Effect of venous and lymphatic congestion on lymph capillary pressure of the skin in healthy volunteers and patients with lymph edema

The aim of the present study was to assess the influence of venous and lymphatic congestion on lymph capillary pressure (LCP) in the skin of the foot dorsum of healthy volunteers and of patients with lymph edema. LCP was measured at the foot dorsum of 12 patients with lymph edema and 18 healthy volunteers using the servo-nulling technique. Glass micropipettes (7-9 microm) were inserted under microscopic control into lymphatic microvessels visualized by fluorescence microlymphography before and during venous congestion. Venous and lymphatic congestion was attained by cuff compression (50 mm Hg) at the thigh level. Simultaneously, the capillary filtration rate was measured using strain gauge plethysmography. The mean LCP in patients with lymph edema increased significantly (p < 0.05) during congestion (15.7 +/- 8.8 mm Hg) compared to the control value (12.2 +/- 8.9 mm Hg). The corresponding values of LCP in healthy volunteers were 4.3 +/- 2.6 mm Hg during congestion and 2.6 +/- 2.8 mm Hg during control conditions (p < 0.01). The mean increase in LCP in patients with lymph edema was 3.4 +/- 4.1 mm Hg, and 1.7 +/- 2.0 mm Hg in healthy volunteers (NS). The maximum spread of the lymph capillary network in patients increased from 13.9 +/- 6.8 mm before congestion to 18.8 +/- 8.2 mm during thigh compression (p < 0.05). No increase could be observed in healthy subjects. In summary, venous and lymphatic congestion by cuff compression at the thigh level results in a significant increase in LCP in healthy volunteers as well as in patients with lymph edema. The increased spread of the contrast medium in the superficial microlymphatics in lymph edema patients indicates a compensatory mechanism for lymphatic drainage during congestion of the veins and lymph collectors of the leg.     

Double-blind investigation of the effects of propranolol and placebo on the pressure of esophageal varices in patients with portal hypertension

This study was aimed at investigating the effects of propranolol on esophageal variceal pressure in patients with portal hypertension. Variceal pressure was measured at endoscopy using a miniature pressure-sensitive gauge in 20 patients with portal hypertension. Measurements were obtained under baseline conditions and 20 min after double-blind administration of propranolol (0.15 mg/kg; n = 10) or an identical amount of placebo (normal saline, 0.3 ml/kg; n = 10). Under baseline conditions, variceal pressure was similar in propranolol and placebo groups (14.1 +/- 5 mm Hg vs. 14.9 +/- 6.6 mm Hg, respectively; not significant). Placebo had no significant effect on variceal pressure (baseline = 14.9 +/- 6.6 mm Hg; placebo = 15.5 +/- 6.6 mm Hg; not significant), and values after placebo administration were closely correlated with baseline values (r = 0.98; y = 1.1 + 0.97 x; p less than 0.0001). In contrast, propranolol caused a significant decrease in the pressure of esophageal varices (from 14.1 +/- 5 mm Hg to 11.3 +/- 4.4 mm Hg; p less than 0.0002). No significant changes in the size of esophageal varices were observed after propranolol or placebo administration. This study shows (a) the endoscopic pressure-gauge technique has a low variability and may be used to assess acute drug-induced changes in variceal pressure; and (b) propranolol causes significant decreases in variceal pressure in patients with portal hypertension and esophageal varices.     

