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Syncope of patients with bradyarrhythmia is perceived as severe sign of low cardiac output caused by bradycardia and as a major criteria for pacemaker implantation (PMI). However, it has been reported that PMI can not always prevent syncope; it has been suggested that not bradycardia but an abnormality of the autonomic nervous system plays a part in syncope. To investigate the relation between autonomic nervous dysfunction and syncope in cases of sinus bradycardia (SB). Thirty-nine patients with SB were divided into two groups according to the presence (group S, n = 16, 46.9 +/- 20.0 years) or absence (group N, n = 23, 40.4 +/- 17.6 years) of syncope or presyncope. Corrected sinus node recovery time (CSNRT) was measured by electrophysiologic study. Pharmacologic autonomic nervous tests were performed as follows in a quiet room. Increased HR by application of 0.04 mg/kg atropine (para-tone), and by 0.004 microgram/kg/min isoproterenol divided by 0.004 (beta-sens) were evaluated, beta-tone was obtained by subtracting HR after application of propranolol (0.2 mg/kg) from that of atropine. Basal beta-sympathetic activity was evaluated by beta-sec that was obtained by beta-tone/beta-sens. Increased SBP by application of 0.4 microgram/kg/min phenylephrine divided by 0.4 (alpha-sens) was evaluated. alpha-tone was obtained by subtracting minimum SBP after 0.2 mg/kg phentolamine from SBP after application of propranolol. Basal alpha-sympathetic activity was evaluated by alpha-sec, that was obtained by alpha-tone/alpha-sens. There were no significant differences in basal clinical characteristics (age, sex, cardiac function) between the groups. The parameters of the functions of parasympathetic and beta-sympathetic receptors (para-tone, beta-sens, beta-tone, beta-sec) showed no significant differences between the groups, alpha-sens was attenuated (P < 0.01) and alpha-sec was augmented (P < 0.0001) significantly in group S. It was suggested that syncope or presyncope in SB patients could be attributed to failure of vasoconstriction mediated by alpha-sympathetic receptor but to severity of sinus node dysfunction.
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The difference between the maximum and minimum QT interval measured from a 12-lead electrocardiogram was defined as an index of spatial inhomogeneous repolarization of the ventricular myocardium. The causal relationship between QT dispersion and incidence of ventricular arrhythmias has been pointed out in various heart diseases, but until now it was discussed mainly related to sinus rhythm. QT dispersion in extrasystole may be more important in the development of arrhythmias. We examined 5 cases (mean age 34 +/- 12 years) with a history of paroxysmal supraventricular tachycardia, who underwent electrophysiologic study. Both atrial and ventricular premature stimuli were given at a basic cycle length of 600 msec respectively. The QT interval and the ventricular activation time (VAT) (period from premature test stimulus to the summit of QRS) of the premature beats were measured in a simultaneously recorded 12-lead electrocardiogram. QT dispersion (the difference between the longest QT interval and the shortest QT interval) and VAT dispersion (the difference between the longest VAT and the shortest VAT) were measured. In atrial premature beats, there were no significant changes in the QT dispersion or VAT dispersion when the coupling interval of the premature beats was shortened. In the ventricular premature beats, however, both the QT dispersion and the VAT dispersion tended to increase with the shortening of the coupling interval. We concluded that only a short coupled ventricular premature beat induces greater QT and VAT dispersion. A ventricular couplet with short coupling interval may contribute to the development of ventricular tachyarrhythmias.
We evaluated the short-term effects of tamsulosin in treating benign prostatic hyperplasia. Twenty-seven patients, aged 57 to 86 years (mean 68.4); complaining of obstructive urinary symptoms who had received no previous treatment for such symptoms were orally administered 0.2 mg of tamsulosin for 4 weeks. Symptoms (total AUA symptom score and AUA symptom subscores) and objective parameters including peak and average flow rate, and post-void residual urine rate were evaluated before and after 1, 2 and 4 weeks of treatment. The mean total AUA symptom score and the mean AUA symptom subscores for incomplete emptying and weak stream were significantly decreased after only 1 week of treatment. The mean AUA symptom subscores for intermittency, urgency and nocturia were significantly decreased after 4 weeks of treatment. The mean AUA symptom subscores for frequency and hesitancy were unchanged after 4 weeks of treatment. The mean peak and average flow rate, and post-void residual urine rate were significantly improved after only 1 week of treatment. In conclusion, tamsulosin improved not only objective parameters but also symptoms only 1 week after the start of treatment.
