Exercise decreases the risk of development of diabetes mellitus, So...
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Biomedical subjects
Publications and source records attributed to C A Nugent.
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UNLABELLED: This study tested the capability of a single 42-microgram dose of inhaled salmeterol xinafoate, a long-acting beta 2-agonist, to protect against bronchoconstrictive effects of exposure to 0.75 ppm sulfur dioxide (SO2) during exercise, for up to 24 h. Ten SO2-responsive adult volunteers with stable asthma were studied under 4 conditions of drug pretreatment/exposure, administered in random order, double-blind: salmeterol/SO2, placebo/SO2, salmeterol/clean air, and placebo/clean air. Each subject underwent 10-min exposure/exercise challenges in a chamber 1, 12, 18, and 24 h after pretreatment. Exercise ventilation rates averaged 29 L/min. Response was measured as the decrement in FEV1 between preexposure and postexposure (lowest value within 30 min). After salmeterol, mean decrement post-SO2 was 7% at 1 h and 12% at 12 h. At 18 and 24 h after salmeterol, and at all times after placebo, mean decrements were 25 to 30%. After 18 and 24 h, salmeterol still improved base-line FEV1 relative to placebo, although improvement was not statistically significant at 24 h. Acute symptom increases accompanied FEV1 decrements. CONCLUSION: In our asthmatic subjects, pretreatment with salmeterol imparted clinically and statistically significant (p < 0.01) protection against bronchoconstriction induced by SO2/exercise for at least 12 h, and maintained an improvement in lung function for as much as 18 h.
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White blood cell (WBC) Na+ and K+ concentrations, plasma (Na+ + K+)ATPase inhibition and blood pressure were determined in normotensive control subjects and patients with essential hypertension. While the untreated hypertensive group had significantly lower WBC K+ concentrations than the normotensive group (mean +/- SEM, 121.6 +/- 4.4 vs. 134.7 +/- 2.8 mEq/kg, p less than 0.05), no significant difference was observed in WBC Na+ concentrations between the 2 groups. The mean of plasma (Na+ + K+)-ATPase inhibition in untreated hypertensive patients was higher than that in normotensive controls (14.8 +/- 1.7 vs. 7.2 +/- 1.8%, p less than 0.05). The correlations between (Na+ + K+)ATPase inhibition and mean blood pressure and between WBC Na+/K+ ratio and mean blood pressure were significant (r = 0.278, p less than 0.05 and 0.270, p less than 0.05, respectively), but both were weak. However, untreated hypertensive patients with higher (Na+ + K+)ATPase inhibition had significantly higher WBC Na+/K+ ratios than untreated patients with less (Na+ + K+)ATPase inhibition. These results suggest a contribution of plasma (Na+ + K+)ATPase inhibition in the production of high blood pressure in a subset of patients with essential hypertension, which results in altered intracellular K+ concentrations.
Two multicenter, double-blind, randomized studies were performed to determine the antihypertensive efficacy and effects on laboratory values of a new, shorter-acting formulation of metolazone in patients with mild to moderate hypertension. After baseline placebo-control periods, 105 patients were randomly assigned to receive single daily doses of either placebo or 0.5, 1.0, or 2.0 mg of the new formulation of metolazone for six weeks in one study, and 164 patients were randomized to receive 0.5, 1.0, or 2.0 mg of the new formulation of metolazone or 2.5 mg of the older, long-acting metolazone in the other. Mean blood pressure reductions in all three metolazone groups were statistically and clinically significant. Blood pressures of 51% to 58% of patients in the 0.5-mg metolazone group were controlled (diastolic blood pressure less than 90 or a fall of greater than or equal to 10 mmHg from baseline). Reductions in mean serum potassium levels were dose-related. We conclude that 0.5 mg of metolazone is safe and effective therapy for hypertension; it will significantly reduce systolic and diastolic blood pressure and minimizes changes in laboratory test values.
Although the common form of osteoporosis associated with aging can be treated, it is best to avoid the problem by not letting the disease develop. Osteomalacia is caused by inadequate or delayed mineralization of bone and is treated by correcting the abnormal intake, loss, or metabolism of vitamin D, phosphate, and calcium. Paget's disease is characterized by osteoclastic resorption of bone with new bone laid down in a disorganized fashion.
