呋塞米治疗产前妊娠高血压性心衰疗效观察

目的:观察呋塞米治疗产前妊娠高血压性心衰患者疗效。方法:将110例产前妊娠高血压性心衰患者随机分为呋塞米治疗组(治疗组)和常规治疗组(对照组),观察两组患者西地兰用量、心衰缓解时间、硝酸甘油的平均速度、治疗前后血压平均下降范围及治疗组用药前后血清钾的变化。结果:治疗组呋塞米平均用量60 mg。西地兰平均用量治疗组0.6 mg,对照组1.4 mg;心衰缓解时间治疗组3.8 h,对照组6.6 h,两组比较差异有统计学意义(P<0.01)。硝酸甘油的平均速度治疗组40μg/min,对照组60μg/min,两组比较差异有统计学意义(P<0.01)。治疗组治疗后收缩压平均下降42.12 mmHg,舒张压平均下降25.33 mmHg;对照组治疗后收缩压平均下降38.62 mmHg,舒张压平均下降23.51 mmHg,两组比较差异有统计学意义(P<0.01)。治疗组治疗前后血清钾平均值分别是3.66 mmol/L、3.37 mmol/L,治疗前后差异无统计学意义(P>0.05)。结论:产前妊娠高血压性心衰在强心、降压的基础上静注呋塞米能够较快的控制心衰,减少西地兰、硝酸甘油的用量,同时又可控制血压,血清钾下降不明显,是一种安全、可靠的治疗产前妊娠高血压性心衰理想药物之一。     

Acute diuretic effect of continuous intravenous infusion of an aqueous extract of Coriandrum sativum L. in anesthetized rats

AIM OF THE STUDY: The present investigation was carried out to evaluate the acute diuretic activity of continuous intravenous infusion of an aqueous extract of the seed of Coriandrum sativum L. Apiaceae (coriander) in rats. MATERIALS AND METHODS: The aqueous extract of coriander seed was administered by continuous intravenous infusion (120 min) at two doses (40 and 100mg/kg) to anesthetized Wistar rats. Furosemide (10mg/kg), a standard diuretic was used as the reference drug. Excretion of water and electrolytes (sodium, potassium and chloride) in urine was measured, and glomerular filtration rate (equal to creatinine clearance) was determined. RESULTS: The crude aqueous extract of coriander seeds increased diuresis, excretion of electrolytes, and glomerular filtration rate in a dose-dependent way; furosemide was more potent as a diuretic and saluretic. The mechanism of action of the plant extract appears to be similar to that of furosemide. CONCLUSIONS: The aqueous extract of coriander seed possesses diuretic and saluretic activity, thus, validating the use of coriander as a diuretic plant in Moroccan pharmacopoeia.     

Release of Furosemide from Multiple-Unit and Single-Unit Preparations Containing Different Viscosity Grades of Sodium Alginate

The release characteristics and the effect of viscosity of sodium alginate on the release rate of furosemide (a rather poorly soluble drug) from hard gelatin capsules (single-unit), and minitablets (multiple-unit) filled in hard gelatin capsules, were evaluated. Swelling and erosion experiments showed a different behavior for each viscosity grade. Polymer characteristics influenced significantly the release of the drug from the preparations prepared and tested. The results indicate that erosion plays a significant role, accelerates release rate and shortens duration of drug release. Low viscosity formulations exhibited a greater erosion, and drug release was completed in 4 hours. Medium viscosity formulations showed intermediate erosion, while hh viscosity formulations exhibited less erosion, and drug release was completed in 8 hours. The minitablets always displayed lower release and dissolution efficiency values than the capsules, and as the viscosity increased, the difference of dissolution efficiency between the two formulations increased accordingly. The results further indicated that the multiple-unit system demonstrated a more pronounced sustained effect than the single-unit, and therefore, it is a more suitable preparation for sustained release delivery of poorly soluble drugs. Analysis of release data indicate a rather zero–order release mechanism, which may be attributed mainly to swelling and an erosion/dissolution process.     

Diuretic bioactivity optimization of furosemide in rats

Furosemide is a loop diuretic widely used by patients with congestive heart failure (CHF) to rid excess body water, reducing blood pressure, and mobilizing edemas. However, due to the narrow window of furosemide absorption, occurring only in the proximal gastrointestinal tract, only immediate release oral formulations are clinically available. Comparisons of bolus and continuous administration of furosemide in intravenous settings demonstrate that continuous administration at lower concentrations produced greater diuretic efficiency and reduced subsequent hospitalization rates in patients experiencing severe CHF. We report a systematic investigation of the diuretic bioactivity profiles of phase inversion micronized furosemide and furosemide co-precipitated with Eudragit L100, as well as their blends with stock furosemide, targeted at reducing the rapid spike in diuresis associated with immediate release formulations while maintaining cumulative urine output. Of the formulations tested, an equal parts blend of micronized furosemide and stock furosemide demonstrated optimal diuretic bioactivity profiles in a rat model.     

