Search PubMed⌕ Search

Biomedical subjects

E Reisin

Publications and source records attributed to E Reisin.

At least 19 recordsLinked to original sources
PubMed2002

Renal and cardiovascular considerations for the nonpharmacological and pharmacological therapies of obesity-hypertension.

Obesity-associated hypertension is a common disease that involves a complex pathogenesis. Failure to control hypertension (HTN) in obese subjects provides a great threat to their renal and cardiovascular functions. The treatment of obesity-associated HTN is often difficult, and requires nonpharmacological and/or pharmacological approaches. Weight reduction is the cornerstone of the therapies of obesity-HTN, as it reverses the multiple components of its pathogenesis. When weight loss cannot be sustained or fails, pharmacological means should then be used. Angiotensin-converting enzyme inhibitors (ACEI) are the drug of choice: they can reduce blood pressure, protect the kidney and heart, and improve the metabolic abnormalities in obese subjects. Angiotensin-2 type-1 receptor blockers have a renoprotective benefit similar to ACEI, and they provide an important alternative to the use of ACEI. Diuretics are very effective in African-American obese hypertensives, but small doses should be used to avoid adverse effects on metabolic profiles. Long-acting calcium channel blockers are also effective and have the advantage of no adverse metabolic effects. Nondihydropyridine calcium channel blockers may provide additional renal and cardiovascular protective effects. The beta-adrenergic receptor blockers can cause further weight gain and metabolic abnormalities in obese subjects; therefore, careful monitoring is needed. There are few clinical data that support the efficacy and benefit of centrally acting alpha-2 agonists and alpha-adrenergic receptor antagonists in the treatment of obesity-HTN.

Cardiovascular Physiological Phenomena↗
PubMed2001

Effects of dehydroepiandrosterone and quinapril on nephropathy in obese Zucker rats.

BACKGROUND: The obese Zucker rat exhibits insulin resistance, develops nephropathy at an early age, and may be a model of diabetic nephropathy. Dehydroepiandrosterone (DHEA) may ameliorate many of the factors that contribute to diabetic nephropathy, while angiotensin-converting enzyme inhibitors are known to be effective. One marker of nephropathy is the expression of alpha-smooth muscle actin. METHODS: We studied the effect of DHEA on the expression of alpha-smooth muscle actin in obese Zucker rats and compared the changes with those in a control group, a group given quinapril, and a group on a low-calorie diet. DHEA (0.6%) added to plain chow, quinapril (0.3 mg/kg) added to drinking water, and a low-calorie diet based on pair-feeding were administered to obese rats from age 4 to 20 weeks. Immunohistochemical expression of alpha-smooth muscle actin, a marker of interstitial and glomerular fibrosis and an early indicator of nephropathy, was measured semiquantitatively in glomeruli, cortical interstitium, and medullary interstitium on a scale of 0 to 4 and was reported as mean +/- SEM. RESULTS: When compared with the obese control group, quinapril exhibited a marked reduction in alpha-smooth muscle actin staining in glomeruli, cortical interstitium, and medullary interstitium (P < 0.0005); DHEA reduced alpha-smooth muscle actin staining in cortical interstitium and medullary interstitium (P < 0. 005), and a low-calorie diet reduced alpha-smooth muscle actin staining in cortical and medullary interstitium (P < 0.005), which was similar to the effects of DHEA. CONCLUSIONS: DHEA was similar to a low-calorie diet in reducing the immunohistochemical staining of alpha-smooth muscle actin in obese Zucker rats. However, quinapril exerted a marked protective effect on the development of fibrosis, as indicated by alpha-smooth muscle actin staining, which was significantly less than that of DHEA at the doses studied.

Actins↗
PubMed2001

Obesity, hypertension, and the heart.

