Drugs online research references
J Am Coll Cardiol. 1996 Apr;27(5):1061-70.
Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome.
Miyazaki T, Mitamura H, Miyoshi S, Soejima K, Aizawa Y, Ogawa S.
Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
OBJECTIVES. We examined the modulatory effects of autonomic nervous system and antiarrhythmic drugs on the ST segment in patients with Brugada syndrome to gain an insight into the mechanism of ST segment elevation. BACKGROUND. Right bundle branch block, ST segment elevation and ventricular tachyarrhythmias define a distinct clinical and electrocardiographic (ECG) syndrome (Brugada syndrome). However, the mechanism of ST segment elevation and the causes of this syndrome are unknown. METHODS. The study included four patients in whom structural heart or coronary artery disease was excluded by noninvasive and invasive tests. High take-off ST segment elevation of either the coved or saddle-back type in precordial leads V1, V2 and V3 was seen in all patients. Three patients experienced recurrent episodes of syncope or aborted sudden cardiac death, and the remaining patient had palpitation. Autonomic receptor stimulation and blockade and intravenous administration of antiarrhythmic drugs were performed during sinus rhythm while the 12-lead ECG was recorded. Metaiodobenzylguanidine (MIBG) scanning and Holter monitoring were also performed. RESULTS. Beta-adrenoceptor stimulation by intravenous isoproterenol consistently reduced (> or = 0.1 mV) ST segment elevation at or 80 ms after the J point in all four patients. Selective alpha-adrenoceptor stimulation by intravenous norepinephrine in the presence of propranolol or by intravenous methoxamine consistently augmented, whereas alpha-adrenoceptor blockade reduced, ST segment elevation in three patients. Intracoronary acetylcholine or intravenous edrophonium or neostigmine augmented ST segment elevation without inducing coronary spasm in three of four patients. Class IA antiarrhythmic drugs also consistently augmented (three patients), whereas class IB drugs had no effect on (two patients) ST segment elevation. No abnormality was found on MIBG imaging or heart rate variability in three patients, suggesting that autonomic dysfunction is not a primary disease process. Class IA drugs had no effect on ST segment in three control patients, suggesting that the ST segment elevation seen in patients with Brugada syndrome in response to the drugs is not a nonspecific response. CONCLUSIONS. ST segment elevation in patients with Brugada syndrome was augmented by selective stimulation of alpha-adrenoceptors or muscarinic receptors or by class IA drugs but was mitigated by beta-adrenoceptor stimulation or alpha-adrenoceptor blockade. These responses might be explained by postulating the presence of an area of early repolarization or a local "depolarized" area in the ventricle causing ST segment elevation in this syndrome. Because only a small number of patients were studied, these possibilities need further evaluation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8609322&dopt=Abstract
Crit Care Med. 1996 Apr;24(4):647-57.
Effect of jet ventilation on heart failure: decreased afterload but negative response in left ventricular end-systolic pressure-volume function.
Weber A, Mathru M, Rooney MW.
Department of Anesthesiology, Loyola University Medical Center, Maywood, IL 60153, USA.
OBJECTIVE: To examine the mechanism of cardiac assist with systolic jet ventilation, specifically effects on loading conditions and left ventricular pressure-volume function. Both systolic and diastolic jet ventilation were compared in the absence and presence of heart failure. DESIGN: Prospective, two-factor, repeated-measures study. SETTING: Animal laboratory. SUBJECTS: Ten anesthetized, closed-chest dogs. INTERVENTIONS: The measurement protocol consisted of two phases: a) apnea, randomized jet ventilation (systole- and diastole-synchronized); b) postjet ventilation apnea, before and after heart failure, induced with a propranolol-imipramine-plasma expansion treatment. MEASUREMENT AND MAIN RESULTS: Systolic and diastolic jet ventilation was associated with mean airway pressures of approximately 7 mm Hg and intrapleural pressures of approximately 3 mm Hg in both heart conditions. In normal hearts, jet ventilation (either mode) decreased transmural left ventricular end-diastolic pressure by 40% to 60% (p < .05), left ventricular end-diastolic volume 25 +/- 8%, and stroke volume by 28% to 30%. Heart failure was associated with decreases (41 +/- 6%) in end-systolic pressure-volume function (i.e., pressure change/volume change or elastance), transmural left ventricular end-systolic pressure (22 +/- 3%), and stroke volume (16 +/- 4%), and increased transmural left ventricular end-diastolic pressure (139 +/- 6%). Application