植物雌激素对血压的影响

目的研究大豆饮食中所含的植物雌激素对健康人血压、血脂谱的影响。方法213名健康受试者(男性108人,绝经后女性105人),年龄50-75岁,随机、双盲接受特定大豆蛋白饮食(试验组)或酪蛋白安慰剂(安慰剂组)干预,为期3个月。建立多变量模型以评价治疗效果。结果饮食干预后,仅在试验组受试者尿液中植物雌激素含量增高。试验组血压较安慰剂组下降明显[收缩压(-7.5±1.2)mm Hg比(-3.6±1.1)mm Hg,P<0.01;舒张压(-4.3±0.8)mm Hg比(-1.9±0.7)mm Hg,P<0.05;平均压(-5.5±1.0)mm Hg比(-0.9±1.0)mm Hg,P<0.008]。试验组血脂水平较安慰剂组有显著改变(P<0.001),其中试验组低密度脂蛋白胆固醇/高密度脂蛋白胆固醇比值显著下降[(-0.33±0.10) mmol/L比(0.04±0.10) mmol/L,P<0.05],甘油三酯水平也有显著下降[(-0.20±0.05)mmol/L比(-0.01±0.05)mmol/L,P<0.05],而脂蛋白(a)水平升高(±95%可信区间)[42(17-67)mg/L比4(-22-31)mg/L,P<0.05]。两组中总胆固醇和低密度脂蛋白胆固醇水平均下降,高密度脂蛋白胆固醇水平升高。副作用的发生率两组相似,并且都没有观察到男性激素水平发生改变。结论在正常血压男性和绝经后女性人群中,大豆饮食对血压和血脂水平有改善作用。     

Tissue fluid pressure, lymph pressure, and fluid transport in rat intestinal villi

Tissue fluid pressure (Pt) and lymph pressure (Pl) as well as fluid transport between initial lymphatics and tissue matrix were determined in the villi of the jejunum in vivo and in vitro. When the intestine was absorbing fluid, free tissue fluid as a micro pool appeared in the villi. Pt and Pl were 2.4 +/- 0.7 and 2.9 +/- 0.8 mm Hg (mean +/- SE), respectively, in the villi in vivo (26 villi of 5 rats) or 0.8 +/- 0.4 and 1.2 +/- 0.5 mm Hg, respectively, in the villi in vitro (30 villi of 5 rats). Pl was significantly (P less than 0.01) higher than Pt. When Evans blue in saline was continuously infused into an initial lymphatic, dye rapidly leaked out into the tissue matrix, but when it was infused into the free tissue fluid, dye did not enter the lymphatics but leaked out of the epithelial layer, apparently due to low hydraulic conductance of the tissue matrix to fluid transport in this direction. Furthermore, in the villi with fat absorption, a retrograde flow of chylous lymph out of the villous tips always occurred, indicating that there are large pores at the villous tips to allow free passage of fluid and chylomicrons. From these findings and other evidences, it is inferred that during fluid absorption a fraction of the lymph may be formed by the transport of the luminal fluid directly into the terminal end of the initial lymphatics via large pores at the villous tips presumably by inhibition of the tissue matrix or by lymphatic suction or both.     

Blood pressure response to hyperventilation test reflects daytime pressor profile

Recent studies show that healthy subjects and patients with moderate hypertension have different pressor responses to hyperventilation, depending on their sympathoadrenergic reactivity. In the present study, we investigated whether a different response to the hyperventilation test is related to differences in the daily blood pressure profiles recorded with noninvasive ambulatory monitoring. Forty-five healthy subjects and 67 patients with essential hypertension of grades 1 and 2 (Joint National Committee VI and World Health Organization) were investigated. Healthy subjects and hypertensive patients responding to hyperventilation with an increase in systolic blood pressure had, during daytime ambulatory blood pressure assessment, peak systolic blood pressure values (146.0+/-5.0 mm Hg, 182.2+/-9.0 mm Hg, respectively) similar to the hyperventilation peak systolic blood pressure values (147.2+/-3.5 mm Hg, 183.0+/-4.7 mm Hg, respectively). Hypertensive patients responding to hyperventilation with a decrease in blood pressure showed clinic systolic blood pressure values (178.4+/-3.2 mm Hg) higher than daytime average ambulatory systolic blood pressure (155.2+/-7.1 mm Hg; P<0.01). Our results indicate that a hyperventilation test yields information on daily peak blood pressure values in healthy subjects and hypertensive patients when it induces a pressor increase and can identify hypertensive patients with the so-called "white coat effect" when it induces a pressor decrease.     