Hypertension occurs more commonly in obese than in lean persons at virtually every age. A variety of endocrine, genetic, and metabolic mechanisms have been linked to the development of obesity hypertension. These include insulin resistance and hyperinsulinemia, increased serum aldosterone levels, salt sensitivity and expanded plasma volume in the presence of increased peripheral vascular resistance, a genetic predisposition, and possibly increased leptin levels. Pressure and volume overload are present in obese hypertensives. This leads to a mixed eccentric-concentric form of left ventricular hypertrophy and increases the predisposition to congestive heart failure. Weight loss, even in modest decrements, is effective in reducing obesity-hypertension, possibly by ameliorating several of the proposed pathophysiologic mechanisms. There are currently no specific recommendations concerning pharmacotherapy of obesity-hypertension because each drug group has pros and cons.

Antihypertensive Agents↗
PubMed2000

Obesity-hypertension: the effects on cardiovascular and renal systems.

Longitudinal and cross-sectional studies suggest that a large number of obese patients have a high prevalence of hypertension. This association causes the following changes: insulin and leptin resistance with a suppressed biologic activity of natriuretic peptide, which contributes to sodium retention with concomitant expanded cardiopulmonary volume and increased cardiac output. The cellular metabolism of cations may be altered in obesity and may lead to changes in vascular responsiveness and increased vascular resistance. These changes lead to structural adaptations in the heart characterized by concentric-eccentric left ventricular hypertrophy. The hypertrophic condition provides the basis for the development of congestive heart failure and cardiac arrhythmias that may explain the higher rates of cardiac sudden death in those patients. In the kidneys, obesity hypertension may initiate a derangement of renal function. The increased deposit of interstitial cells and of extracellular matrix between the tubules induces higher interstitial hydrostatic pressure and tubular sodium reabsorption. The consequent increase in renal flow and glomerular filtration enhances albuminuria excretion and the susceptibility to the development of renal damage. In summary, the hemodynamic and structural adaptations related to obesity hypertension is the cause of greater risk for adverse cardiovascular and renal events.

Animals↗
PubMed2000

A comparison of nisoldipine ER and amlodipine for the treatment of mild to moderate hypertension.

This multicentre, double-blind, double-dummy, randomised trial compared the efficacy and tolerability of nisoldipine extended release (10-40 mg) and amlodipine (2.5-10 mg) in 161 patients. The primary end point was a between-treatment comparison of change from baseline to week 8 in mean office diastolic blood pressure (DBP). The least squares mean reductions in systolic (S)BP/DBP (+/- standard error) for nisoldipine and amlodipine were -11.7/-9.3 +/- 1.4/0.8 and -14.3/-12.0 +/- 1.4/0.8 mmHg, respectively. The DBP treatment difference was 2.7 mmHg (90% confidence interval: 1.1 to 4.3 mmHg; p = 0.005). Tolerability profiles were similar between treatments. The drug acquisition cost per mmHg DBP reduction was 40% lower with nisoldipine; an acquisition cost analysis revealed that amlodipine was 80% more expensive than nisoldipine for treating hypertension. In summary, nisoldipine and amlodipine provide clinically equivalent antihypertensive efficacy; however, nisoldipine is more economical than amlodipine.

Adult↗
PubMed1999

A low-calorie unrestricted protein diet attenuates kidney damage in uninephrectomized spontaneously hypertensive rats.

