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Biomedical subjects

M D Carlson

Publications and source records attributed to M D Carlson.

64 records · Page 4Linked to original sources
PubMed1989

Programmed ventricular stimulation in patients with left ventricular dysfunction and ventricular tachycardia: effects of acute hemodynamic improvement due to nitroprusside.

To assess the electrophysiologic effects of acute hemodynamic improvement in patients with left ventricular systolic dysfunction, 12 patients with a left ventricular ejection fraction less than 0.40 and a history of sustained monomorphic ventricular tachycardia were studied. All patients had underlying coronary artery disease. Patients underwent programmed cardiac stimulation in random order during a baseline period and with nitroprusside infusion. Mean pulmonary capillary wedge pressure decreased from 20 +/- 8 mm Hg at baseline study to 8 +/- 3 mm Hg during nitroprusside infusion (p less than 0.0001). Pulmonary artery, right atrial and systemic arterial pressures also decreased with nitroprusside (p less than 0.01). Cardiac output did not change. Left ventricular dimensions, determined by two-dimensional echocardiography, decreased significantly during nitroprusside infusion. The right ventricular effective refractory period, measured during ventricular drive trains at cycle lengths of 400 and 600 ms, were similar during baseline and nitroprusside periods (271 +/- 30 versus 274 +/- 31 ms at 600 ms, and 249 +/- 25 versus 246 +/- 18 ms at 400 ms). In 2 patients no ventricular arrhythmias were induced during either study period; in the other 10, ventricular tachyarrhythmias were induced during both periods. The mean number of extrastimuli required to induce a ventricular tachyarrhythmia was similar during the baseline period (1.8 +/- 0.6) and during nitroprusside infusion (1.9 +/- 0.7). As well, the mean cycle length of ventricular tachycardia induced was similar during the baseline period (347 +/- 61 ms) and during nitroprusside infusion (342 +/- 70 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Glutamate uptake into synaptic vesicles: competitive inhibition by bromocriptine.

The ATP-dependent uptake of L-glutamate into synaptic vesicles has been well characterized, implicating a key role for synaptic vesicles in glutamatergic neurotransmission. In the present study, we provide evidence that vesicular glutamate uptake is selectively inhibited by the peptide-containing halogenated ergot bromocriptine. It is the most potent inhibitor of the agents tested: the IC50 was determined to be 22 microM. The uptake was also inhibited by other ergopeptines such as ergotamine and ergocristine, but with less potency. Ergots devoid of the peptide moiety, however, such as ergonovine, lergotrile, and methysergide, had little or no effect. Although bromocriptine is known to elicit dopaminergic and serotonergic effects, its inhibitory effect on vesicular glutamate uptake was not mimicked by agents known to interact with dopamine and serotonin receptors. Kinetic data suggest that bromocriptine competes with glutamate for the glutamate binding site on the glutamate translocator. It is proposed that this inhibitor could be useful as a prototype probe in identifying and characterizing the vesicular glutamate translocator, as well as in developing a more specific inhibitor of the transport system.

Adenosine Triphosphate↗
PubMed1989

Cardiac conduction abnormalities during percutaneous balloon mitral or aortic valvotomy.

To evaluate the electrophysiologic changes in the cardiac conduction system that occur during percutaneous mitral or aortic balloon valvotomy, we prospectively studied the conduction system in 19 patients (10 mitral, 8 aortic, and 1 both) undergoing this procedure. A His bundle electrogram was recorded in all patients, and when sinus rhythm was present, the atrioventricular (AV) node effective refractory period was measured. Holter monitoring was performed during and for 24 hours after the procedure. Follow-up electrocardiograms (ECG) were available in 11 patients 2.3 +/- 1.5 months after the procedure. The AV node effective refractory period before (276 +/- 86 msec) and after valvotomy (298 +/- 85 msec) were not significantly different. The maximum His-Purkinje conduction time (HV interval) observed during valvotomy (66 +/- 20 msec) was significantly longer (p less than 0.01) than that measured before (57 +/- 10 msec) or after (60 +/- 18 msec) valvotomy. The mean HV intervals before and after valvotomy were not significantly different. The mean QRS complex duration increased from 95 +/- 28 to 112 +/- 28 msec during valvotomy and remained significantly prolonged (109 +/- 26 msec) 24 hours after the procedure (p less than 0.01). A new intraventricular conduction defect (QRS complex duration greater than 100 msec) or bundle branch block occurred in five of 13 patients who had normal QRS duration before the procedure. The change in HV interval did not correlate with the change in QRS complex duration. In four patients, the newly acquired intraventricular conduction defect was still present on follow-up ECG tracing. Complete heart block was not observed in any patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Sensitivity of an automatic external defibrillator for ventricular tachyarrhythmias in patients undergoing electrophysiologic studies.

An automatic advisory external defibrillator (AED) was activated during all arrhythmias occurring at the time of 77 electrophysiologic studies in 45 patients. Sustained ventricular tachycardia (VT) occurred during 55 studies in 31 patients and nonsustained VT was induced during 10 studies in 9 patients. Ventricular fibrillation was induced 5 times in 5 patients and atrial arrhythmias with a rapid ventricular response occurred during 7 studies in 4 patients. The AED detection algorithm advised "shock" during 36 of 55 (65%) episodes of sustained VT and all 5 episodes of ventricular fibrillation. The device correctly advised "shock" for all 6 episodes of nonsustained VT that spontaneously terminated after analysis was complete. Thus, the sensitivity of the device for all ventricular arrhythmias analyzed was 47 of 66 (71%). The device recommended "shock" for all 31 episodes of rapid VT and 1 of 2 episodes of atrial fibrillation associated with systemic hypotension (32 of 33, 97%). The 19 episodes of VT for which "no shock" was advised were comparatively slow and were hemodynamically well tolerated. The device recommended "no shock" during all 21 episodes of normal sinus rhythm and all 20 episodes of rapid atrial pacing (cycle length 400 ms) analyzed. "No shock" was advised during 4 episodes of sustained narrow QRS complex supraventricular tachycardia and 4 brief episodes of nonsustained VT that terminated before analysis was complete. Thus, in this study the specificity of the AED for wide complex tachycardias was 100%.

