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Biomedical subjects

J N Cohn

Publications and source records attributed to J N Cohn.

At least 433 records · Page 24Linked to original sources
PubMedDate not supplied

Cutaneous administration of nitroglycerin: a review.

Chronic administration of nitroglycerin may have important therapeutic effects in patients with angina, acute myocardial infarction, congestive heart failure and peripheral vascular disease. Because of unpredictable oral absorption and short duration of action, topical preparations provide an alternative mode of administration. New controlled release transdermal preparations appear to produce constant plasma nitroglycerin concentrations of 0.2-0.3 ng/ml that persist for up to 24 hours. Additional clinical trials of the therapeutic response to this drug form are necessary, particularly in regard to the relative hemodynamic efficacy and side-effect profile of sustained vs. fluctuating plasma nitroglycerin concentrations.

Administration, Topical↗
PubMedDate not supplied

Pathophysiologic and prognostic implications of measuring arterial compliance in hypertensive disease.

Structural alterations of the arterial wall precede atherosclerosis and cardiovascular events. Endothelial dysfunction appears to be the earliest marker for this structural change that makes the vasculature sensitive to the adverse effects of pressure, lipids, diabetes, smoking and other so-called risk factors. Reduced arterial compliance or elasticity provides an index to the structural abnormalities associated with aging and disease states. Preliminary studies suggest that an alteration in pulsewave oscillations induced at small artery branch points serves as a guide to endothelial dysfunction and reduced nitric oxide bioactivity. Additional studies are urgently needed to document the usefulness of clinical measurement of arterial compliance as a marker for the vascular abnormality that leads to cardiovascular disease and as a guide to efficacy of therapeutic interventions.

Arteries↗
PubMedDate not supplied

Acute hemodynamic and hormonal effects of central versus peripheral sympathetic inhibition in patients with congestive heart failure.

Indoramin, an alpha 1 antagonist, and guanabenz, an alpha 2 agonist, were given to 10 patients with severe congestive heart failure to compare the hemodynamic and hormonal effects of a reduction in sympathetic tone obtained through inhibition of postsynaptic alpha 1 receptors versus the decrease in sympathetic activity achieved by stimulating central or presynaptic peripheral alpha 2 adrenoceptors. Both drugs produced similar reduction in systemic arterial pressure. However, only indoramin significantly decreased systemic and pulmonary vascular resistances from 1529 +/- 526 to 1071 +/- 356 and from 721 +/- 422 to 412 +/- 257 dynes X s X cm-5, respectively, and increased stroke index from 26.6 +/- 9.5 to 33.3 +/- 9.5 ml/m2 (all p less than 0.01). Heart rate fell significantly only after guanabenz. Plasma norepinephrine, unchanged after indoramin, fell in each patient after guanabenz; the mean value decreased from 746 +/- 332 to 461 +/- 255 pg/ml (p less than 0.01). Plasma renin activity increased only after indoramin. The data demonstrate: (a) a decrease in sympathetic activity due to blockade of alpha 1 adrenoreceptors produces marked peripheral and pulmonary vasodilation; (b) noradrenergic transmitter release in heart failure is regulated by alpha 2 receptors; (c) an alpha 2-mediated decrease in sympathetic activity and in plasma norepinephrine has a bradycardic effect but does not produce a vasodilator effect. Although the acute hemodynamic effects of indoramin were more prominent than those of guanabenz, the more favorable neurohumoral effects of guanabenz suggest the possibility of long-term benefit in the treatment of heart failure.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Effect of salt on the vascular lesions of spontaneously hypertensive rats.

High salt intake accelerates hypertension in humans and increases cardiovascular morbidity and mortality. The temporal relation between blood pressure (BP) elevation and appearance of vascular lesions during salt-loading was studied in the spontaneously hypertensive rat (SHR). Starting at 5 weeks of age, SHRs and normotensive Wistar-Kyoto rats (WKYs) were given 1% NaCl in their drinking water SHRs and WKYs on tap water served as controls. Animals from each group were sacrificed at 10 and 20 weeks of age, and the aorta and intrarenal vessels were studied by light and electron microscopy. Neither BP nor vascular morphology of WKYs were affected by 1% NaCl. In SHRs, the course of BP was not affected by the addition of salt for at least 11 weeks, but vascular changes were significantly aggravated within 5 weeks. Thus, aortic intimal lesions progressed more rapidly so that, by 20 weeks of age, 50% of the animals had 3+lesions while, in control SHRs, they did not exceed the 2+grade. Salt-loading resulted in significant thickening of the aortic media between the 10th and 20th week of age while control SHRs showed no increment within the same time interval. Also, small intrarenal arterial vessels of salt-treated SHRs had significantly narrower lumina and greater wall thickness at both 10 and 20 weeks of age. In addition, they showed intimal proliferations and necrotizing lesions which were absent from control SHRs at these ages. These results show that, in this experimental model, the aggravation of vascular changes is not merely a sequela of further elevation of BP. Since the adverse effect of salt on the vessels was not seen in WKYs, it is likely that this effect is related to genetic factors or to higher susceptibility of hypertensive vessels.

