鼠残肾修复过程中Pax-2^+细胞的影响,探讨血管紧张素转化酶抑制剂(ACEI)及血管紧张素1型受体阻断剂(ARB1)非血液动力学肾保护作用的可能机制。方法5/6肾切除术制作SD大鼠残肾模型,术后分别以NS(模型组)、美托洛尔(普通降压药组)、贝那普利(贝那普利组)及缬沙坦(缬沙坦组)灌胃治疗,定期测血肌酐、尿素氮及24h尿蛋白;于设定时间采集肾脏标本,免疫组化及流式细胞术监测残肾Pax-2^+细胞,流式细胞术分离Pax-2^+细胞;RT-PCR检测Pax-2^+细胞AT1R、AT2R和Pax-2 m RNA表达,Westernblot检测TGF-β1及VEGF表达。结果模型组大鼠术后,残肾Pax-2^+细胞数及Pax-2^+细胞的Pax-2 m RNA的表达量逐渐减低(P<0.05);与模型组比较,贝那普利组及缬沙坦组残肾Day30,Day90 Pax-2^+细胞数及Pax-2^+细胞的Pax-2 m RNA的表达升高(P<0.05),普通降压药组与模型组各期间无统计学差异(P>0.05);贝那普利组及缬沙坦组残肾d90肾小球硬化指数明显低于模型组(P<0.05),普通降压药组及模型组间无统计学差异(P>0.05)。结论 5/6肾切除术后,大鼠残肾Pax-2^+细胞及其Pax-2 mRNA表达逐渐减少,出现肾小球硬化及CRF,ACEI及ARB1对残肾Pax-2^+细胞具有保护作用,这种保护作用可能是其非血液动力学肾保护作用重要机制。展开更多
In this study,we investigated the effect of captopril(CPT) on glomerular filtration rate(GFR),effective renal plasma flow(ERPF),filtration fraction(FF),urinary albumin excretion(UAE) and daily urinary excretion of thr...In this study,we investigated the effect of captopril(CPT) on glomerular filtration rate(GFR),effective renal plasma flow(ERPF),filtration fraction(FF),urinary albumin excretion(UAE) and daily urinary excretion of thromboxane B2(TXB2) and 6-keto-prostaglandin F1a(6-keto-PGFla) in 29 normotensive non-insulin-dependent diabetes(NIDDM) patients without clinically discernible nephropathy.Before treatment,urinary excretion 6-keto-PGF1a was significantly increased(P<0.05) in 29 NIDDM patients compared with 25 health subjects matched for age and sex.The values of GFR and FF were significantly higher(P<0.01 and P<0.005,respectively) in NIDDM than in normal volunters,whereas ERPF was comparable in both groups.Meanwhile we observed that UAE of early NIDDM was increased before treatment.After CPT treatment,GFR,FF,UAE and urinary excretion of 6-keto-PGFla were significantly reduce(all P<0.005) compared with those of NIDDM before treatment. These data indicated that CPT is effective in lowering glomerular filtration pressure and ameliorating microalbuminuria in the normotensive early NIDDM.展开更多
The purpose of this review is to objectively evaluate the biochemical and pathophysiological properties of 0.9% saline （henceforth： saline） and to discuss the impact of saline infusion, specifically on systemic aci...The purpose of this review is to objectively evaluate the biochemical and pathophysiological properties of 0.9% saline （henceforth： saline） and to discuss the impact of saline infusion, specifically on systemic acid-base bal- ance and renal hemodynamics. Studies have shown that electrolyte balance, including effects of saline infusion on serum electrolytes, is often poorly understood among practicing physicians and inappropriate saline prescribing can cause increased morbidity and mortality. Large-volume （〉2 L） saline infusion in healthy adults induces hyperohloremia which is associated with metabolic acidosis, hyperkalemia, and negative protein balance. Saline overload （80 ml/kg） in rodents can cause intestinal edema and contractile dysfunction associated with activation of sodium-proton exchanger （NHE） and decrease in myosin light chain phosphorylation. Saline infusion can also adversely affect renal hemody- namics. Microperfusion experiments and real-time imaging studies have demonstrated a reduction in renal perfusion and an expansion in kidney volume, compromising 02 delivery to the renal perenchyma following saline infusion. Clinically, saline infusion for patients post abdominal and cardiovascular surgery is associated with a greater number of adverse effects including more frequent blood product transfusion and bicarbonate therapy, reduced gastric blood flow, delayed recovery of gut function, impaired cardiac contractility in response to inotropes, prolonged hospital stay, and possibly increased mortality. In critically ill patients, saline infusion, compared to balanced fluid infusions, in- creases the occurrence of acute kidney injury. In summary, saline is a highly acidic fluid. With the exception of saline infusion for patients with hypochloremic metabolic alkalosis and volume depletion due to vomiting or upper gastroin- testinal suction, indiscriminate use, especially for acutely ill patients, may cause unnecessary complications and should be avoided. More education regarding saline-related effects and adequate electrolyte management is needed.展开更多