Algorithms↗
PubMed1979

Nerve outgrowth by dorsal root ganglia in vitro: stimulation by inhibitors of DNA metabolism in the absence of exogenous nerve growth factor.

Dorsal root ganglia from 8-day chick embryos can be stimulated to extend nerve processes in culture by inclusion of cytosine arabinoside (Ara-C) in the culture medium, in the absence of exogenous nerve growth factor (NGF). The degree of stimulation is dose dependent, and is not mimicked by either free cytosine or free arabinose. Since Ara-C is known to inhibit DNA synthesis, other inhibitors of DNA synthesis were tested. Hydroxyurea, fluorodeoxyuridine, and 3 mM thymidine all stimulated nerve outgrowth in the absence of exogenous NGF. In addition, bromodeoxyuridine also stimulated nerve outgrowth. In all cases, stimulation was observable after 24 h of culture, with maximal outgrowth achieved by 72 h of culture. The experimental response was never as large as the response to NGF, but was up to seven times greater than control outgrowth. In all cultures, nerve processes were characterized by growth cones at their distal tips, colchicine-sensitivity, and a high tubulin content visualized by immunofluorescence with anti-tubulin antibody.

Animals↗
PubMedDate not supplied

NMDA, AMPA, and benzodiazepine binding site changes in Alzheimer's disease visual cortex.

Quantitative receptor autoradiography was used to measure the laminar distribution of [3H]glycine and [3H]glutamate binding to the N-methyl-D-aspartate (NMDA) receptor complex, [3H]D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) binding to the AMPA receptor, and [3H]flunitrazepam binding to the benzodiazepine (BDZ) receptor in three areas of visual cortex in control and Alzheimer's disease (AD) postmortem human brains (primary or striate visual cortex, visual association cortex, and higher-order visual association cortex, corresponding to Brodmann Areas 17, 18, and 21, respectively). In Area 17, binding to the NMDA, AMPA, and BDZ receptors was not significantly altered in the AD brains (except in layer VI for [3H]glycine and layer III for [3H]AMPA, where binding was reduced in the AD brains). Ligand binding to the two EAA receptors in Area 18 was, however, significantly reduced in the AD brains (layers I through III for [3H]glycine and layers III through VI for [3H]AMPA). In Area 21, binding to both the NMDA and BDZ receptors but not to the AMPA receptor, was significantly reduced in almost all laminae of the AD brains (layers I through VI for [3H]glycine and layers I through V for [3H]flunitrazepam). This hierarchical pattern of laminar binding loss with increasing complexity of association visual cortices is consistent with the increasing numbers of neurofibrillary tangles found in those areas, implicating NMDA and BDZ receptor bearing cells in AD neuropathology. AMPA receptor losses do not parallel the pathology, suggesting that AMPA receptors are not directly correlated with the pathology.

Aged↗
PubMedDate not supplied

How to manage atrial fibrillation: an update on recent clinical trials.

The latter half of the 1990s was a time of extraordinary progress in the understanding and management of atrial fibrillation (AF). Evidence that "AF begets AF" has generated considerable interest regarding the mechanisms responsible for this phenomenon and has sparked the development of new concepts in both pharmacologic and nonpharmacologic therapy. The recognition that, in some patients, AF is initiated and possibly maintained by atrial tachycardia originating in the pulmonary veins has challenged accepted notions regarding the mechanisms responsible for arrhythmia. New antiarrhythmic drugs, devices, ablation techniques, and pacing techniques have been developed and tested. Strategies for the use of existing therapies have been evaluated, and new indications for existing therapies are under consideration. This article reviews several studies published in 1999 and 2000 that addressed the mechanisms and the management of AF.

Amiodarone↗
PubMedDate not supplied

Late results with concomitant coronary artery bypass grafting and ICD implantation.

BACKGROUND: To determine the influence of left ventricular function on the long-term survival of patients with coronary artery disease and lethal ventricular arrhythmias, who undergo concomitant coronary artery bypass grafting (CABG) and implantable cardiovertor defibrillator (ICD) implantation, we studied survival in 54 consecutive patients who underwent CABG and ICD implantation. METHODS: Group I consisted of 35 patients with left ventricular ejection fraction (LVEF) < or = 35% (mean 25.3 +/- 5.6) and Group II consisted of 19 patients with LVEF > 35% (mean 47.5 +/- 6.6). The two groups were similar with regards to age, gender, clinical presentation, induced arrhythmias, and the number of grafts placed at the time of surgery. RESULTS: Two in-hospital deaths (3.7%) occurred, both in Group I. During follow-up (42.5 +/- 21.8 months), there were 10 deaths in Group I (1 noncardiac, 1 sudden, and 8 heart failure), and 1 death in Group II (heart failure) (p < 0.04). CONCLUSIONS: Concomitant CABG and ICD implantation can be performed with an acceptable in-hospital mortality, even in patients with poor left ventricular function. Although freedom from sudden cardiac death remains excellent, overall long-term survival is limited by refractory heart failure, especially in those patients with left ventricular dysfunction at the time of surgery.

Adult↗