Screening for suicide risk in inmates.
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Adult↗
Biomedical subjects
L G Sherman
Publications and source records attributed to L G Sherman.
Piretanide, a potent diuretic with potassium-sparing properties, for the treatment of congestive heart failure.
The diuretic and clinical efficacy and safety of piretanide, a new high-ceiling loop diuretic, was determined in patients with mild to moderately severe congestive heart failure. Piretanide (n = 20) administered orally in a daily dosage of up to 24 mg was compared with placebo (n = 18) for 28 days, using a double-blind, randomized, parallel design. Patients were hospitalized during the first 5 days of the study when dosage titration was established and 24-hour fractionated urine collections were obtained. Piretanide caused significant diuresis for 3 hours after ingestion with a natriuretic response noted for up to 6 hours. While occasional kaliuretic response was noted, it did not significantly increase 24-hour urinary potassium excretion. Only one patient treated with the highest allowed dose of piretanide developed mild hypokalemia. An improvement in New York Heart Association functional class status was noted after piretanide therapy. In contrast, patients who received placebo exhibited no significant improvement. BUN increased in nine piretanide-treated patients; two were discontinued from the study because of progressive azotemia. However, there was no significant increase in serum creatinine levels. Other blood, physical, ECG, and audiometric examinations also revealed no significant abnormalities. The study suggests that oral piretanide is a relatively safe and effective diuretic for treating congestive heart failure with a potential advantage of having potassium-sparing properties.
Adult↗
Sustained improvement of cardiac function in patients with congestive heart failure after short-term infusion of dobutamine.
Fifteen patients with congestive cardiomyopathy (six idiopathic and nine alcoholic) manifested by heart failure (New York Heart Association class III or IV) were randomly assigned to a protocol in which dobutamine (n = 8) or 5% dextrose in water (n = 7) was infused continuously for 72 hr. The dose of dobutamine was titrated to increase cardiac output to twice the baseline values. The patients were evaluated before infusion, shortly after infusion, and 1, 2, and 4 weeks thereafter. Functional class improved in six of eight dobutamine-treated patients but in only two of seven control patients during the 4 week observation period. Maximal exercise time and left ventricular ejection fraction increased significantly above baseline only in the dobutamine group. However, neither dobutamine nor placebo infusion produced significant changes shortly after infusion in heart rate, cardiac index, or total peripheral vascular resistance at rest or during exercise at similar workloads. The group receiving dobutamine did show a reduction in systemic systolic and pulmonary arterial mean and diastolic pressure at rest (123 +/- 5 to 108 +/- 6, 32 +/- 5, to 24 +/- 3, and 26 +/- 4 to 20 +/- 2 mm Hg, respectively). In addition, total body oxygen consumption during similar workloads was lower after dobutamine infusion than before.(ABSTRACT TRUNCATED AT 250 WORDS)
Catecholamines↗
Nifedipine in chronic stable angina: a double-blind placebo-controlled crossover trial.
Thirty patients with chronic stable angina pectoris were randomized in a double-blind prospective placebo-controlled crossover trial to assess the efficacy of nifedipine (30 to 60 mg/day orally) in controlling symptoms and objective signs of myocardial ischemia using a symptom-limited treadmill exercise test. Adverse effects that occurred during both nifedipine and placebo treatment were minor and generally well tolerated. Twenty-three patients were analyzed from the crossover phase of the study. Nifedipine significantly reduced the frequency of angina by 55% and nitroglycerin consumption by 59%, and increased exercise time by 34%. These changes were significantly greater than those in the placebo group. Hemodynamic evaluation during exercise revealed a significant reduction in systolic and diastolic blood pressures in the nifedipine group at the onset of angina and at maximal exercise without significant differences in heart rate responses in the nifedipine and placebo groups. The pressure-rate product during submaximal exercise was significantly smaller in the nifedipine group than in the placebo group, but did not differ significantly in the 2 groups at the onset of angina or on maximal exercise. Furthermore, S-T segment depressions that occurred during exercise at the same pressure-rate products were smaller in the nifedipine period than in the placebo period. Thus, it appears that the antianginal effects of nifedipine are caused by a reduced myocardial oxygen demand for a specific work load and possibly by an increased blood supply to ischemic myocardium.
Adult↗
Nursing and computers: the present and implications for the future.
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Computers↗
Renin-angiotensin system inhibition in acute myocardial infarction in dogs. Effects on systemic hemodynamics, myocardial blood flow, segmental myocardial function and infarct size.