BACKGROUND/AIMS: Uninephrectomized, spontaneously hypertensive rats (UNX-SHR) develop glomerular hyperfiltration, hyperfusion, and interstitial infiltrate of the remnant kidney. Consequently, UNX-SHR is a useful animal model to investigate mechanisms involved in the progression of hypertensive renal disease. METHODS: Body weight; tail systolic blood pressure (SBP); urine excretion of protein, urea, and electrolytes; and serum biochemistry were determined in UNX-SHR at 2 months of age prior to uninephrectomy (week 0), prior to treatment (week 8) with a low-calorie (LC) or control diet, and one month after diet treatment (week 12). The LC diet was modified to allow equal intake of protein, sodium phosphorus, and other nutrients in both groups. RESULTS: UNX-SHR treated with the LC diet had significantly lower body weights and SBP at the end of the experiment than did the controls (p < 0.0001). Changes in serum biochemistry and 24-hour urinary excretion of protein, sodium, potassium, and urea nitrogen in both groups were not statistically significant. The final glomerular filtration rate and renal plasma flow were similar in both groups, but the LC diet significantly reduced the glomerular damage index (0.0007), mesangial expansion index (p < 0.002), volume of interstitium per cortex (p < 0.0003), tubular interstitium volume fraction (p < 0.0008), glomerular volume (p < 0.02), and remnant kidney weight (p < 0.01). CONCLUSION: We demonstrated that in UNX-SHR, the prevention of renal damage by LC diet may involve diminished glomerular growth and interstitial infiltrate without changes in renal hemodynamics. Consequently, LC diet, regardless of protein ingestion, may be an important tool in the prevention of renal damage in hypertension. Additional studies of obese-hypertensive rats may confirm the beneficial effect of a LC diet and weight reduction on the renal damage of obesity-hypertension.

Animals↗
PubMed1999

Obesity-associated hypertension: hypothesized link between etiology and selection of therapy.

The association of obesity and hypertension is characterized hemodynamically by an increase in absolute circulating intravascular volume that induces increased cardiac output and total peripheral resistance that remains inappropriately normal. These changes constitute the hemodynamic basis for the increase in blood pressure in obesity. Obesity-associated hypertension is also characterized by an abnormal renal response, including increased renal blood flow and a rise in glomerular and interstitial pressures. These hemodynamic changes induce the following structural changes in the heart: enlarged left atrial, ventricular and aortic root diameters as well as increased posterior septal wall thickness and left ventricular mass. The hemodynamic changes in the kidneys generate higher glomerular volume and increased interstitial infiltrate, which may cause compression of the tubules and blood vessels of the renal medulla. Weight reduction is an effective tool in the control of blood pressure, and significantly reduces the metabolic and hemodynamic derangements that occur with obesity. However, since weight reduction compliance is difficult to maintain, pharmacological agents are often needed to control blood pressure. Angiotensin-converting enzyme inhibitors, calcium channel blockers and alpha- adrenergic blocking agents may be the most appropriate therapy for obesity-associated hypertension since they intervene with some of the previously described pathophysiological conditions.

Antihypertensive Agents↗
PubMed1998

Nocturnal reduction of blood pressure and the antihypertensive response to a diuretic or angiotensin converting enzyme inhibitor in obese hypertensive patients. TROPHY Study Group.

During a 12-week, multicenter study to evaluate the efficacy and safety of lisinopril and hydrochlorothiazide (HCTZ) for the treatment of obesity-related hypertension, ambulatory blood pressure (ABP) monitoring was performed both at baseline and at study completion in 124 patients. Patients were randomized to three groups: placebo, lisinopril (10, 20, or 40 mg/day), or HCTZ (12.5, 25, or 50 mg/day). All groups were matched with regard to sex, race, age, body mass index, and waist/hip ratio. The primary analysis of ABP data revealed that both lisinopril and HCTZ effectively lowered mean 24-h systolic (SBP) and diastolic (DBP) blood pressure compared with placebo, (mean change from baseline SBP/DBP: -12.0/-8.2, -10.6/-5.5, and -0.3/-0.5 mm Hg, respectively); however, lisinopril lowered DBP better than HCTZ (P < .05). Secondary analyses of groups revealed that men responded better to lisinopril than HCTZ (-11.9/-7.3 v -6.6/-3.5 mm Hg, respectively), whereas women responded well to both drugs. White patients responded better to lisinopril than HCTZ, whereas black patients showed a significant response to HCTZ only. Response to treatment was also influenced by patient classification of 24-h blood pressure profiles, ie, "dipper" or "nondipper." Overall, the majority of obese hypertensives were nondippers. Nondippers (n = 82) responded well to both drugs (-10.4/-6.9 v -12.5/-5.7 mm Hg, P < .05 v placebo), whereas dippers (n = 42) responded to lisinopril (-11.7/ -9.4 mm Hg, P < .05 v placebo and HCTZ), but not HCTZ (-5.6/-4.1 mm Hg, P = NS v placebo). Results of 24-h ABP data show that both lisinopril and HCTZ are effective therapies for obesity-related hypertension and that response to treatment is influenced by sex, race, and dipper/nondipper status.

