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Biomedical subjects

R A Shiroff

Publications and source records attributed to R A Shiroff.

10 recordsLinked to original sources
PubMed1980

Validation of dynamic radiography in the dog and evaluation of ischemic dyssynergy.

If a collimated radiation detector (sodium iodide crystal) and a collimated X-ray source are positioned at right angles, scattered radiation will be sensed and the detector will generate a signal as tissue enters and leaves the "sensitive volume" formed by the intersection of the field of view of the detector and incident beam. This technique, called dynamic radiography, was used to identify and quantify the components of epicardial motion in anesthetized open-chested dogs. The data so obtained were validated by two independent optical methods: biplane cinematography and a technique that measures the shadow cast by the heart using a light beam-cadmium sulfide photocell. Displacement measured by dynamic radiography appeared to be the time integral of the scalar product of the velocity vector and the vector normal to the surface area within the sensitive volume, i.e., that component of displacement of myocardial mass that was perpendicular to the surface of the myocardium. In other words, the dynamic radiographic signal was proportional to the mass of tissue within the sensitive volume. Good agreement in terms of absolute motion, its direction, and phase was noted between predicted dynamic radiographic signals and those observed. Thus validated, this technique was found to be reliable in quantifying motion abnormalities produced by acute coronary ligation.

Animals↗
PubMed1979

Effect of coadministration of procainamide and isoniazid on each other's acetylation pathway.

The effect of isoniazid (INH) and procainamide (PA) on each other's acetylation pathway was studied in 7 normal subjects (3 rapid acetylators, 3 slow acetylators, 1 of indeterminate phenotype). Oral PA (6 mg/kg) was administered every 4 h for a total of seven doses. Following the final dose subjects received a single 300-mg oral dose of INH. Analysis of the parent drugs and their acetylated metabolites in plasma and urine revealed no effect on the acetylation of either drug. In 2 subjects (1 rapid, 1 slow acetylator) increasing doses of PA were given and the effect on INH (300 mg) acetylation measured. High mean circulating levels of PA (7.1 microgram/ml) appeared to inhibit acetylation of INH in the rapid acetylator whereas a mean PA plasma level of 8.6 microgram/ml had no effect on INH acetylation in the slow acetylator. However, the results from this study suggest that alterations of INH acetylation by PA are unlikely to be of clinical significance.

Administration, Oral↗
PubMed1978

Propranolol rebound--a retrospective study.

To assess the effects of sudden withdrawal of propranolol on inpatients with coronary artery disease, 102 patients admitted for cardiac catheterization were evaluated. Criteria for inclusion in the study were angiographically documented coronary artery disease, propranolol therapy at a mean daily dose of at least 80 mg and abrupt discontinuation of propranolol therapy before catheterization. There were 55 patients (mean age 52.5) who discontinued propranolol therapy (mean daily dose 127 mg) and a control group of 47 patients (mean age 53) who continued to receive propranolol (mean daily dose 143 mg). The criteria for morbidity were death, myocardial infarction or change in pain pattern. In the withdrawal group there were no deaths, one myocardial infarction judged to be related to catheterization and only one instance of a change in pain pattern. Thus, propranolol rebound appears to occur infrequently among hospitalized patients with reduced activity.

Adult↗
PubMed1978

Diffuse coronary artery disease in diabetic patients: fact or fiction?

To compare angiographically-determined coronary artery disease in diabetic patients with controls, 1,653 patients coming to cardiac catheterization were reviewed retrospectively to find 37 diabetic and 79 control patients matched for sex, age (+/- 3 years), and risk factors (hypertension, hyperlipidemia, and smoking). The severity of coronary artery disease was assessed using an angiographic grading system. The following results were obtained: 16 of 37 diabetic patients (43%) had three-vessel disease compared to 20 of 79 controls (25%). Seventy-six of 111 (68%) diabetic vessels were diseased compared to 110 of 237 control vessels (46%) (P less than 0.005). The total coronary score reflecting total extent of disease for diabetic patients was 371 (mean 10.0 +/- (SEM) compared to 594 for controls (mean 7.5 +/- 0.7, (P less than 0.01). Diabetic patients had a statistically similar number of diffusely diseased vessels as controls (28% vs 22%). There were only three of 76 diabetic vessels (4%) considered inoperable compared to seven of 110 (6%) control vessels. We conclude that diabetic patients with chest pain have more coronary artery disease than nondiabetics, but no more diffuse or inoperable disease.

Coronary Disease↗
PubMed1978

The effect of hydralazine and other drugs on the kinetics of procainamide acetylation by rat liver and kidney N-acetyltransferase.