Acute left anterior descending coronary artery occlusion was produced in 21 conscious, chronically instrumented dogs. Forty minutes after coronary occlusion, nine dogs were given i.v. teprotide, 25 micrograms/kg/min, followed by oral doses of captopril, 10 mg/kg every 8 hours for 24 hours. The remaining 12 dogs served as saline-infused controls. In all dogs, acute coronary occlusion increased plasma renin activity and peripheral vascular resistance and reduced cardiac output, but did not change mean aortic blood pressure significantly. Teprotide significantly (p less than 0.05) decreased peripheral vascular resistance (from 3804 +/- 1158 to 2876 +/- 816 dy-sec-cm-5) (+/- SD) and mean aortic pressure (from 117 +/- 12 to 107 +/- 15 mm Hg), and increased cardiac output (from 2.63 +/- 0.67 to 3.12 +/- 0.74 l/min). Teprotide also produced a relative increase in flow to the renal and splanchnic circulations compared with the saline-treated controls. There were, however, no differences in segmental systolic shortening, blood flow in the normal or ischemic myocardium, or infarct size. These results indicate that the renin-angiotensin system may play an important role in dogs with acute coronary occlusion and that blockade of this system lowers systemic blood pressure and improves cardiac output. However, direct effects of renin-angiotensin system blockade on the myocardium are lacking; there were no changes in myocardial blood flow, myocardial mechanics or infarct size.
Animals↗
The effect of verapamil on mechanical performance of acutely ischemic and reperfused myocardium in the conscious dog.
The effect of verapamil, an inhibitor of transmembrane calcium flux, was studied in intact conscious dogs with myocardial ischemia produced by inflating a balloon cuff implanted on the left anterior descending coronary artery. Six dogs received a continuous infusion of verapamil (10 microgram/kg per min) beginning prior to coronary occlusion, and six received normal saline infusions. Systolic ejection shortening (SES) was measured from subendocardial ultrasonic crystals implanted in the central ischemic zone (IZ) and border zone (BZ), and in a nonischemic control zone (CZ). Hearts were paced at a constant heart rate with periodic introduction of closely coupled extrasystoles. SES was measured both for normally paced beats and during postextrasystolic potentiation (PESP). Regional myocardial blood flow was measured by injecting radioactive microspheres before, during, and after coronary occlusion. There were no significant differences between verapamil-treated dogs and saline control dogs in mean aortic pressure, heart rate, left ventricular end-diastolic pressure or dP/dt, cardiac output, or regional myocardial blood flow in IZ, BZ, or CZ. Differences in mechanical performance between two groups were noted, however. In the IZ, SES was abolished completely for normally paced beats in both groups but was significantly preserved for PESP beats in the verapamil-treated animals. In the BZ, SES was significantly reduced for normally paced beats only in the saline controls, and PESP responses were preserved to a significantly greater degree in the verapamil-treated animals. These results indicate that verapamil pretreatment exerts beneficial effects upon mechanical performance of ischemic myocardium. Since no changes in systemic hemodynamics or regional myocardial blood flow were observed, the effect may be due to the calcium-antagonistic properties of the agent.
Acute Disease↗
Dobutamine infusion in conscious dogs with and without acute myocardial infarction. Effects on systemic hemodynamics, myocardial blood flow, and infarct size.
We infused dobutamine (20 microgram/kg per min) intravenously, once before and once after coronary artery occlusion, in 10 chronically instrumented dogs. Both infusions increased cardiac output and left ventricular dP/dt and dP/dt/P, but divergent effects on heart rate and aortic blood pressure were observed. Dobutamine decreased heart rate and increased mean aortic blood pressure before coronary artery occlusion, whereas after occlusion it increased heart rate while mean aortic blood pressure remained unchanged. A greater decrease in total peripheral vascular resistance occurred during dobutamine infusion after coronary artery occlusion than before. These differences may relate to withdrawal of enhanced sympathetic tone after coronary occlusion. Similar infusions of normal saline (n = 9) produced no systemic hemodynamic changes either before or after coronary artery occlusion. Myocardial blood flow increased to both non-ischemic and ischemic regions of the heart during dobutamine infusion, but the endocardial:epicardial blood flow ratio did not change significantly. In addition, infarct size, measured by nitroblue tetrazolium stain, was smaller in the dobutamine group (10 +/- 1 g) than in the normal saline group (15 +/- 2 g). Neither left ventricular weight nor risk zone differed between the two groups. These results indicate that dobutamine may be a useful inotropic agent during acute myocardial infarction.
Animals↗