Accurate diagnosis of convulsive syncope: role of an implantable subcutaneous ECG monitor.
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Convulsive syncope due to transient bradycardia is recognized as a cause of treatment-resistant seizures. However, the diagnosis may be difficult to make with conventional electrocardiographic devices if attacks are infrequent. We present a case of apparent epilepsy in which a new implantable electrocardiographic event recorder (the 'Reveal' insertable loop recorder) was used to show that attacks were caused by prolonged asystole of up to 36 s in duration. The insertable loop recorder may have an important role in the investigation of patients with treatment-resistant seizures, particularly where there is a strong suspicion of an underlying cardiac arrhythmia. (+info)
Activation of GABAA but not GABAB receptors in the NTSblocked bradycardia of chemoreflex in awake rats.
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In the present study we analyzed effects of bilateral microinjections of muscimol (a GABAA agonist) and baclofen (a GABAB agonist) into the nucleus tractus solitarius (NTS) on bradycardic and pressor responses to chemoreflex activation (potassium cyanide, 40 micrograms/rat iv) in awake rats. Bilateral microinjections of muscimol (25 and 50 pmol/50 nl) into the NTS increased baseline mean arterial pressure (MAP): 119 +/- 8 vs. 107 +/- 2 mmHg (n = 6) and 121 +/- 8 vs. 103 +/- 3 mmHg (n = 6), respectively. Muscimol at 25 pmol/50 nl reduced the bradycardic response to chemoreflex activation 5 min after microinjection; with 50 pmol/50 nl the bradycardic response to chemoreflex activation was reduced 5, 15, 30, and 60 min after microinjection. Neither muscimol dose produced an effect on the pressor response of the chemoreflex. Effects of muscimol (50 pmol/50 nl) on basal MAP and on the bradycardic response of the chemoreflex were prevented by prior microinjection of bicuculline (a GABAA antagonist, 40 pmol/50 nl) into the NTS. Bilateral microinjections of baclofen (12.5 and 25 pmol/50 nl) into the NTS produced an increase in baseline MAP [137 +/- 9 vs. 108 +/- 4 (n = 7) and 145 +/- 5 vs. 105 +/- 2 mmHg (n = 7), respectively], no changes in basal heart rate, and no effects on the bradycardic response; 25 pmol/50 nl only attenuated the pressor response to chemoreflex activation. The data show that activation of GABAA receptors in the NTS produces a significant reduction in the bradycardic response, whereas activation of GABAB receptors produces a significant reduction in the pressor response of the chemoreflex. We conclude that 1) GABAA but not GABAB plays an inhibitory role in neurons of the lateral commissural NTS involved in the parasympathetic component of the chemoreflex and 2) attenuation of the pressor response of the chemoreflex by activation of GABAB receptors may be due to inhibition of sympathoexcitatory neurons in the NTS or may be secondary to the large increase in baseline MAP produced by baclofen. (+info)
Glycine toxicity after high-dose i.v. infusion of 1.5% glycine in the mouse.
(19/860)
Glycine 1.5% is the most widely used irrigating fluid during endoscopic procedures. To investigate if glycine toxicity is a mechanism promoting a fatal outcome when the solution is absorbed, we administered glycine 200 or 300 ml kg-1 dissolved in sterile water or normal saline, and also normal saline alone, over 60 min by i.v. infusion to 100 mice under methoxyflurane anaesthesia. Survival rates were 29% after 1.5% glycine, 21% after 1.5% glycine in normal saline, 67% after normal saline and 100% in controls. Both solutions containing glycine induced bradycardia and prolongation of the PQ interval and QRS duration, while only 1.5% glycine increased the water content of the myocardium. These results suggest that glycine promotes bradycardia and death, regardless of whether hyponatraemia or hypo-osmolality is present. We conclude that glycine toxicity is an important factor that increases the risk of administration of an irrigating fluid. (+info)
Nocturnal oxygen desaturation in coronary artery disease.
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Nocturnal oxygen desaturation and sleep apnea may provoke myocardial ischemia and arrhythmias in patients with coronary artery disease (CAD). Additionally, these factors may accelerate coronary atherosclerosis in the long term and they may play a role in the progression of the disease process. On the other hand, studies related to this subject are limited. This study was conducted to investigate the nocturnal oxygen desaturation and apneas during sleep in patients with CAD and to assess the possible association of these factors with CAD. We studied 22 male patients with CAD confirmed by coronary angiography who did not have symptomatic pulmonary disease and fourteen male healthy controls without known heart disease. Patients were randomly selected from men undergoing coronary angiography. Controls were age and sex matched and selected from the population registry. The normal controls were of similar body mass index to the patients. None of them were obese. The patients and controls underwent standard polysomnography. Men with CAD and controls had a similar apnea-hypopnea index (2.3 +/- 3.8 vs. 1.2 +/- 1.7). Mean oxygen desaturation index was higher among patients than controls (2.1 vs. 0.5, p < 0.05). Patients with CAD spent 3.1% (9.7 +/- 13.6) of total sleep time desaturated, while the same proportion in controls were 0.5% (1.9 +/- 4.1)(p < 0.05). Although both groups of patients were of similar heart rates at initial, the development of bradycardia during sleep was significantly higher in patients compared with controls (43.3% vs. 25.3%, p < 0.05). The results demonstrate that sleep disordered breathing, in particular nocturnal oxygen desaturation, occurs more common in patients with CAD compared to controls. Additionally, patients are at higher risk of developing bradycardia during sleep. This findings suggest that oxygen desaturation during sleep might contribute to the progression of CAD. (+info)
Muscle metaboreflex contribution to sinus node regulation during static exercise: insights from spectral analysis of heart rate variability.