The objectives of this study were to investigate 1) the tissue distribution of procainamide acetylase activity in the rat and 2) the kinetics of procainamide acetylation by rat liver and kidney N-acetyltransferase and 3) to determine the effect of drugs thought to be similarly acetylated on procainamide acetylation. The cytosol fraction (100,000 X g) of tissue homogenates served as the source of N-acetyltransferase. Of the tissues studied the liver possessed the greatest acetylase activity followed by the kidney, lung, intestine and spleen. The apparent procainamide Michalis constant (Km) for liver and kidney was 2.03 X 10(-4) and 2.09 X 10(-4) M in the presence of 4.2 X 10(-4) M acetyl CoA. The liver Km for procainamide with "infinite" acetylCoA concentration was 4.36 X 10(-3) M. The liver Km for acetyl CoA in the presence of "infinite" PA concentration was 2.44 X 10(-3) M. Hydralazine, para-aminobenzoic acid, isoniazid, and sulfapyridine competitively inhibited procainamide acetylation by liver and kidney N-acetyltransferase.

Acetylation↗
PubMed1978

The quantitative disposition of procainamide and N-acetylprocainamide in the rat.

The objectives of this study were to investigate: 1) the rat acetylator phenotype, 2) the systemic availability of oral procainamide (PA), 3) the kinetic disposition of PA and its N-acetyl metabolite (NAPA) and 4) the relationship between PA dose and steady-state blood PA and NAPA levels. The rat acetylator phenotype seems to be monomorphic in type. The systemic availability of PA was estimated to be 78%. The half-life (T 1/2) of PA elimination was 55 minutes and that of NAPA was 51 minutes. PA clearance was 64 ml/kg/min and NAPA clearance 22.4 ml/kg/min. The apparent distribution volume for PA was 4.92 liters/kg and for NAPA 1.64 liters/kg. Acetylation accounted for 38% of PA disposition, urinary excretion 34% and other metabolism 28%. Urinary excretion of NAPA accounted for 72% of administered drug. Steady-state blood PA levels showed a linear increase with dose whereas NAPA did not. The latter observation suggests saturation of PA acetylation at higher PA doses.

Acetylation↗
PubMed1977

Echocardiographic diagnosis of intraventricular clot.

The literature contains many reports of the echocardiographic findings in left atrial myxoma and clot; however, descriptions of left ventricular thrombus or tumor are rare. We discuss here the echocardiographic findings in a patient with a large apical left ventricular thrombus which was confirmed both angiographically and pathologically. The importance of echocardiographically examining the area below the mitral valve near the apex of the left ventricle, where most of the thrombi are located, is stressed.

Diagnosis, Differential↗
PubMed1976

Distribution of coronary artery disease. Prediction by echocardiography.

To assess the sensitivity of standard echocardiography in detecting ventricular motion abnormalities in patients with coronary artery disease (CAD) without prior myocardial infarction, 56 consecutive patients with a history of angina pectoris were studied during an angina-free period. In the 48 patients with adequate echocardiograms, the amplitude of septal and posterior wall motion in the high, mid, and low left ventricle was determined and used to predict prospectively in a blinded fashion the sites of angiographically-determined CAD. Twenty-eight of 35 patients (80%) with disease of the left anterior descending artery (LAD) had diminished interventricular septal motion (P less than 0.001) and 14 of 27 patients (52%) with disease of posterior vessels had diminished posterior wall motion on echocardiogram. When abnormalties of echocardiographic wall motion were compared with left ventriculography, the results were similar. Echocardiography may aid in predicting the presence and distribution of CAD, especially LAD disease.

Adult↗
PubMed1976

Persistence of biologic activity after disappearance of propranolol from the serum.

In order to evaluate the duration of the biologic effects of propranolol after the drug was discontinued, we evaluated a variety of noninvasively determined hemodynamic parameters. Significant depression was found in the heart rate (18 per cent), cardiac output (13 per cent) (determined echocardiographically), and the triple product of blood pressure, heart rate, and systolic ejection time (16 per per cent) during administration or propranolol (200 mg. per day) to 9 normal volunteers. Significant depression of these parameters was present 12 hours after discontinuing the drug. By 12 hours, serum propranolol levels had returned 90 per cent toward their base line; however, at the same time, the heart rate and cardiac output had returned only 19.4 and 14.3 per cent toward their base-line values, and the triple product had returned 41 per cent toward its baseline. By 36 hours no biologic effect was seen. Thus if propranolol were discontinued 2 days prior to cardiac surgery, no significant biologic effect would remain to complicate the patient's postoperative course.

Adult↗