Antihypertensive effect of diltiazem in a slow-release formulation for mild to moderate essential hypertension

The antihypertensive efficacy and frequency of adverse reactions following administration of diltiazem in a new slow-release formulation were compared with placebo in 34 patients with mild to moderate essential hypertension in a randomized, double-blind, crossover study. After 6 weeks of treatment with diltiazem (240 or 360 mg/day), average supine blood pressure (BP) decreased from 165 +/- 21/101 +/- 5 mm Hg at baseline to 152 +/- 16/93 +/- 4 mm Hg compared with 160 +/- 19/100 +/- 7 mm Hg with placebo (p less than 0.01/p less than 0.001). Standing BP decreased from 162 +/- 20/107 +/- 6 mm Hg at baseline to 150 +/- 14/101 +/- 5 mm Hg compared to 159 +/- 18/107 +/- 8 mm Hg with placebo (p less than 0.01/p less than 0.001). The supine heart rate after diltiazem was 65 +/- 7 beats/min and after placebo 69 +/- 9 beats/min (p less than 0.01). There were no hematologic side effects. Only minor differences between diltiazem and placebo were observed in some of the biochemical laboratory values. Four patients were withdrawn due to side effects during treatment with diltiazem and 2 with placebo. Diltiazem in a slow-release formulation given twice a day lowered blood pressure significantly as monotherapy in patients with mild to moderate hypertension and was well tolerated.     

Fluorescence microlymphography of the upper extremities. Evaluation with a new computer programme.

BACKGROUND: To evaluate the initial lymphatics of the superficial skin in healthy volunteers using fluorescence microlymphography and to establish controls values for comparison with lymphedema patients. METHODS: Fluorescence microlymphography was performed on the hand dorsum, on the lower and the upper arm in 12 healthy subjects (58.7+/-8.0 years). At each of these sites 10 microl FITC-dextran was injected subepidermally using a steel cannula. The studies were recorded on video tape using a fluorescence microscope and a CCD video camera. Final magnification was 24 and 62. The maximum spread of the fluorescent contrast medium was measured 10 minutes after injection. The area of the visualized lymph capillaries was determined using a computer programme. SETTING: University Hospital, Department of Medicine, Division of Vascular Medicine (Angiology). RESULTS: The mean area of the visualised lymph capillary network 95.3+/-41.3 mm2 (42-174 mm) at the upper and 89.4+/-45.5 mm2 (44-171 mm). The maximum spread was 4.8+/-3.5 mm (1.9-13.6 mm) and 4.4+/-3.7 mm, respectively. The mean diameter of the lymph capillaries was 84.1+/-19.9 microm and 75.5+/-14.8 microm, respectively. CONCLUSIONS: The extension of the lymph capillary network at the upper and lower arm are comparable to those at the lower extremities. Considering the two-dimensional nature and the irregular shape of the network the area measurement seems to be more appropriate than the maximum spread in one direction.     

Clinical and experimental studies on the efficiency of nifedipine on smooth muscle strips of the esophagus (author's transl)

Based on in vivo studies on isolated muscle strips of the LES and on manometric in vivo studies on 8 mongrel dogs, 6 healthy volunteers, 6 patients with achalasia and 3 subjects with diffuse esophageal spasm we could demonstrate that nifedipine causes a long-lasting relaxation of smooth muscle, the esophagus and LES. In 8 dogs resting pressure at the LES was decreased by 20 mg nifedipine from 18.5 +/- 1.8 mm Hg to 8.2 +/- 0.9 mm Hg. This pressure decrease could not be reversed by pentagastrin stimulation (3.0 microgram/kg KG PG). The resting pressure in LES was decreased from 26.8 +/- 3.8 mm Hg to 16.4 +/- 2.1 mm Hg in healthy volunteers and from 45.5 +/- 2.6 mm Hg to 14.5 +/- 0.4 mm Hg in patients with achalasia. In 3 patients with diffuse esophageal spasm nifedipine (20 mg) caused a mean decrease of 38% of the contraction amplitude. Further clinical studies have to be done to clarify if the spasmolysis by nifedipine may be important in the treatment of spastic or hypertonic motility disorders of the LES and the esophagus.     