文摘目的观察贝那普利及缬沙坦对大鼠残肾修复过程中Pax-2^+细胞的影响,探讨血管紧张素转化酶抑制剂(ACEI)及血管紧张素1型受体阻断剂(ARB1)非血液动力学肾保护作用的可能机制。方法5/6肾切除术制作SD大鼠残肾模型,术后分别以NS(模型组)、美托洛尔(普通降压药组)、贝那普利(贝那普利组)及缬沙坦(缬沙坦组)灌胃治疗,定期测血肌酐、尿素氮及24h尿蛋白;于设定时间采集肾脏标本,免疫组化及流式细胞术监测残肾Pax-2^+细胞,流式细胞术分离Pax-2^+细胞;RT-PCR检测Pax-2^+细胞AT1R、AT2R和Pax-2 m RNA表达,Westernblot检测TGF-β1及VEGF表达。结果模型组大鼠术后,残肾Pax-2^+细胞数及Pax-2^+细胞的Pax-2 m RNA的表达量逐渐减低(P<0.05);与模型组比较,贝那普利组及缬沙坦组残肾Day30,Day90 Pax-2^+细胞数及Pax-2^+细胞的Pax-2 m RNA的表达升高(P<0.05),普通降压药组与模型组各期间无统计学差异(P>0.05);贝那普利组及缬沙坦组残肾d90肾小球硬化指数明显低于模型组(P<0.05),普通降压药组及模型组间无统计学差异(P>0.05)。结论 5/6肾切除术后,大鼠残肾Pax-2^+细胞及其Pax-2 mRNA表达逐渐减少,出现肾小球硬化及CRF,ACEI及ARB1对残肾Pax-2^+细胞具有保护作用,这种保护作用可能是其非血液动力学肾保护作用重要机制。
文摘In this study,we investigated the effect of captopril(CPT) on glomerular filtration rate(GFR),effective renal plasma flow(ERPF),filtration fraction(FF),urinary albumin excretion(UAE) and daily urinary excretion of thromboxane B2(TXB2) and 6-keto-prostaglandin F1a(6-keto-PGFla) in 29 normotensive non-insulin-dependent diabetes(NIDDM) patients without clinically discernible nephropathy.Before treatment,urinary excretion 6-keto-PGF1a was significantly increased(P<0.05) in 29 NIDDM patients compared with 25 health subjects matched for age and sex.The values of GFR and FF were significantly higher(P<0.01 and P<0.005,respectively) in NIDDM than in normal volunters,whereas ERPF was comparable in both groups.Meanwhile we observed that UAE of early NIDDM was increased before treatment.After CPT treatment,GFR,FF,UAE and urinary excretion of 6-keto-PGFla were significantly reduce(all P<0.005) compared with those of NIDDM before treatment. These data indicated that CPT is effective in lowering glomerular filtration pressure and ameliorating microalbuminuria in the normotensive early NIDDM.
文摘The purpose of this review is to objectively evaluate the biochemical and pathophysiological properties of 0.9% saline （henceforth： saline） and to discuss the impact of saline infusion, specifically on systemic acid-base bal- ance and renal hemodynamics. Studies have shown that electrolyte balance, including effects of saline infusion on serum electrolytes, is often poorly understood among practicing physicians and inappropriate saline prescribing can cause increased morbidity and mortality. Large-volume （〉2 L） saline infusion in healthy adults induces hyperohloremia which is associated with metabolic acidosis, hyperkalemia, and negative protein balance. Saline overload （80 ml/kg） in rodents can cause intestinal edema and contractile dysfunction associated with activation of sodium-proton exchanger （NHE） and decrease in myosin light chain phosphorylation. Saline infusion can also adversely affect renal hemody- namics. Microperfusion experiments and real-time imaging studies have demonstrated a reduction in renal perfusion and an expansion in kidney volume, compromising 02 delivery to the renal perenchyma following saline infusion. Clinically, saline infusion for patients post abdominal and cardiovascular surgery is associated with a greater number of adverse effects including more frequent blood product transfusion and bicarbonate therapy, reduced gastric blood flow, delayed recovery of gut function, impaired cardiac contractility in response to inotropes, prolonged hospital stay, and possibly increased mortality. In critically ill patients, saline infusion, compared to balanced fluid infusions, in- creases the occurrence of acute kidney injury. In summary, saline is a highly acidic fluid. With the exception of saline infusion for patients with hypochloremic metabolic alkalosis and volume depletion due to vomiting or upper gastroin- testinal suction, indiscriminate use, especially for acutely ill patients, may cause unnecessary complications and should be avoided. More education regarding saline-related effects and adequate electrolyte management is needed.