The purpose of this study was to identify the best of three methods of treating hypertensive outpatients in order to minimize dietary sodium levels and thereby decrease the need for antihypertensive drugs. Forty-eight outpatients with hypertension were randomly assigned to three treatment programs: (1) advice; (2) an intensive educational program; and (3) small-group management plus feedback. This last program had a problem-solving format in which patients shared ideas and provided mutual support for dietary change. Only these group management patients were told the results of their sodium determinations. In a one-year study, group management plus the feedback to patients of information on the sodium content of their urine was more effective in decreasing dietary sodium intake than advice or an intensive educational effort.
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We examined the role of dietary electrolytes and humoral factors in causing seasonal changes in blood pressure. Normal subjects had no seasonal difference in blood pressure, although urinary sodium and norepinephrine were significantly higher in winter than in summer. In patients with essential hypertension blood pressure, urinary sodium and norepinephrine excretion and plasma norepinephrine concentration were significantly higher in winter. Plasma renin activity, plasma and urinary aldosterone and urinary kallikrein excretion were not significantly different between the two seasons in both normal subjects and hypertensive patients. In conclusions, the blood pressure of patients with essential hypertension has a seasonal variation with higher pressures in the winter than in the summer. Increased sympathetic nervous activity and an increased load of sodium presented to the kidney for excretion may be contributing factors in the rise in blood pressure in winter in patients with essential hypertension.
Two sisters were found to have Bartter's syndrome. Both had hypokalemia, hyperreninemia, normal BPs, and decreased pressor responses to angiotensin II. During a water diuresis, patient 1 had an abnormally low distal tubular fractional reabsorption of chloride initially, but this normalized after hypokalemia was corrected for one year. Patient 2 had no demonstrable defect in chloride transport. Hypokalemia in Bartter's syndrome may be caused by some hereditary mechanisms other than defective reabsorption of chloride in the distal tubules.
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The ability of glucagon and several of its semi-synthetic analogues to stimulate glucose production in isolated rat hepatocytes was measured and compared for relative potencies. The order of decreasing biological activities of glucagon in this assay was as follows: glucagon greater than [HArg12]-glucagon greater than [des-Asn28, Thr29][homoserinehydrazide27]-glucagon approx. equal to [des-His1]-glucagon greater than [des-Asn28, Thr29][homoserinelactone27]-glucagon greater than [des-Asn28, Thr29]-[n-butylhomoserineamide27]-glucagon greater than glucagon1-21. Qualitatively, these results are similar to those obtained previously in the hepatic plasma membrane adenylate cyclase assay. Minor exceptions were noted for the hydrazide derivative and the partial agonist [des-His1]-glucagon, both of which were slightly more potent relative to glucagon in the glycogenolytic assay than in the adenylate cyclase assay. The assay provides important insight into glucagon structure-function relationships.
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Compliance was compared in 52 previously noncompliant hypertensive patients randomly assigned for eight weeks to either a nurse-operated hypertension clinic (control) or a patient-operated hypertension group] (experimental). Control patients listened to audiotapes on hypertension and its management and met individually with a nurse who adjusted their drug regimens. Experimental patients were trained to take their own blood pressure (BP) and select their own drugs in a group program emphasizing informed self-help. After the eight-week training period and at two- and six-month follow-up visits, both groups had significantly lower BPs. Compared with control patients, experimental patients had lower diastolic BPs, better pill counts, and better attendance (all P < .05). This study suggests that training noncompliant patients in groups to manage their own hypertension may achieve better results than traditional management programs.
Sex histories and serum samples were obtained from 27 hypertensive men before and after 3 months of therapy with either 100 mg of hydrochlorothiazide or 0.25 mg of reserpine daily. Sera were analyzed for testosterone, dihydrotestosterone, estradiol, luteinizing hormone and prolactin. Both drugs effectively lowered pressure. The incidence of impaired sexual performance was low and insignificantly different in the two treatment groups. There were no significant changes in serum hormone concentrations as a result of drug therapy.
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Patients with abnormalities due to bronchogenic carcinoma, noted on chest films, have decreased peripheral blood lymphocytes and increased total white cells compared to patients with benign lesions. Precision studies of 40 patients revealed that a low percentage of lymphocytes averaged over a three-week period distinguished bronchogenic carcinoma patients from patients with benign lesions with 95 percent overall accuracy. Lesions as small as 1.0 cm were correctly predicted to be malignant. Mean 8 AM plasma cortisol levels were elevated in patients with bronchogenic carcinoma and there was a negative correlation of 8 AM plasma cortisol levels with precentage of lymphocytes. Increased levels of endogenous cortisol may account for lymphocytopenia in bronchogenic carcinoma patients.