Metabolic complications associated with use of diuretics

Diuretics are commonly used therapeutic agents that act to inhibit sodium transport systems along the length of the renal tubule. The most effective diuretics are inhibitors of sodium chloride transport in the thick ascending limb of Henle. Loop diuretics mobilize large amounts of sodium chloride and water and produce a copious diuresis with a sharp reduction of extracellular fluid volume. As the site of action of diuretics moves downstream (thiazide and potassium-sparing diuretics), their effectiveness declines because the transport systems they inhibit have low transport capacity. Depending on the site of action diuretics can influence the renal handling of electrolyte-free water, calcium, potassium, protons, sodium bicarbonate, and uric acid. As a result, electrolyte and acid-base disorders commonly accompany diuretic use. Glucose and lipid abnormalities also can occur, particularly with the use of thiazide diuretics. This review focuses on the biochemical complications associated with the use of diuretics. The development of these complications can be minimized with careful monitoring, dosage adjustment, and replacement of electrolyte losses.     

托伐普坦片和呋塞米注射液治疗心力衰竭的临床疗效及安全性分析

目的 探索托伐普坦片和呋塞米注射液治疗心力衰竭的临床疗效及安全性.方法 120例心力衰竭患者,依据单双号随机化分为观察组与对照组,各60例.对照组采用呋塞米治疗,观察组采用托伐普坦片治疗.对比两组临床疗效、不良反应发生情况及脑钠素(BNP)、左心室舒张末期内径(LVEDD)、左心室收缩末期内径(LVESD)、左心室射血...     

Modification of ethanol-induced motor impairment by diet,diuretic, mineralocorticoid,or prostaglandin synthetase inhibitor

Ethanol-induced motor impairment in rats was measured following a number of different dietary or drug treatments. A low sodium diet combined with injections of the diuretic furosemide, but not a low sodium diet alone, increased motor impairment while a high sodium diet decreased impairment. Blood ethanol measurements indicated that both effects were probably mediated by changes in blood ethanol levels. However, the synthetic mineralocorticoid, DOCA, and the nonsteroidal anti-inflammatory, indomethacin, both altered ethanol-induced motor impairment without concomitant changes in blood ethanol levels. The aldosterone antagonist, spironolactone, failed to produce any effect. Since all treatments can modulate activity in the renin-angiotension system, this system appears to play a role in altering some of the behavioral properties of ethanol.     

Effect of Na−K-ATPase inhibition on hydrogen ion and potassium secretion

The purpose of the present study was to examine whether in vivo inhibition of renal Na–K-ATPase affects renal H⁺ and potassium (K) secretion. Infusion of digoxin, furosemide, or ethacrynic acid into one renal artery of HCO₃ loaded dogs caused similar increases in urine flow, fractional Na and Cl excretion, and fractional water excretion. Glomerular filtration rate and urinary HCO₃ concentration fell comparably in all experiments. Maximal HCO₃ reabsorption was not depressed by any of the drugs infused, however only digoxin inhibited renal Na–K-ATPase activity. Furthermore, unilateral digoxin infusion resulted in a marked depression in the urine to bloodpCO₂ gradient (U-BpCO₂) and prevented the rise in fractional K excretion secondary to HCO₃ infusion observed in the contralateral control kidney. At all urinary HCO₃ concentrations, U-BpCO₂ was significantly higher in urine obtained from furosemide or ethacrynic acid infused kidneys than in urine obtained from digoxin infused kidneys. In addition, furosemide or ethacrynic acid administration markedly enhanced fractional K excretion in both kidneys. The systemic infusion of tris(hydroxymethyl)aminomethane (THAM; pK 8.0) failed to return U-BpCO₂ in the digoxin infused experimental kidneys to control levels, whereas THAM caused a marked rise in U-BpCO₂ in the control kidney. These data demonstrate that the in vivo inhibition of renal Na–K-ATPase by digoxin causes a defect in the secretion of both H⁺ and K. This defect likely results from the dissipation of the Na dependent lumen negative potential difference (PD) by digoxin, since a lumen negative PD favors both H⁺ and K secretion in the collecting duct. Furthermore, these data do not support the notion that furosemide or ethacrynic acid affect tubular transport through the inhibition of renal Na–K-ATPase activity.