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Biomedical subjects

B F Hoffman

Publications and source records attributed to B F Hoffman.

At least 91 records · Page 5Linked to original sources
PubMed1981

The diagnosis and treatment of neuroleptic-induced Parkinsonism.

Basal ganglia side-effects caused by neuroleptic drugs are frequently ignored, misdiagnosed, or mistreated by the patient or physician. Such side-effects must be anticipated and appropriate management instituted so that patient compliance with the drug regimen is increased and the therapeutic relationship is maintained. Side-effects can be detected in frequent and complete examinations of the head and neck, limbs, and chest and back. The various medications for drug-induced parkinsonism are reviewed, with an emphasis on the indications for selection and the effects of each drug. Common errors in the diagnosis and management of side-effects of neuroleptic drugs are summarized.

Antipsychotic Agents↗
PubMed1981

Neurosyphilis in a young man.

New cases of neurosyphilis are comparatively rare. The epidemiology and clinical presentation of neurosyphilis are described. The article describes the presentation of general paresis in a 34 year old man, 10 years after he had been ineffectively treated with penicillin for secondary syphilis. The various laboratory tests for syphilis are reviewed. The Venereal Disease Research Laboratories (VDRL) is currently the best screening test and the Fluorescent Treponema Antibody-Absorption test (FTA-ABS) is the current recommended specific test for syphilis. Central nervous system involvement is confirmed in the laboratory by a positive VDRL on the cerebrospinal fluid. Physicians should be on the alert for this cause of dementia which may, once again, be increasing in frequency.

Adult↗
PubMed1981

In vivo and in vitro antiarrhythmic and arrhythmogenic effects of N-acetyl procainamide.

We studied the effects of N-acetyl procainamide (NAPA) on isolated canine cardiac tissues by using standard microelectrode techniques. NAPA (10-40 mg/l) does not suppress the rate of phase 4 depolarization of Purkinje fibers and does not change resting membrane potential, action potential amplitude or maximum upstroke velocity of phase O of the action potentials of Purkinje fibers or ventricular muscle cells. In contrast, action potential duration of both types of cells is significantly prolonged by NAPA in a dose-dependent manner. In toxic concentrations (80-240 mg/l), NAPA can produce a "secondary plateau" at about -55 mV during phase 3 of the action potential of Purkinje fibers driven at cycle lengths of 2000 to 4000 msec. Early afterdepolarizations and single or multiple spontaneous action potentials were often triggered during the secondary plateau. When NAPA is given to conscious or anesthetized dogs (50-100 mg/kg i.v.), ventricular extrasystoles occur at constant coupling intervals if the basic rate of ventricular activation is slow (60 per minute or slower). Single extrasystoles, or the first extrasystole in a salvo, appear at coupling intervals of 400 to 600 msec. The single and multiple extrasystoles induced by NAPA may be caused by action potentials triggered during the secondary plateau and may degenerate into ventricular fibrillation. In doses of up to 100 mg/kg i.v., NAPA exerts slight antiarrhythmic effects in dogs with 24-hr myocardial infarcts.

Acecainide↗
PubMed1980

Method for recording electrical activity of the sinoatrial node and automatic atrial foci during cardiac catheterization in human subjects.

A method for recording electrical activity of the sinoatrial (S-A) node and automatic atrial foci in human subjects is described. To record S-A nodal electrograms, an electrode catheter was inserted percutaneously into the femoral vein and advanced under fluoroscopic control to the superior vena caval-right atrial junction. The distal terminal of the catheter was placed in the area of the S-A node and the proximal terminal on the free right atrial wall or in the right atrial lumen. Polarity was reversed from the conventional electrocardiographic recording; high amplification (about 100 microV/cm) and selective filters (0.1 to 20 hertz) were used. S-A nodal electrograms recorded with this method in human subjects were similar to electrograms obtained previously from the dog and rabbit and revealed negatively directed diastolic and upstroke slopes preceding the P wave of the electrocardiogram. Sinoatrial conduction time measured from the S-A nodal electrograms in 15 cases was 34.9 +/- 2.1 ms(mean +/- standard error of the mean) for a sinus cycle length of 736.4 +/- 38.6 ms. The coronary sinus electrograms in a patient with coronary sinus rhythm were recorded by the same technique except that the distal terminal of the catheter was placed at the coronary sinus ostium. A negatively directed diastolic slope preceding the P wave was consistently recorded. This method for recording electrograms of the S-A node and ectopic automatic atrial foci should prove useful in (1) assessment of both normal and abnormal S-A nodal function, (2) direct determination of conduction time from the S-A nodal pacemaker to the atrium, and (3) localization of automatic atrial foci.