of jet ventilation (either mode) during heart failure did not affect stroke volume but significantly (p < .05) attenuated transmural left ventricular end-diastolic pressure by 30% to 40%, left ventricular end-diastolic volumes by 33 +/- 9%, and transmural left ventricular end-systolic pressure by 11% to 19% (p < .05). After jet ventilation, left ventricular elastance was decreased 36 +/- 8% in normal hearts and 35 +/- 11% in failing hearts. Stroke volume, however, returned to baseline levels because of increases in transmural left ventricular end-diastolic pressure in both heart conditions, and also in failing hearts, because transmural left ventricular end-systolic pressure remained decreased approximately 30% (p < .05). CONCLUSIONS: Jet ventilation did not decrease stroke volume in failing hearts because of the afterload-reducing benefit (decreased transmural left ventricular end-systolic pressure) of increased intrapleural pressure in dilated ventricles. Moreover, jet ventilation did not have positive effects on myocardial function and had negative effects on left ventricular elastance in the postjet ventilation period in both normal and failing hearts. Cardiac assist by jet ventilation was not cycle specific, suggesting no selective benefit of jet ventilation over conventional positive-pressure ventilation during heart failure. These studies demonstrate a negative inotropy associated with jet ventilation that, during heart failure, may compromise the general benefit of positive-pressure-mediated increases in intrapleural pressure.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8612418&dopt=Abstract
J Pharmacol Exp Ther. 1996 May;277(2):1076-89.
Functional classification of antidepressants based on antagonism of swim stress-induced fos-like immunoreactivity.
Duncan GE, Knapp DJ, Johnson KB, Breese GR.
Department of Psychiatry, School of Medicine, University of North Carolina at Chapel Hill, USA.
Autoradiographic analysis of 14C-2-deoxyglucose (2-DG) uptake and immunocytochemical assessment of Fos-like immunoreactivity (Fos-LI) were used to assess swim stress-induced changes in metabolic activity in brain and to define the effect of chronic treatment with antidepressants from different pharmacological classes. Saline-treated rats processed in the forced swim test exhibited marked increases in Fos-LI in limbic cortical regions, lateral septum, medial amygdala and paraventricular nucleus of the hypothalamus (PVN). Uptake of 2-DG was increased by swim stress in some of the same brain regions where Fos-LI was induced, with the notable exception of a lack of a change in the PVN. Rats received injections for 3 wk with imipramine, desipramine, fluoxetine, nisoxetine, tranylcypromine or mianserin before being processed in the forced swim test. Chronic treatment with imipramine and desipramine alone induced Fos-LI in the central nucleus of the amygdala and the dorsolateral bed nucleus of the stria terminalis. After tranylcypromine treatment, Fos-LI was induced in many brain regions including limbic cortex, amygdala and paraventricular nucleus of the hypothalamus. None of the other antidepressants induced Fos-LI in any brain region examined. Chronic administration of imipramine, desipramine and nisoxetine antagonized the swim induced expression of Fos-LI in the PVN and in limbic cortical regions, including the medial prefrontal ventrolateral orbital and cingulate cortices. Chronic treatment with fluoxetine, tranylcypromine and mianserin did not alter swim stress-induced Fos-LI in any brain region. Thus, only antidepressant drugs that affect norepinephrine uptake (i.e., imipramine, desipramine and nisoxetine) antagonized swim stress-induced Fos-LI. In contrast to the action of chronic imipramine on Fos-LI induced by swim, chronic administration of imipramine did not antagonize the stress-induced changes in 2-DG uptake in limbic cortical regions. Acute administration of propranolol, which blocks beta-adrenergic receptors, reduced the number of cells staining for Fos-LI in limbic cortical regions, resembling the effects produced by chronic imipramine, desipramine and nisoxetine. In the PVN, neither propranolol nor prazosin (an alpha 1 antagonist) blocked the swim-induced Fos-LI, suggesting that swim-induced Fos-LI in the PVN is not under control of beta- or alpha 1-adrenergic receptors. These latter results imply that adaptation of noradrenergic receptors by chronic imipramine may not be related to the antagonism of stress-induced Fos-LI. The clear functional differences of the various antidepressant agents on swim stress-induced Fos-LI after chronic administration provide a functional classification of antidepressant drug action not previously identified.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627519&dopt=Abstract
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