Adult↗
PubMed1997

Nonpharmacologic approaches to hypertension. Weight, sodium, alcohol, exercise, and tobacco considerations.

Weight loss decreases blood pressure, and this change can be sustained over the long-term when the lower weight is maintained. Salt restriction may be effective in blood pressure control only in salt-sensitive individuals. Heavy drinkers (those who drink more than three drinks [30 mL] daily) experience deleterious effects such as hypertension and more cardiovascular risk factors. Consequently, they should be advised to reduce alcohol intake to less than 30 mL daily. Endurance training with dynamic exercise appears to be beneficial for hypertensive patients, although recommendation guidelines are still imprecise. Finally, smoking cessation has not been proven to decrease blood pressure levels but should nonetheless be recommended because of its favorable effects on cardiovascular morbidity and mortality.

Alcohol Drinking↗
PubMed1997

Comparative results of early and delayed cannulation of arteriovenous graft in haemodialysis.

OBJECTIVE: To determine whether arteriovenous graft (AVG) can be cannulated for haemodialysis 24-48 h following placement. DESIGN AND MATERIALS: Thirty-six upper extremity Gore-Tex PTFE arteriovenous grafts were cannulated for haemiodialysis 24-36 h (n = 18) and at 10-14 days (n = 18) following insertion. The determinant parameters were compression time to control bleeding, venous back pressure, haematoma, infection and occlusion. MAIN RESULTS: In a 40 day follow-up, there were no significant difference in cannulation of AVG at 24-36 h vs. 10-14 days using the predetermined parameters. CONCLUSION: Early graft cannulation produced no adverse results than late cannulation when the diameter of the tunneller matched the diameter of the graft. Early graft cannulation was safe and recommended.

Arm↗
PubMed1997

Lisinopril versus hydrochlorothiazide in obese hypertensive patients: a multicenter placebo-controlled trial. Treatment in Obese Patients With Hypertension (TROPHY) Study Group.

Because obesity-associated hypertension has unique hemodynamic and hormonal profiles, certain classes of antihypertensive agents may be more effective than others as monotherapy. Thus, we compared the efficacy and safety of the angiotensin-converting enzyme inhibitor lisinopril and the diuretic hydrochlorothiazide in a 12-week, multicenter, double-blind trial in 232 obese patients with hypertension. Patients with an office diastolic pressure between 90 and 109 mm Hg were randomized to treatment with daily doses of lisinopril (10, 20, or 40 mg), hydrochlorothiazide (12.5, 25, or 50 mg), or placebo. Mean body mass indexes were similar for all patients. At week 12, lisinopril and hydrochlorothiazide effectively lowered office diastolic (-8.3 and -7.7 versus -3.3 mm Hg, respectively; P<.005) and systolic (-9.2 and -10.0 versus -4.6 mm Hg, respectively; P<.05) pressures compared with placebo. Ambulatory blood pressure monitoring confirmed that lisinopril and hydrochlorothiazide effectively lowered 24-hour blood pressure compared with placebo (P<.001). Significant dose-response differences were observed between treatments. Sixty percent of patients treated with lisinopril had an office diastolic pressure <90 mm Hg compared with 43% of patients treated with hydrochlorothiazide (P<.05). Responses to therapies differed with both race and age. Neither treatment significantly affected insulin or lipid profiles; however, plasma glucose increased significantly after 12 weeks of hydrochlorothiazide therapy compared with lisinopril (+0.31 versus -0.21 mmol/L; P<.001). Hydrochlorothiazide also decreased serum potassium levels by 0.4 mmol/L from baseline. In conclusion, lisinopril was as effective as hydrochlorothiazide in treating obese patients with hypertension. Treatment with angiotensin-converting enzyme inhibitors may show greater efficacy as monotherapy at lower doses compared with thiazide diuretics, may have a more rapid rate of response, and may offer advantages in patients at high risk of metabolic disorders.