Norepinephrine transporter blockade with atomoxetine induces hypertension in patients with impaired autonomic function

Atomoxetine, a selective norepinephrine transporter blocker, could increase blood pressure by elevating norepinephrine concentration in peripheral sympathetic neurons. This effect may be masked in healthy subjects by central sympatholytic mechanisms. To test this hypothesis we studied the pressor effect of 18 mg of atomoxetine (pediatric dose) in 21 patients with damage of the central (10 subjects) and peripheral (11 subjects) autonomic nervous system. Atomoxetine was administered in a randomized, crossover, placebo-controlled fashion, and blood pressure and heart rate were measured at baseline and for 60 minutes after drug intake. Atomoxetine acutely increased seated and standing systolic blood pressure in patients with central autonomic failure by 54+/-26 (mean+/-standard deviation; P=0.004) and 45+/-23 mm Hg (P=0.016), respectively, as compared with placebo. At the end of the observation period the mean seated systolic blood pressure in the atomoxetine group was in the hypertensive range (149+/-26, range 113 to 209 mm Hg). However, in patients with peripheral autonomic failure, atomoxetine did not elicit a pressor response; seated and standing systolic blood pressure increased by 4+/-18 mm Hg (P=0.695) and 0.6+/-8 mm Hg (P=0.546) with atomoxetine as compared with placebo. In conclusion, atomoxetine induces a dramatic increase in blood pressure in patients with central autonomic failure even at very low doses. These findings suggest that a functional central sympatholytic pathway is essential to avoid hypertension in patients treated with this drug. Caution should be exercised when this medication is used in patients with milder form of autonomic impairment.     

Remission of mild to moderate hypertension after treatment with carteolol, a beta-adrenoceptor blocker with intrinsic sympathomimetic activity

Previous studies have indicated that some hypertensive patients, following a period of effective treatment with certain antihypertensive drugs, may experience prolonged normotension after drug withdrawal. We have studied the ability of carteolol, a nonselective beta-adrenoceptor antagonist with intrinsic sympathomimetic activity, to produce such remissions of hypertension. Thirty-four patients whose diastolic blood pressure was controlled at 90 mm Hg or less with carteolol monotherapy (2.5 to 5.0 mg/d for an average of 328 days) were randomized to a nine-month, double-blind, placebo-controlled drug-withdrawal trial. Those patients randomized to continue carteolol therapy had initially responded to carteolol treatment with reduction in blood pressure from 151 +/- 4/99 +/- 2 to 132 +/- 4/80 +/- 2 mm Hg. Those randomized to treatment with placebo had initially responded with blood pressure reductions from 154 +/- 4/97 +/- 2 to 137 +/- 4/81 +/- 2 mm Hg. Changes in mean systolic and diastolic blood pressure (mm Hg +/- SEM) from baseline during carteolol therapy to the final visit at nine months were not different for patients receiving placebo (13 +/- 5/6 +/- 4 mm Hg, recumbent; 11 +/- 6/4 mm Hg, standing) or carteolol (11 +/- 5/7 +/- 3 mm Hg, recumbent; 12 +/- 6/7 +/- 3 mm Hg, standing). The final mean recumbent diastolic blood pressure (86.9 mm Hg) was the same in both groups. Prolonged normotension may follow a period of carteolol treatment, again suggesting the potential importance of periodic withdrawal of antihypertensive medication.     

