Disease relevance of Bradycardia

• The tilt test alone (i.e., without isoproterenol) induced symptomatic bradycardia or hypotension in 1 of the 9 patients with positive electrophysiologic tests (11 percent), 4 of the 15 patients with negative electrophysiologic tests (27 percent), and none of the controls [1].
• Each mutation caused heritable, progressive conduction-system disease (sinus bradycardia, atrioventricular conduction block, or atrial arrhythmias) and dilated cardiomyopathy [2].
• Provocation of bradycardia and hypotension by isoproterenol and upright posture in patients with unexplained syncope [1].
• These transgenic animals exhibit decreased systolic function and inward I(Ca,L), low levels of connexin43 and connexin40, sinus bradycardia, and prolonged atrioventricular (AV) node conduction followed by complete heart block and sudden death [3].
• These data implicate cardiomyocyte iNOS overexpression as sufficient to cause cardiomyopathy, bradyarrhythmia, and sudden cardiac death [4].

Psychiatry related information on Bradycardia

• Presently, there are rare reports of gynecomastia, bradycardia, inhibition of acetylcholinesterase, headache, lethargy, diarrhea, and rash in patients receiving ranitidine [5].
• Effects of brain epinephrine depletion on thermoregulation, reflex bradycardia, and motor activity in rats [6].
• There are no differences in cardiovascular AEs, including bradycardia, between placebo and donepezil groups in the clinical trials published to date, even in a very sick vascular dementia population with high rates of comorbidity and concomitant medication use [7].
• Classical conditioning of tone-signaled bradycardia modifies 2-deoxyglucose uptake patterns in cortex, thalamus, habenula, caudate-putamen and hippocampal formation [8].
• A 17-year-old male with anorexia nervosa developed atypical prolongation of his corrected QT interval (QTc) when placed on isoproterenol for profound sinus bradycardia [9].

High impact information on Bradycardia

• Symptomatic bradycardia developed in two patients and was treated with atropine [10].
• We used the "upright-tilt test" (duration, less than or equal to 10 minutes) with or without an infusion of exogenous catecholamine (isoproterenol [1 to 5 micrograms per minute], given intravenously) to elicit bradycardia, hypotension, or both in 24 patients with recurrent syncope and in 18 control subjects [1].
• Despite normal morphological development of the circulatory system, EPAS1-deficient mice display pronounced bradycardia [11].
• Thioridazine (Mellaril) hydrochloride cardiotoxicity is manifested by bradycardia and prolongation of the QT interval [12].
• Sinus bradycardia following ritodrine withdrawal [13].

Chemical compound and disease context of Bradycardia

• Severe bradycardia with clonidine [14].
• Both patients continued to receive digoxin without recurrence of bradycardia [15].
• The other patient, who had never taken methyldopa alone, did not demonstrate bradycardia with digoxin alone [15].
• Hypotension and bradycardia following diazoxide and hydralazine therapy [16].
• When cardiovascular responses to phenylephrine were recorded while chronic ICV infusions were in progress, awake rats receiving hypertonic NaCl were still normotensive on day 2 yet reflex bradycardia was already attenuated [17].

Biological context of Bradycardia

• Neonatal bradycardia was more common after atenolol but the systolic blood-pressure of the babies was the same in both groups [18].
• Activation of carotid chemoreflex by nicotine increased CBF by 121 +/- 9% from 32 +/- 4 mL++/min (P < .05) with the heart rate controlled and caused bradycardia (-32 +/- 5 beats per minute) without the heart rate controlled [19].
• Captopril abolished the increases in arterial pressure, hindquarters, and left renal resistance, but both bradycardia and increased mesenteric resistance persisted, indicating that baroreflex activation might be buffering a non-renin-angiotensin system pro-hypertensive mechanism [20].
• These effects promote reflex bradycardia, vasodilation and hypotension (Bezold-Jarisch reflex) and also modulate renin release and vasopressin secretion [21].
• 3. Intravenous capsaicin caused hypotension, bradycardia and rapid shallow breathing, together with a decrease in nasal vascular resistance and little change in nasal airways resistance [22].

Anatomical context of Bradycardia

• The intrinsic heart rate (IHR) was determined in 17 patients with symptomatic sinus bradycardia by administering atropine 0.04 mg/kg and propranolol 0.2 mg/kg, i.v. In this way, sick sinus (SSS) patients with intrinsic sinus node (SN) dysfunction could be distinguished from those patients with disturbed autonomic regulation of SN function [23].
• Nucleus tractus solitarii lesions abolished the reflex bradycardia to a phenylephrine-induced elevation in arterial pressure [24].
• Selective knockout of mouse ERG1 B potassium channel eliminates I(Kr) in adult ventricular myocytes and elicits episodes of abrupt sinus bradycardia [25].
• Clonidine (30 micrograms) produced hypotension and bradycardia after injection into the lateral ventricle [26].
• RESULTS: The gamma-MSHs caused an increase in MAP, CBF and HR, whereas phenylephrine caused an increase in MAP and CBF and baroreceptor reflex-mediated bradycardia [27].

Gene context of Bradycardia

• Conduction disorders were associated with LQT2, whereas sinus bradycardia was associated with LQT1 [28].
• All HR effects were probably mediated by CRF(1) because injection of the CRF(2)-selective agonist mouse urocortin II was ineffective, and the baseline bradycardia by i.c.v. CRF was preserved in CRF(2)-deficient mice [29].
• While the pressor response to ET-1 was significantly inhibited after i.v. injection of phentolamine, the bradycardia was blocked by pentolinium [30].
• Treatment with both AVP and oxytocin did not augment baroreflex-mediated bradycardia greater than AVP alone [31].
• The NPY-induced bradycardia is attributed to not yet characterized NPY receptor subtypes other than Y1, Y2 and Y5, or a complex receptor interaction [32].

Analytical, diagnostic and therapeutic context of Bradycardia

• Microinjections of glutamate into the NRV resulted in inhibition of the tail-flick reflex, hypertension, and mild bradycardia [33].
• Data in these patients were compared with those in a control group of 18 patients without bradyarrhythmias (group 2) who were not given theophylline [34].
• OBJECTIVES: We attempted to demonstrate that theophylline, an adenosine receptor antagonist, can reverse bradyarrhythmias after orthotopic heart transplantation [34].
• METHODS: Twenty-nine transplant recipients (group 1) were given theophylline after bradyarrhythmias developed after transplantation [34].
• Bilateral vagotomy suppressed the bradycardia induced by i.c.v. administered nifedipine [35].

References