Adult↗
PubMed1997

Reciprocating gait orthosis powered with electrical muscle stimulation (RGO II). Part I: Performance evaluation of 70 paraplegic patients.

Seventy paraplegics were fitted with an improved Reciprocating Gait Orthosis powered with or without (low-level injury) electrical stimulation of the thigh muscles (RGO II) as a secondary rehabilitation phase after the acute period. The patients comprised a broad cross-section of the paraplegic population applying for medical services and varied in age from 16 to 55 years, time since injury ranging from less than 1 to 15 years, injury levels ranging from C-6/7 to T-11/12, and varying levels of spasticity, contractures, scoliosis and other related medical and physiologic problems. The success/failure ratio was dependent on the injury level, which was 1:1 for paraplegics with injury level at C-6/7; 1.67:1 for those with injury of T-1/3; and about 4:1 for paraplegics with injury level from T-3 to T-12. Lack of motivation and medical problems unrelated to the RGO II treatment were the primary reasons for failure. The duration of treatment (outpatient service three times per week) ranged from 2 to 48 weeks (mean: 16). Forty-one patients who completed the RGO II rehabilitation and were sent home with the orthosis for independent use (for at least 6 months and up to 3 years) were surveyed by a staff member for analysis of the meaning and impact of the RGO II on the patient's life and health, and potential problems. It was shown that 80.5% of the 41 patients were regular users and 19.5% were non-users. Thirty-eight of the 41 patients declined an offer to return the RGO II equipment for a full refund, while three patients were willing to return the orthosis. It was concluded that the RGO II is viable orthosis for restoring standing and limited walking in paraplegics while providing sufficient function, safety, and reliability. The most appropriate patients for the use of such an orthosis consist primarily of those with T-3 to T-12 injury level and good motivation, although highly selected patients with higher injury levels also can benefit from its use. Regular use of the RGO II, even for exercise only, had a general positive impact on the patients' health and outlook.

Adolescent↗
PubMed1997

Reciprocating gait orthosis powered with electrical muscle stimulation (RGO II). Part II: Medical evaluation of 70 paraplegic patients.

Medical evaluation was performed on a group of paraplegics who were trained to walk with the Reciprocating Gait Orthosis powered with electrical muscle stimulation (RGO II). The evaluation included changes in spasticity, cholesterol level, bone metabolism, cardiac output and stroke volume, vital capacity, knee extensors torque, and heart rate at the end of a 30-meter walk. After an average of 14 weeks of training during which patients walked for 3 hours per week, significant reductions in spasticity, total cholesterol and low-density lipids, hydroxyproline/creatinine ratio, and increased knee extensor torque were evident. The data also showed that improvements occurred in the calcium/creatinine ratio, serum calcium and alkaline phosphatase levels, cardiac output and stroke volume, and vital capacity, yet these improvements were not statistically significant. The final heart rate at the end of a 30-meter walk showed that the RGO II required only a moderate level of exertion, which was found to be the lowest among the other mechanical or muscle stimulation orthoses available to paraplegics. It was concluded that the limited but reasonable level of functional regain provided by the RGO II is associated with a general improvement in the paraplegic's physiological condition if used for a minimum of 3 to 4 hours per week.

Bone Resorption↗
PubMed1997

Accuracy of formula-derived creatinine clearance in paraplegic subjects.