Placebo: its hypotensive effect and influence on certain psychological parameters and dependency on dosage prescribed to patients

The main purpose of this study is to estimate the influence of taking a number of placebo tablets to obtain hypotensive effects and some psychological parameters with essential hypertension. 197 patients (102F/95M) aged between 18-80 years (average age 52.3) with essential hypertension were included in the research in two outpatients clinics. The patients who participated in research, stayed for at least seven days without any pharmacological treatment. They had a diastolic pressure (DBP) between 95-114 mm Hg and systolic pressure (SBP) up to 200 mm Hg. 92 patients had taken one tablet a day and 105 patients had taken two tablets in the morning. This was before the placebo was included and two weeks after their blood pressure had been taken by standard methods (sphygmomanometer). They were monitored daily throughout the period using traditional methods and ABPM (SpaceLabs 90121). The patients completed two psychological tests. 97 records (52F/45M) qualified for statistical analysis (80% of measurements were undertaken properly, and the time between measurements was less than two hours). Psychological questionnaires were correctly completed by 92 patients. The visible results of decreasing systolic and diastolic value of blood pressure were obtained after using one (group 1) and two (group 2) placebo tablets. They were monitored by a standard method and recorded by ABPM. In group 1 SBP decreased from 164 +/- 11.4 mm Hg to 158 +/- 8.8 mm Hg (p < 0.01, on standard method) and from 149.5 +/- 17.8 to 144.5 +/- 8.3 mm Hg daily (p < 0.05, ABPM). DBP in this examined group decreased from 106.2 +/- 2.8 to 102 +/- 3.9 mm Hg (p < 0.01, stand. method), and from 103.2 +/- 2.6 to 98.6 +/- 1.2 mm Hg daily (p < 0.05, ABPM). In the second group SBP decreased from 169 +/- 12.8 to 157.6 +/- 17.9 mm Hg (p < 0.001, stand. method), and in ABPM from 148.5 +/- 15.8 to 139.6 +/- 16.2 mm Hg (p < 0.01). In this same group, DBP decreased from 104.4 +/- 2.6 to 98 +/- 3.4 mm hG (p < 0.001, stand. method), and from 107.4 +/- 5.8 mm Hg to 95.5 +/- 4.2 mm Hg-daily (p < 0.001, ABPM). There were no differences between heart rate in all groups of patients. In both groups there were significant statistical differences in negative symptoms, physical symptoms and anexity, but a more optimistic mood was observed by group 2. More effective hypertensive treatment was observed within the group which was treated with two placebo tablets. This group was characterized by more optimistic mood compared to the group which was treated with one placebo tablet a day.     

Effects of dipyridamole on the hypoxemic pulmonary hypertension of patients with chronic obstructive pulmonary disease

Based on the hypothesis that blood platelets contribute to the pathogenesis of hypoxemic pulmonary hypertension in patients with chronic obstructive pulmonary disease (COPD), the effect of a prolonged treatment with dipyridamole, a platelet-inhibiting drug, on hypoxemic pulmonary hypertension was evaluated in a double-blind cross-over study. Eight patients with COPD, pulmonary hypertension [mean systolic pressure 52.2 +/- (SD) 9.7 mm Hg; mean diastolic pressure 25.8 +/- (SD) 6.8 mm Hg] and shortened platelet regeneration time [mean 5.2 +/- (SD) 1.2 days] received, in a cross-over random sequence, the following two 3-month treatments: (a) dipyridamole 100 mg and acetylcysteine 100 mg every 6 h; (b) acetylcysteine, 100 mg every 6 h. Dipyridamole significantly prolonged the platelet regeneration time [mean 6.5 +/- (SD) 1.0 days; p less than 0.05]. There was no significant effect on diastolic pulmonary pressure. However, systolic pressure was significantly (p less than 0.05) lower after dipyridamole [46.8 +/- (SD) 16 mm Hg] than after placebo [56.1 +/- (SD) 14 mm Hg]. These results suggest that dipyridamole can slow the progression of hypoxemic pulmonary hypertension in patients with COPD.     

Efficacy and safety of an oral fixed low-dose perindopril 2 MG/indapamide 0.625 MG combination: a randomized, double-blind, placebo-controlled study in elderly patients with mild to moderate hypertension.

