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Biomedical subjects

J N Cohn

Publications and source records attributed to J N Cohn.

At least 307 records · Page 17Linked to original sources
PubMed1981

Neurohumoral control mechanisms in congestive heart failure.

Neurohumoral vasoconstrictor systems may play an important role in the hemodynamic derangement and natural history of congestive heart failure (CHF) by raising impedance to left ventricular ejection and shifting blood centrally to augment cardiac filling. Activation of the sympathetic nervous system, and renin-angiotensin system, and the antidiuretic hormone-vasopressin system can be demonstrated in clinical CHF by increased plasma levels of norepinephrine, renin activity, and arginine vasopressin. Because the magnitude of increase in each of these hormones varies widely from patient to patient, profiling of the neurohumoral response might provide new insight into the mechanisms of regulation of the circulation in CHF and into specific management with drugs to inhibit or reverse the vasoconstrictor process. Preliminary encouraging experience with converting-enzyme inhibitors to block formation of angiotensin II and alpha-receptor blockers to inhibit norepinephrine-induced vasoconstriction raise the possibility that selective therapy may eventually have a place in long-term management of CHF. Controlled trials in a larger patient population are now required.

Angiotensin II↗
PubMed1981

Pirbuterol: a new oral sympathomimetic amine for the treatment of congestive heart failure.

Fourteen patients with refractory congestive heart failure (CHF) were given a single oral dose ranging from 5 to 30 mg of the new sympathomimetic drug pirbuterol. Hemodynamic measurements and plasma pirbuterol levels were obtained at control and then serially for 6 hours following drug administration. The optimal pirbuterol dose range was determined to be 20 to 30 mg. Ten patients received 20 to 30 mg pirbuterol. In this group cardiac index was significantly increased (1.9 to 2.6 L/min/m2, p less than 0.001). Pulmonary artery wedge pressures fell significantly (24 to 20 mm Hg, p less than 0.02). Decreases were also noted in mean pulmonary artery pressure (36 to 31 mm Hg, p less than 0.02), aortic diastolic pressure (71 to 65 mm Hg, p less than 0.05), systemic vascular resistance (1782 to 1201 dynes. sec. cm-5, p less than 0.001), and pulmonary vascular resistance (265 to 175 dynes.sec.cm-5, less than 0.001). Systolic and mean aortic pressure and heart rate showed no significant change from control. Hemodynamic effects persisted for 5 hours. Pirbuterol was clinically well tolerated. The mechanism of action is unclear at this time, but both inotropic and vasodilator effects are possible. Pirbuterol orally has a marked and prolonged salutary hemodynamic effect and offers promise in CHF treatment.

Administration, Oral↗
PubMed1981

Physiologic basis of vasodilator therapy for heart failure.

In congestive heart failure, an increase in impedance to left ventricular ejection appears to be an important factor in impairing left ventricular performance. Arteriolar narrowing and decreased arterial compliance will decrease the left ventricular ejection fraction, whereas reduction in venous capacitance will shift blood centrally and increase cardiac filling. These vascular events may result from activation of the sympathetic nervous system and the renin-angiotensin system. Vasodilator drugs, by relaxing the increased vascular tone, will reduce ventricular volume and increase stroke volume, and thus improve the patient's hemodynamic and myocardial metabolic state. Translation of this acute hemodynamic response into a therapeutic benefit from long-term therapy is an attractive but not yet entirely proved thesis. Long-term controlled trials must eventually establish the place of vasodilator drug therapy in the management of different types of congestive heart failure. Furthermore, additional insight is needed into the potential for selective therapy that is tailored to counteract specific mechanisms of vasoconstriction in individual patients.

Heart Failure↗
PubMed1981

Effect of captopril on renal function in patients with congestive heart failure.