Animals↗
PubMedDate not supplied

Short-term systemic hemodynamic adaptation to beta-adrenergic inhibition with atenolol in hypertensive patients.

Early systemic hemodynamic adjustments to antihypertensive therapy with the cardioselective beta inhibitor, atenolol, were investigated in 12 hospitalized men, mean age 52 years, with uncomplicated mild-to-moderate essential hypertension. Twice daily measurements of cardiac output (CO) by CO2 rebreathing, blood pressure by cuff, and heart rate were performed in all subjects for 3 days before and 5 days after initiation of oral atenolol therapy (50 or 100 mg daily). Cardiac output by CO2 rebreathing was checked with dye dilution just before, and 4 hours and 4 days after the start of therapy. Plasma volume (radioiodinated albumin) was measured before therapy and on Day 5 of therapy. The CO results obtained with the two methods were not significantly different (r = 0.88, p less than 0.01, n = 12). A reduction in heart rate, 18 +/- 2 beats/min (mean +/- SE), occurred in all patients while taking atenolol. By 4 hours after the first dose of atenolol, CO fell from 5.49 +/- 0./30 to 4.24 +/- 0.21 liters/min (p less than 0.01), while the control mean arterial pressure (MAP) of 108 +/- 4 mm Hg was not significantly changed, 110 +/- 4 mm Hg. At 24 hours, CO returned near baseline (5.10 +/- 0.21 liters/min) but MAP was reduced (95 +/- 3 mm Hg, p less than 0.001) and remained so thereafter. CO remained at baseline at 48 hours (5.50 +/- 0.29 liters/min) but fell again (p less than 0.01) to 4.81 +/- 0.11 on Day 4 and to 4.68 +/- 0.25 liters/min on Day 5 of atenolol therapy. Plasma volume, 3110 +/- 100 ml before therapy, was reduced to 2850 +/- 100 by Day 5 of atenolol therapy (p less than 0.01). The findings indicate a delayed onset of the antihypertensive action of atenolol. The transient return to baseline of CO on Day 2 and 3 of atenolol therapy suggests a reverse autoregulatory adjustment to the initial fall in CO.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Left ventricular dysfunction and heart failure. Mechanistic and therapeutic distinctions.

Dysfunction of the left ventricle may result from a variety of insults, all of which may initiate a self-perpetuating process of ventricular remodeling which may progress to end-stage heart disease. Symptoms of heart failure may or may not co-exist with this ventricular remodeling. Treatment and prevention of these two largely distinct entities differ. Symptoms may respond to diuretics, vasodilators and digoxin. Progressive ventricular remodeling may be slowed by angiotensin converting enzyme inhibitors, hydralazine + isosorbide dinitrate and beta blockers. Prevention of symptomatic heart failure is dependent on early recognition of ventricular dysfunction and aggressive treatment to slow its progression. Development of more effective and targeted therapies will be dependent on expanded insight into the cellular and molecular mechanisms contributing to the remodeling process.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Bradycardia with traumatic hyphema in children.

Eleven patients, aged 4 to 18 years, who were admitted to the hospital with the diagnosis of traumatic hyphema were placed on 24-hour cardiac (Holter) monitors. Ten of the 11 patients had episodes of bradycardia and bradyarrhythmias. Blood pressures monitored during the same period showed that the bradycardia was not hemodynamically significant. Cardiac monitoring was repeated on six patients 3 months later, and nocturnal cardiac rhythms were compared; the minimum heart rates immediately following the eye injury were significantly lower (p = .03) than those measured 3 months later. While these data do not establish a relationship between bradyarrhythmias and the frequently-observed occurrence of somnolence, it does appear that episodes of bradyarrhythmias represent a common physiologic response to traumatic hyphema, and they can be expected to resolve spontaneously.

Adolescent↗
PubMedDate not supplied

ACE inhibition and vascular remodeling of resistance vessels: vascular compliance and cardiovascular implications.

The arterial circulation is composed of conduit arteries that store blood in systole (capacitive function), small branch points that contribute to pressure oscillations and reflected waves (oscillatory function), and arterioles that control blood flow (resistance function). These vessels are lined by endothelial cells that secrete nitric oxide and other substances that influence smooth-muscle tone, growth, and structural remodeling. The role of endothelial function is greater in thin-walled vessels than in conduit arteries, including proximal elastic vessels with thick walls. Thus, endothelial dysfunction is most likely to raise resistance and alter pressure oscillations than to produce early changes in the conduit artery wall. Later structural changes, facilitated by endothelial dysfunction, lead to reduced large artery compliance and widened pulse pressure as markers of risk for a cardiovascular event. Angiotensin-converting enzyme inhibitors, particularly those with vascular effects, tend to restore endothelial function and may result in regression of the structural alterations. Pulse contour analysis is the most sensitive means of assessing both capacitive oscillatory and resistance vessel function of the vasculature. Noninvasive radial artery tonometry with computer analysis of diastolic pressure decay provides independent measures of capacitive function, oscillatory function, and resistance, which allows screening and monitoring of arterial function. Such monitoring should lead to more individualized management that could supplement pressure monitoring as a guide to the efficacy of therapeutic intervention.

Angiotensin-Converting Enzyme Inhibitors↗