Adolescent↗
PubMed1980

Methods for recording electrograms of the sinoatrial node during cardiac surgery in man.

Recent reports have shown that it is possible to record extracellular electrograms from the rabbit and dog sinoatrial (SA) node. We applied similar techniques to record SA nodal activity in 23 patients who underwent cardiac surgery for various forms of heart disease. Both a bipolar technique, using pairs of electrodes at various interelectrode distances, and a unipolar technique, using an exploring and an indifferent electrode, were used. To record SA nodal electrograms, polarity was reversed from the conventional electrocardiographic recording; high amplification (100 microV/cm) and low-pass filters (0.15-20 Hz) were used. SA nodal electrograms were recorded from eight of 12 patients using the bipolar method and from nine of 11 patients using the unipolar method. There were no significant differences in the success rate or quality of the recording between the two methods. However, the unipolar method allowed a more accurate localization of the SA node. Human SA nodal electrograms resembled those of the dog and rabbit and showed two distinct slopes: a diastolic slope and an upstroke slope preceding the P wave of the ECG, SA conduction times were 32.4 +/- 2.8 msec (mean +/- SEM) at sinus (PP) cycle lengths of 587.6 +/- 35.6 msec for the bipolar method, and 38.2 +/- 3.2 msec at sinus (PP) cycle lengths of 712.2 +/- 50.7 msec for the unipolar method. These methods for recording of extracellular SA nodal electrograms in man may prove useful in 1) localization of the SA node during open heart surgery and 2) assessment of SA nodal function in health and disease.

Adolescent↗
PubMed1980

Electrical activity from the sinus node region in conscious dogs.

In an attempt to understand the way automatic cells in the sinus node (SN) control the cardiac rhythm, we studied extracellular electrograms recorded from the SN region in conscious dogs. A SN electrode, containing 48 silver terminals arranged 1.5 mm apart, was implanted over the node, and an indifferent electrode was implanted on the superior vena cava. Through terminals of the SN electrode paired with the vena caval electrode, "unipolar" electrograms were recorded at 100 microV/cm and with a time constant of 0.1 second. Low amplitude and low frequency deflections (dV/dt less than or equal to 20 mV/sec) which resulted from electrical activity of the node could be differentiated from the more rapid deflections due to atrial electrical activity. Electrical activity due to the inherent automaticity of what appeared to be groups of automatic cells was recognized as a slow negative-going diastolic slope followed by a slow negative-going, or negative and then positive-going, SN potential. Impulse propagation toward the SN electrode terminal in groups of automatic cells appeared as a slow positive-going deflection interrupting the diastolic slope. Adjacent groups of automatic cells located near the sites of earliest atrial activation discharged asynchronously before the earliest atrial activity; this suggests that multiple groups of automatic cells might initiate atrial activation. In addition to changes in rate and in location of the pacemaking groups of automatic cells, significant beat-to-beat variation in the sinoatrial interval contributed to the changes in atrial rate in "sinus arrhythmia." These studies provide a better understanding of SN function in conscious animals.

Animals↗
PubMed1980

Pharmacologic antagonism of beta adrenergic blockade in dogs. II. Hemodynamic effects of simultaneous intravenous infusion of isoproterenol and dopamine during chronic propranolol administration.