The efficacy and safety of 12 weeks treatment with an oral fixed low-dose perindopril 2 mg + indapamide 0.625 mg (Per/Ind) combination in elderly and very elderly patients (65-85 years) with mild to moderate systolic and diastolic hypertension (SDH) or isolated systolic hypertension (ISH) were investigated vs placebo. This trial was a multinational randomized double-blind study with doubling of active drug dosage in nonresponders. Intention to treat analysis was performed in 383 patients (age 72.4 years; ISH 32%). 58.5% remained on their initial dosage. Per/Ind decreased supine diastolic and systolic blood pressure (sDBP/sSBP) by 13.2+/-8.0 mm Hg and 22.5+/-13.9 mm Hg (P <.0001) versus placebo -7.3+/-9.0 mm Hg and -12.3+/-15.2 mm Hg, respectively. In ISH (n = 123), Per/Ind decreased sSBP by 23.0+/-11.8 mm Hg (P <.0001). Overall response and normotension rates was 81.3% with Per/Ind (P <.0001). Adverse event rates (including hypokalemia) were similarly low in both groups. Analysis in the over-75 year subgroup showed similar safety and efficacy results. Fixed low-dose Per/Ind is a safe and effective treatment of hypertension including isolated systolic hypertension in the elderly.     

The use of isosorbide in the treatment of severe, uncontrolled hypertension

Isosorbide dinitrate was administered sublingually and compared with placebo in a double-blind, randomized fashion to determine its effectiveness and safety in the rapid control of severe arterial hypertension. In 11 patients who received 10 mg of isosorbide dinitrate, blood pressure (BP) dropped from 205 +/- 8/131 +/- 3 to 166 +/- 9/106 +/- 5 mm Hg at 120 minutes. In eight patients who received placebo, BP dropped from 203 +/- 8/130 +/- 3 to 193 +/- 11/122 +/- 5 mm Hg at 120 minutes. When 10 mg of isosorbide dinitrate was administered sublingually after 120 minutes to placebo-pretreated patients, their BP dropped to 161 +/- 7/105 +/- 6 mm Hg at 240 minutes. Our study group (19 patients) was compared with a "control" group (six patients) whose BP (203 +/- 12/132 +/- 8 mm Hg) was treated only with conventional antihypertensive medications and bed rest; five (83%) of the six controls achieved steady BP control at 24 hours vs nine (47%) of the 19 study patients pretreated with isosorbide. There were no side effects, including hypotension, orthostatic effect, and reflex tachycardia. Sublingual isosorbide safely and effectively lowers systolic and diastolic BP in patients with severe, uncontrolled arterial hypertension.     

Bovine casein hydrolysate (c12 Peptide) reduces blood pressure in prehypertensive subjects

BACKGROUND: About one in four adults suffer from prehypertension. People with prehypertension are at risk of developing hypertension, being a biomarker for cardiovascular disease risk. The use of milk-derived protein hydrolysates containing peptides with angiotensin-converting enzyme (ACE) inhibiting properties may reduce blood pressure (BP) and thus the risk of developing hypertension. METHODS: We investigated the BP-lowering effect of a casein-derived protein hydrolysate (C12 Peptide) during a 4-week intervention period in prehypertensive subjects. After a 2-week run-in period, 48 Taiwanese volunteers were randomly assigned to either placebo or C12 Peptide tablets for 4 weeks, followed by a 2-week off-treatment period. After the run-in period, BP was measured weekly. RESULTS: Baseline values for systolic BP (mean +/- SEM) in the placebo and C12 Peptide groups were 137.1 +/- 3.1 and 137.9 +/- 2.4 mm Hg, respectively; those for diastolic BP were 85.2 +/- 2.1 and 86.9 +/- 2.0 mm Hg, respectively. Four weeks repeated daily intake of 3.8 g C12 Peptide reduced significantly systolic and diastolic BP by 10.7 +/- 1.6 mm Hg and 6.9 +/- 1.2 mm Hg, respectively, compared to baseline. Furthermore, plasma angiotensin II and aldosterone levels were reduced significantly (P < .05). The placebo group showed a BP reduction of 3.6 +/- 2.4 and 2.7 +/- 1.6 mm Hg in systolic and diastolic BP, respectively (P = not significant). No evidence of side effects was observed. CONCLUSIONS: This study shows that C12 Peptide reduces BP in prehypertensive people.     