The usefulness of formula-derived creatinine clearance (CC) is not well established among the paraplegic population. We prospectively collected 24-hour-urines from paraplegic subjects, obtaining 81 collections from 42 patients over 27 months. After validation, 57 collections were used to obtain measured CC. CCs were also estimated using several formulae. Measured CC and estimated CC were then compared. In the case of the Cockroft-Gault formula, the overall correlation was excellent, with an r value of 0.88 and p = 0.0001. In our study 40, 70, and 93% of the estimated CCs were within 10, 20, and 33% of the measured CCs. These numbers are similar to the ones reported by Cockroft and Gault. Also, the data on measured creatinine clearance in paraplegics compared favorably with parallel data obtained from nonparaplegics (91 24-hour-urine collections, 65 validated). We conclude that the Cockroft-Gault formula (and other formulae) estimate creatinine clearance as accurately in the paraplegic population as they do in the nonparaplegic population.

Adult↗
PubMed1996

Obesity-related hypertension: its physiological basis and pharmacological approaches to its treatment.

Obesity-related hypertension is a common pathological disorder that can occur at any age and in any sex or race. Some of the metabolic, endocrinologic, adrenergic, and hemodynamic changes associated with this condition are reversed, in part, by weight reduction, which coincidentally decreases blood pressure (BP) in obese hypertensive patients. However, a major problem for obese hypertensives is dietary noncompliance. Consequently, a pharmacologic approach to obesity-related hypertension that meets the specific requirements of this complex pathological condition should be recommended when the initial nonpharmacological approach falls. Diuretics and beta-adrenergic blocking agents have been shown to be effective in decreasing BP in obese hypertensives, but they also decrease insulin sensitivity and increase cholesterol and lipoprotein concentrations. Calcium channel blockers, alpha 1-adrenoreceptor blocking, and angiotensin-converting enzyme inhibitor agents may offer an efficient and safe antihypertensive approach in obese hypertensive patients.

Antihypertensive Agents↗
PubMed1995

Obesity-related hypertension: mechanisms, cardiovascular risks, and heredity.

Recent investigations cast some doubts on the status of insulin resistance as a trigger in hyperinsulinemia-associated hypertension or obesity-related hypertension, or both. Major epidemiological studies have shown that central adiposity is a powerful risk factor for stroke or coronary artery disease when accompanied by hypertension or hypertriglyceridemia. New heredity studies have failed to identify a common gene that may explain obesity-related hypertension.

Animals↗
PubMed1993

Low calorie unrestricted protein diet attenuates renal injury in hypertensive rats.

In the present investigation we researched the effects of low calorie diet without protein restriction on the renal function and glomerular injury of uninephrectomized spontaneously hypertensive rats. We compared the findings with those that occurred in two different groups of uninephrectomized spontaneously hypertensive rats: one treated with oral hydralazine (10 mg/kg per day) and a second fed regular food. The low calorie diet and hydralazine treatment significantly reduced intra-arterial blood pressure in each group (p < 0.05 and p < 0.001, respectively). The control group showed at the end of the experiment a slight but not significantly different increase in the intra-arterial blood pressure. Low calorie diet was more effective in protecting the kidney function. Creatinine clearance after treatment was significantly higher in uninephrectomized spontaneously hypertensive rats on a low calorie diet than in either the hydralazine-treated or control groups (p < 0.01). The 24-hour urinary protein excretion in the low calorie diet group was significantly lower than in the control group (p < 0.05) and lower but not statistically different from the hydralazine-treated group. The mean glomerular injury index of the remaining kidney in the low calorie diet group was lower than in either the hydralazine-treated or control groups (p < 0.05), and the mean mesangial expansion index in the low calorie diet group was significantly lower than in the control group (p < 0.05). The favorable effect of low calorie diet on renal function was independent of protein restriction or sodium and potassium content.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