Angiotensin converting enzyme inhibitors can improve haemodynamics in patients with congestive heart failure and may enhance sodium excretion in hypertensive patients. In a metabolic unit we assessed the effects of one of these agents on renal function in nine patients with stable New York Heart Association functional class 3 or 4 congestive heart failure. Single blinded, the patients received placebo for three days, 25 to 100 mg of captopril three times a day for three days, and three more days of placebo. Mean blood pressure decreased during captopril, with little change in heart rate or respiration. Serum urea was slightly higher during captopril administration. The mean change in creatinine clearance during captopril was insignificant, but it decreased more than 25% in three of nine patients. Decreases in creatinine clearance correlated with lower blood pressure during captopril and were most obvious in patients with high baseline plasma renin activity. Urine output and both sodium and potassium excretion decreased during captopril. Thus captopril failed to improve natriuresis in patients with congestive heart failure and close monitoring of kidney function is necessary when using this agent in patients with congestive heart failure, particularly when blood pressure falls to lower levels.

Aged↗
PubMed1981

Effects of minoxidil on hemodynamics in patients with congestive heart failure.

Vasodilators used in chronic congestive heart failure are not optimal in that nitrates are predominant venodilators, prazosin is associated with tolerance development, and hydralazine produces chronic toxicity. Therefore, we studied the acute hemodynamic effects of a single dose of minoxidil in 18 patients with chronic left ventricular failure caused by ischemic or primary cardiomyopathy. Peak effects were observed 5 hours after single oral doses of minoxidil, averaging 15.3 +/- 1.4 mg (SEM). Heart rate rose slightly, from 85.4 +/- 2.9 to 90.9 +/- 3.2 beats/min, after minoxidil (p less than 0.02) and mean arterial pressure fell slightly, from 88.0 +/- 2.3 to 84.9 +/- 2.5 mm Hg (p less than 0.05). Cardiac index increased from 2.34 +/- 0.l4 to 2.95 +/- 0.29 l/min/m2 after minoxidil (p less than 0.02) and systemic vascular resistance fell from 19.6 +/- 1.5 to 15.0 +/- 1.3 units (p less than 0.01). Minoxidil did not affect right atrial, pulmonary arterial and pulmonary wedge pressures. Hemodynamic effects of minoxidil persisted for at least 8 hours after a single dose. Minoxidil appears to be an effective arterial dilating agent in patients with heart failure and resembles hydralazine in its actions. Because of its potency, prolonged duration of action and relatively low toxicity, minoxidil may be a useful vasodilator for heart failure. However, its long-term effect must be further evaluated.

Adult↗
PubMed1981

Site of premature ventricular contractions demonstrated by echocardiography.

Abnormal ventricular activation in Wolff-Parkinson-White Syndrome (WPW) can be identified by echocardiography, but the effects of premature ventricular contractions have been demonstrated. We examined motion of the interventricular septum (IVS) and left ventricular posterior wall (LVPW) by surface echocardiography in 12 awake dogs using a method developed and validated in our laboratory. Premature ventricular contractions (PVCs) were induced by right (RV) and left ventricular (LV) pacing (6 dogs), injection of dopamine (2 dogs) and phenylephrine (2 dogs), and posterior myocardial infarction (MI) caused by embolization of the circumflex coronary artery (2 dogs), and posterior myocardial infarction (MI) caused by embolization of the circumflex coronary artery (2 dogs). PVCs induced by RV and LV septal pacing showed early IVS systolic posterior motion beginning 40.0 msec (range 26--48 msec) after the pacing impulse, while LVPW showed normal motion beginning 78.8 msec (range 63--116 msec) after the pacing impulse and accompanied by decreased posterior IVS motion. PVCs induced by LVPW pacing demonstrated early LVPW systolic anterior motion beginning 43.3 msec (range 31--68 msec) after the pacing impulse, while IVS showed a normal motion which began 97.3 msec (range 76--130 msec) after the pacing impulse and was accompanied by reduced anterior motion of the LVPW. PVCs induced by dopamine and phenylephrine showed a similar echocardiographic pattern to RV and LV septal pacing, while PVCs induced by MI exhibited a pattern similar to LVPW pacing. This study demonstrates that early IVS or LVPW contraction can be demonstrated by echocardiogram, and also indicates where the site of early excitation after PVCs is.