Association between supine hypertension and orthostatic hypotension in autonomic failure

Supine hypertension occurs commonly in primary chronic autonomic failure. This study explored whether supine hypertension in this setting is associated with orthostatic hypotension (OH), and if so, what mechanisms might underlie this association. Supine and upright blood pressures, hemodynamic responses to the Valsalva maneuver, baroreflex-cardiovagal gain, and plasma norepinephrine (NE) levels were measured in pure autonomic failure (PAF), multiple-system atrophy (MSA) with or without OH, and Parkinson's disease (PD) with or without OH. Controls included age-matched, healthy volunteers and patients with essential hypertension or those referred for dysautonomia. Baroreflex-cardiovagal gain was calculated from the relation between the interbeat interval and systolic pressure during the Valsalva maneuver. PAF, MSA with OH, and PD with OH all featured supine hypertension, which was equivalent in severity to that in essential hypertension, regardless of fludrocortisone treatment. Among patients with PD or MSA, those with OH had higher mean arterial pressure during supine rest (109+/-3 mm Hg) than did those lacking OH (96+/-3 mm Hg, P=0.002). Baroreflex-cardiovagal gain and orthostatic increments in plasma NE levels were markedly decreased in all 3 groups with OH. Among patients with PD or MSA, those with OH had much lower mean baroreflex-cardiovagal gain (0.74+/-0.10 ms/mm Hg) than did those lacking OH (3.13+/-0.72 ms/mm Hg, P=0.0002). In chronic autonomic failure, supine hypertension is linked to both OH and low baroreflex-cardiovagal gain [corrected]. The finding of lower plasma NE levels in patients with than without supine hypertension suggests involvement of pressor mechanisms independent of the sympathetic nervous system.     

Antihypertensive effect of sustained-release isosorbide dinitrate for isolated systolic systemic hypertension in the elderly

A double-blind, randomized trial was performed in 40 patients, mean age (+/- standard deviation) 80 +/- 4 years, with isolated systolic systemic hypertension to evaluate the antihypertensive effect of oral sustained-release isosorbide dinitrate (ISDN), 20 to 40 mg twice daily, vs placebo. After 12 weeks of treatment, supine systolic blood pressure (BP) decreased from 192 +/- 10 to 162 +/- 12 mm Hg with ISDN (p less than 0.001) and from 189 +/- 10 to 175 +/- 15 mm Hg with placebo (p less than 0.001). On the basis of variance analysis, the decrease in systolic BP was significantly lower with ISDN (27 mm Hg) than with placebo (13 mm Hg). Similar results were observed for supine and erect systolic BP measured at 8 AM and 4 PM, 8 and 12 hours after drug intake. No significant differences in diastolic BP, heart rate or side effects occurred. After the ISDN tapering off-period (2 weeks), systolic BP increased significantly but did not change with placebo. The study provided evidence that in elderly patients with systolic hypertension, sustained-release ISDN induced a selective and sustained decrease in systolic BP, antihypertensive effect was observed 8 and 12 hours after drug administration, and no tolerance phenomenon was noted.     

Effect of the HMG-CoA reductase inhibitors on blood pressure in patients with essential hypertension and primary hypercholesterolemia