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BACKGROUND: It is currently assumed that during static exercise, central command increases heart rate (HR) through a decrease in parasympathetic activity, whereas the muscle metaboreflex raises blood pressure (BP) only through an increase in sympathetic outflow to blood vessels, because when the metaboreflex activation is maintained during postexercise muscle ischemia, BP remains elevated while HR recovers. We tested the hypotheses that the muscle metaboreflex contributes to HR regulation during static exercise via sympathetic activation and that the arterial baroreflex is involved in the HR recovery of postexercise muscle ischemia. METHODS AND RESULTS: Eleven healthy male volunteers performed 4-minute static leg extension (SLE) at 30% of maximal voluntary contraction, followed by 4-minute arrested leg circulation (ALC). Autonomic regulation of HR was investigated by spectral analysis of HR variability (HRV), and baroreflex control of heart period was assessed by the spontaneous baroreflex method. SLE resulted in a significant increase in the low-frequency component of HRV that remained elevated during ALC. The normalized high-frequency component of HRV was reduced during SLE and returned to control levels during ALC. Baroreflex sensitivity was significantly reduced during SLE and returned to control levels during ALC when BP was kept elevated above the resting level while HR recovered. CONCLUSIONS: The muscle metaboreflex contributes to HR regulation during static exercise via a sympathetic activation. The bradycardia that occurs during postexercise muscle ischemia despite the maintained sympathetic stimulus may be explained by a baroreflex-mediated increase in parasympathetic outflow to the sinoatrial node that overpowers the metaboreflex-induced cardiac sympathetic activation. (+info)
Large-magnitude, transient, bradycardic events in rabbits.
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We propose that heart period sequences are organized similarly to sentences, with a lexicon of recurrent, similarly shaped words. These words should fulfill four criteria: universality, nonrandomness, central statistical tendencies, and specific associated physiology. Here we describe a large-magnitude, transient bradycardia (LMTB) and assess whether it constitutes a word. LMTBs were seen in 11 of 12 adult female rabbits. All shape parameters were different than those of the beat-randomized and phase-randomized surrogate sequences (P < 0.05-0.001). LMTBs were 8. 4 +/- 2.9 beats and 2.64 +/- 0.87 s long and were characterized by bradycardia of 77 +/- 49 ms over 1.09 +/- 0.49 s with a recovery to baseline over 1.56 +/- 0.61 s. The LMTBs had a slower recovery than onset in 9 of 11 rabbits and were highly peaked in 10 of 11 rabbits (P < 0.05). Scalar, magnitude, and shape parameters had values with central statistical tendencies. About 76% of LMTBs were accompanied by hypotension (mean -6.1 +/- 3.9 mmHg) that lagged 2 beats behind the onset of the bradycardia and that correlated with the bradycardia (-10.5 +/- 4.1 ms/mmHg). Thus transient bradycardic events are a distinct "word" in the lexicon of heart rate variability. (+info)
Bradycardia-induced coronary angiogenesis is dependent on vascular endothelial growth factor.
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A marked coronary angiogenesis is known to occur with chronic bradycardia. We tested the hypothesis that vascular endothelial growth factor (VEGF), an endothelial cell mitogen and a major regulator of angiogenesis, is upregulated in response to low heart rate and consequential increased stroke volume. Bradycardia was induced in rats by administering the bradycardic drug alinidine (3 mg/kg body weight) twice daily. Heart rate decreased by 32% for 20 to 40 minutes after injection and was chronically reduced by 10%, 14%, and 18.5% after 1, 2, and 3 weeks of treatment, respectively. Arterial pressure and cardiac output were unchanged. Left ventricular capillary length density (mm/mm(3)) increased gradually with alinidine administration; a 15% increase after 2 weeks and a 40% increase after 3 weeks of alinidine treatment were documented. Left ventricular weight, body weight, and their ratio were not significantly altered by alinidine treatment. After 1 week of treatment, before an increase in capillary length density, VEGF mRNA increased >2-fold and then declined to control levels after 3 weeks of treatment. VEGF protein was higher in alinidine-treated rats than in controls after 2 weeks and increased further after 3 weeks of treatment. Injection of VEGF-neutralizing antibodies over a 2-week period completely blocked alinidine-stimulated angiogenesis. In contrast, bFGF mRNA was not altered by alinidine treatment. These data suggest that VEGF plays a key role in the angiogenic response that occurs with chronic bradycardia. The mechanism underlying this VEGF-associated angiogenesis may be an increase in stretch due to enhanced diastolic filling. (+info)
Propofol, bradycardia and the Bezold-Jarisch reflex in rabbits.
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Propofol may cause profound bradycardia and asystole, which are mediated indirectly via cardiac innervation but could involve direct effects on the sino-atrial (SA) node and the conducting system of the heart. To test the hypothesis that propofol may also activate Bezold-Jarisch reflexes to cause bradycardia, 5-hydroxytryptamine (5-HT), veratridine and propofol were injected into the left ventricle of the heart in both intact and vagotomized rabbits. 5-HT and veratridine produced an acute, rapid, dose-dependent decrease in mean heart rate (delta HR) and a decrease in mean arterial pressure (delta MAP) together with transient but severe depression and abolition of renal sympathetic nerve activity (RSNA). Bilateral vagotomy greatly attenuated these responses; for example, at the highest dose of 5-HT (8 micrograms kg-1), delta HR, delta MAP and duration of abolition of RSNA were reduced by 57% (P < 0.001), 53% (P < 0.05) and 79% (P < 0.05), respectively. In contrast, reductions in delta HR and delta MAP produced by propofol were statistically significant only at very high doses (8 mg kg-1). Propofol depressed but did not abolish RSNA, and bilateral vagotomy had no effect on any of these responses. These results indicate that the cause of acute bradycardia after administration of propofol does not involve the Bezold-Jarisch reflex. (+info)