Animals↗
PubMed1981

The effectiveness of cardiology consultation. Concordance with diagnostic and drug recommendations.

In an effort to characterize the effectiveness of cardiology consultation, the outcomes of consultants' recommendations for diagnostic actions and cardiac drugs were quantitatively examined in 394 cases. Drug recommendations were made more frequently (49 percent) than diagnostic recommendations (38 percent) and were associated with a higher rate of concordance (82 percent to 64 percent). Recommendations to start therapy with a drug, especially an antihypertensive or an antianginal, were associated with a lower concordance rate than recommendations to continue or discontinue drug therapy. Consultees' responses to recommendations for diagnostic action did not vary significantly according to the type of action suggested. Nonconcordance with diagnostic suggestions was particularly high when a service made a large number of consult requests. Concordance was increased if the consultant left a follow-up note. Consultees' responses to drug and diagnostic recommendations were independent of one another. The study represents the first systematic assessment of cardiology consultation activities and provides a methodology for subsequent studies.

Adult↗
PubMed1981

Postsynthetic variants of creatine kinase MM.

MYocardial CK-MM has been found to undergo postsynthetic modification after AMI. Studies by isoelectric focusing of normal heart extracts, serial serum samples from patients with AMI, normal sera, and sera from patients with DMD revealed the presence of four variants, designated MM-I, MM-II, MM-III and MM-IV, at pH values 6.90, 6.62, 6.36, and 6.20, respectively. The MM variants, together with two MB variants, could also be demonstrated by electrophoresis on cellulose acetate. Heart extract contained primarily MM-I. Serum samples obtained early after infarction (9 to 12 hr) showed predominantly MM-I, MM-II, and MM-III. With increase in time after infarction (24 to 96 hr), there was a gradual shift in which MM-I and MM-II decreased while MM-III and MM-IV increased. These results could be mimicked by incubating an extract of human heart with normal serum for increasing time intervals. Normal serum and serum from DMD patients--both of which contain steady-state levels of MM isoenzyme activity--showed all four variants. There was, however, a preponderance of MM-I and MM-II in normal serum, whereas serum from DMD patients showed a preponderance of MM-II and MM-III. We conclude that the process of postsynthetic modification after AMI probably starts at the site of injury in the myocardium because the variants can be demonstrated in the serum within a few hours after infarction. Further modification then occurs in the circulation after enzyme release from the site of injury has ceased. These data suggest that analysis of CK variants may provide a unique means of assessing the time of onset of necrosis in AMI and may have potential for detecting reinfarction and for monitoring the duration of enzyme release from the site of injury.

Creatine Kinase↗
PubMed1980

Hemodynamic effects of oxdralazine and hydralazine in hypertension.

Oxdralazine, a pyridazine shown to induce prolonged arteriolar dilation in animals, was given orally in doses of 15 to 30 mg to 7 subjects with hypertension. Arterial pressure fell in 2 hr (average mean of 16 mm Hg), peaking in 3 to 4 hr, and was sustained for more than 6 hr. Cardiac output and heart rate rose in 2 hr (2.1 l/min and 17 bpm) and were elevated at 6 hr (3.1 l/min and 22 bpm). Pulmonary arterial pressure and pulmonary arteriolar resistance did not change. In 6 subjects receiving oxdralazine with hydralazine 50 to 75 mg at 1-wk intervals, hydralazine induced earlier, less sustained decreases in arterial pressure and systemic vascular resistance and less of a rise in heart rate than oxdralazine alone. Circulating norepinephrine levels (radioenzymatic method) 3 hr after oxdralazine rose from a mean of 159 to 294 pg/ml, a greater (p less than 0.05) effect than after hydralazine. At the doses tested, oxdralazine is a potent systemic arteriolar dilator with longer-sustained action and more prominent reflex sympathetic stimulation than hydralazine.

Adult↗