Certain hydroxymethylglutaryl coenzyme A reductase inhibitors, ie, statins, may cause vasodilation by restoring the endothelial dysfunction that frequently accompanies hypertension and hypercholesterolemia. Several studies have found that a blood pressure reduction is associated with the use of statins, but conclusive evidence from controlled trials is lacking. After an 8-week placebo and diet run-in period, 30 persons with moderate hypercholesterolemia and untreated hypertension (total cholesterol 6.29+/-0.52 mmol/L, systolic and diastolic blood pressure 149+/-6 and 97+/-2 mm Hg) were randomized in a double-blind manner to placebo or pravastatin (20 to 40 mg/d) in a crossover design. In 25 participants who completed the 32-week trial, pravastatin decreased total and LDL cholesterol (both -1.09 mmol/L, P=0.001), systolic and diastolic blood pressure (-8 and -5 mm Hg, both P=0.001), and pulse pressure (-3 mm Hg, P=0.011) and blunted the blood pressure increase caused by the cold pressor test (-4 mm Hg, P=0.005) compared with placebo. It also reduced the level of circulating endothelin-1 (P=0.001). The blood pressure results were virtually unchanged in stratified analyses according to gender and age and in intention-to-treat analyses that included the 5 patients who dropped out of the study. When the participants were taking either placebo or pravastatin, blood pressure was not significantly correlated with total or LDL cholesterol or with circulating endothelin-1. Pravastatin decreases systolic, diastolic, and pulse pressures in persons with moderate hypercholesterolemia and hypertension. This antihypertensive effect may contribute to the documented health benefits of certain statins.     

Role of erythropoietin in cortisol-induced hypertension

The mechanism of cortisol-induced hypertension remains unknown. We investigated a possible role of erythropoietin (EPO) as a mediator of hypertension in healthy male subjects treated with cortisol. In Study 1, blood pressure (BP) and serum EPO concentrations were measured on alternate days in nine subjects treated with 80 mg of cortisol per day for 5 days. In Study 2 the same parameters were measured in eight subjects randomised to cortisol (80 mg/day) or placebo and 10 subjects randomised to cortisol (200 mg/day) or placebo for 5 days. In Study 1, cortisol caused a significant increase in systolic BP (SBP) (115 +/- 2 vs 126 +/- 2 mm Hg, control vs day 5, P < 0.001) and serum EPO concentrations (14.5 +/- 2.7 vs 24.3 +/- 2.7 mU/mL, P < 0.001). In Study 2 both doses of cortisol increased SBP (118 +/- 2 vs 113 +/- 2 mm Hg, 80 mg cortisol vs placebo, P < 0.05 and 129 +/- 3 vs 113 +/- 2 mm Hg, 200 mg cortisol vs placebo, P < 0.001). Serum EPO concentrations were significantly increased at 200 mg cortisol (25.2 +/- 11.9 vs 15.9 +/- 3.5 mU/mL, P < 0.01) but not 80 mg cortisol (21.3 +/- 2.9 vs 14.9 +/- 3.1 mU/mL). In the 200 mg group there was a positive correlation between the change in SBP and the change in serum EPO concentration (r2 = 0.43, P < 0.05). These results point to a possible role for EPO as the mediator of cortisol-induced hypertension. Journal of Human Hypertension (2000) 14, 195-198.     

长期小剂量氢氯噻嗪的降压疗效观察

目的观察原发性高血压病患者长期服用小剂量氢氯噻嗪的降压疗效。方法232例轻、中度高血压病患者服用氢氯噻嗪12.5mg,每日1次,每月发放一次药物并测量血压,观察1年。比较服药6周及1年的降压疗效及生化指标的变化。结果(1)观察结束时资料完整的观察对象为231例,治疗后6周的收缩压、舒张压、平均动脉压下降值分别为(6.01±16.05)mmHg(1mmHg=0.133kPa)、(2.90±10.33)mmHg、(3.94±10.68)mmHg;治疗1年的收缩压、舒张压、平均动脉压下降值分别为(10.45±17.28)mmHg、(8.45±11.06)mmHg、(9.12±10.88)mmHg。1年时血压下降值高于6周时血压下降值,差异有统计学意义(P<0.05)。治疗6周时的降压达标率为20.3%,治疗1年时降压达标率为35.1%,差异有统计学意义(P<0.05)。(2)观察结束时未发现有症状的低钾血症,但血尿酸值明显增加,与基线值比较差异有统计学意义(P<0.05)。结论长期服用小剂量氢氯噻嗪可有效降低轻、中度原发性高血压患者的血压,对电解质、糖、脂代谢无明显不良影响。