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Patients with spinal cord lesions frequently show autonomic hyperreflexia. The mechanism of autonomic hyperreflexia has been thought to be an acute general autonomic overactivity in response to cutaneous or visceral stimuli, but it remains uncertain. Several kinds of experiments suggest that amplified spinal sympathetic reflexes in the decentralized cord are attributable to the denervation supersensitivity of denervated neurons, which is a well-known phenomenon in denervated muscle fibers. In the present study, changes in the supersensitivity of motoneurons after cordotomy were studied in the spinal cord of neonatal rats. Responses to bath-applied noradrenaline (NA) were recorded from a ventral root of the isolated spinal cord of 6-day-old rats. In normal spinal cords, NA induced depolarization in motoneurons dose-dependently. alpha 1-antagonist prazosin (3 microM) inhibited the deporalization induced by NA, and alpha 2-antagonist rauwolscine (1 microM) potentiated it. In one group of rats, cordotomy was performed 4 days after birth by complete transection of the spinal cord at vertebrate 8th-10th thoracic level, and NA response was examined two days later (when they were 6 days old). In cordotomized rats, NA-induced depolarization was increased with respect to both amplitude and duration. alpha 1- as well as alpha 2-antagonists inhibited the NA response in the spinalized rats. Especially, both antagonists shortened the duration of NA response as compared to normal level. It is concluded that the denervation supersensitivity to NA appears 2 days after cordotomy in the spinal motoneurons of neonatal rats and that the supersensitivity to NA is attributable to the upregulation of both alpha 1- and alpha 2-adrenoceptors on the motoneurons, indicating that a new type of alpha 2-adrenoceptor function appears.
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Although the surgical results of the modified Fontan operation continues to improve, there are various advantages and disadvantages in terms of the post operative condition associated with the Fontan modifications. Late morbidity and mortality are mainly due to arrhythmias, thromboembolic complications, systemic venous hypertension and infective endocarditis. We reported our experience of the modified Fontan operation to determine an appropriate procedure for each patient. Seven patients (ranging from the age 1-14 years) underwent a modified Fontan operation including a lateral tunnel (n = 1), extracardiac conduit (n = 2) and autogenous atrial tunnel (n = 4). There was one hospital death due to sepsis in which the patient underwent lateral tunnel procedure. The mean follow up of another six patients was 20 months (ranging from 1-39 months) and all patients were classified as NYHA class I, and remained in normal sinus rhythm without any thromboembolic complications. When using the autogenous atrial tunnel, there are potential advantages; it is not associated with thromboembolism or endocarditis and has growth potential. However, in high-risk patients with increased pulmonary vascular resistance, impaired ventricular function and pre-operative atrial arrhythmias, it appears reasonable to use an extracardiac conduit.
Amplification of the c-myc gene has been reported in non-small cell lung cancer (NSCLC). We performed dual color fluorescence in situ hybridization (FISH) to detect amplifications of the c-myc gene on chromosome 8 to evaluate the relationship between these possible abnormalities and pathological stage. Tumor tissue samples were obtained from 29 patients of NSCLC in Stage I (n = 15) and III (n = 14) who underwent lobectomy at Saitama Cancer Center. Samples were analyzed for chromosome 8 centromere and c-myc gene by dual color FISH. The numerical aberration rate of chromosome 8 was 36.8 +/- 20.3% in Stage I and 40.6 +/- 24.8% in Stage III. The amplification rate of c-myc gene was 48.3 +/- 15.2% in Stage I and 57.4 +/- 17.0% in Stage III. There was a significnat difference in the numerical aberration rate of chromosome 8 between patients who survived for 5 years or more (28.8 +/- 17.5%) and those who survived less than 5 years (44.7 +/- 23.1%). The amplification rate of c-myc gene was not different between patients who survived more and less than 5 years survival, and who survived more and less than 3 years. The 5 year-survival rate in patients who showed 40% or more of chromosome 8 aberrations (n = 13) was 15.4%, which revealed significantly less than that of patients who showed less than 40% of aberrations (n = 16) (56.3%). There was no difference between the 5 year-survival rate in patients whose amplification rates of c-myc gene were equal or more than 50% (n = 16) and less than 50% (n = 13) (25.0% and 53.9%). The rate of chromosome 8 aberrations and the c-myc gene amplification rate were not correlated with pathological stage. However, the rate of chromosome 8 aberration showed correlation in terms of longevity of survival rate, therefore we considered the rate of chromosome 8 aberration to be an additional prognostic factor of patient with NSCLC.
An experimental study was performed to investigate the influence of hypothyroidism on wound healing. A state of severe hypothyroidism was induced initially by performing a total thyroidectomy on rat models; subsequently wounds were made by making long midline abdominal incisions and then suturing them. The parameters used to evaluate the process of wound healing of these incisions were the assay of type-I collagen, type-III collagen (procollagen peptide PIPC and P III P, each being the precursor of collagen), type-IV collagen, and hydroxyproline. The assays were repeated at specific times and compared to assays of similar parameters taken from a control group. In the state of hypothyroidism, a decrease was observed in type-IV collagen and hydroxyproline during the proliferative phase of wound healing. This indicated that the state of hypothyroidism constitutes an important factor in delaying wound healing.