Chronic beta adrenergic blockade was induced in eight dogs with 240 to 360 mg of oral propranolol dailty for 2 to 6 weeks. Beta blockade was confirmed by a minimal heart rate response to isoproterenol, 0.06 micrograms/kg/min, in a pentobarbital-anesthetized, open-chest preparation. Subsequent to confirmation of beta blockade, hemodynamic effects of isoproterenol and dopamine were examined individually and in combination. A desirable balance of arterial pressure and cardiac output was achieved by combining isoproterenol, 0.2 to 2.0 micrograms/kg/min, with dopamine, 5 to 20 micrograms/kg/min. This combination increased mean arterial pressure (109 +/- 9 versus 81 +/- 7), cardiac output (4.3 +/- .5 versus 2.8 +/- .3 L/min) and heart rate 156 +/- 4 versus 120 +/- 7) (p less than 0.05). The hemodynamic effects of combined isoproterenol-dopamine were superior to the effects of either drug alone and suggest a method for effective circulatory support of man during chronic beta adrenergic blockade.

Animals↗
PubMed1979

Participation of slow inward current in the Purkinje fiber action potential overshoot.

We used microelectrode techniques to study the relationship of canine Purkinje fiber membrane potential and the action potential (AP) overshoot. At the maximum diastolic potential, -93.0 +/- 0.5 (SE) mV, AP overshoot was +37.7 +/- 0.4 mV. There was a range of membrane potentials (MP) less negative than the maximum diastolic potential from which action potentials were elicited with an overshoot greater than the control. Starting at an MP of less than -78.7 +/- 0.4 mV, AP overshoot was less than control. A maximum overshoot of +40.2 +/- 0.4 mV occurred at an MP of -85.4 +/- 0.4 mV. The relationship of the maximum upstroke velocity (Vmax) of phase 0 depolarization to MP was sigmoidal. Peak Vmax, 497 +/- 13 V/s, occurred at MP greater than or equal to -89.3 +/- 0.5 mV. The increase in overshoot was enhanced as perfusate [Ca2+] increased and decreased as [Ca2+] decreased. Slow-channel blocking agents and tetrodotoxin (TTX) depressed the peak of the curve relating overshoot to MP. TTX also decreased Vmax. The effect of TTX on overshoot but not on Vmax was reversed with Ca2+, 8.1 mM. The increase in overshoot for action potentials initiated during the terminal part of phase 3 was due to a slow, delayed component of the upstroke and appears to result from the slow inward current.

Action Potentials↗
PubMed1979

Pharmacologic antagonism of beta-adrenergic blockade in dogs. I. Hemodynamic effects of isoproterenol, dopamine, and epinephrine in acute propranolol administration.

Hemodynamic effects of isoproterenol, dopamine, and epinephrine were studied before and after acute beta-adrenergic blockade in 16 open-chest, anesthetized mongrel dogs. Beta blockade was induced with 1 mg. per kilogram of intravenous propranolol. Cardiac output measurements were obtained by thermal dilution, and pressure recordings were obtained in the right ventricle, pulmonary artery, left atrium, left ventricle, and aorta. Derived parameters included stroke volume, pulmonary and systemic vascular resistances, and peak left ventricular dP/dt. In the presence of propranolol, epinephrine became a lethal drug in large doses and did not increase cardiac output in standard doses. Dopamine, in 25 to 50 mcg. per kilogram per minute doses, increased arterial pressure and systemic resistance; cardiac output was diminished compared with dopamine, 10 mcg. per kilogram per minute, prior to propranolol, as a result of increased resistance and decreased LV contractility. Isoproterenol, 0.6 to 0.9 mcg. per kilogram per minute, 15 to 20 times standard dosages, had moderately positive inotropic effects and increased cardiac output. Left ventricular systolic pressure with isoproterenol after propranolol was reduced when compared with effects of smaller doses prior to propranolol. These observations suggest that none of the catecholamines studied would be optimal for circulatory support in heart failure in the presence of propranolol. The present results define a pharmacologic basis for design of appropriate drug combinations for circulatory support in beta-blocked animals.

Adrenergic beta-Antagonists↗