Biomedical subjects
Publications and source records attributed to G Watanabe.
An internal thoracic artery graft holder, designed for use during coronary artery bypass grafting, is described. This new holder is atraumatic and holds the internal thoracic artery graft securely during anastomosis. The use of this instrument facilitates the use of an arterial graft for coronary artery bypass grafting.
Electrophysiologic features and surgical results were examined in 55 pediatric patients who underwent surgical accessory pathway division for Wolff-Parkinson-White syndrome. There were 31 male and 24 female patients ranging in age from 4 months to 15 years (mean age, 9.8 +/- 4.2 years; 25 patients were less than 10 years old; 4 patients were less than 12 months). Eleven of these patients had associated congenital heart disease and underwent concomitant surgical procedures to treat those conditions. Preoperative effective refractory period of antegrade accessory pathways, the right atrium, atrioventricular node, and cycle length during reentrant tachycardia were shorter in pediatric patients than in adult patients. Antegrade accessory pathways showed right predominance more frequently in the pediatric group than in the adult group. Surgical techniques included an endocardial approach (an epicardial approach was used in 1 patient) and concomitant operation for combined heart disease. The early mortality rate was 3.6%, whereas no late deaths occurred during the follow-up period of 96.8 +/- 54.9 months (maximum follow-up, 205 months). The absolute cure rate was 92%. There were no significant differences in early and late mortality between pediatric and adult patients. Surgical treatment of the Wolff-Parkinson-White syndrome in pediatric patients is as safe and effective as in adults. Considering the potential complications from prolonged fluoroscopic exposure during catheter ablation, surgical division of accessory pathways in children is a promising modality for the treatment of Wolff-Parkinson-White syndrome in selected cases.
Eight male patients ranging from 15 to 51 years old (mean age, 36.3 years) underwent surgical treatment of ventricular tachycardia (VT) associated with arrhythmogenic right ventricular dysplasia. One patient had an associated left ventricular aneurysm. The earliest activation site was detected for 15 lesions, and delayed potentials were recorded during sinus rhythm in all patients. On the basis of the epicardial mapping, the origins of the VT foci in the right ventricle were resected. Cryoablation on the surrounding myocardium was performed. There were no surgical deaths or postoperative fatal complications. During long-term follow-up, there has been no recurrence of VT and no congestive heart failure in the 6 patients without left ventricular involvement. The 2 patients with LV involvement died late of either congestive heart failure or development of VT originating from the left ventricle. In conclusion, a surgical approach consisting of myocardial excision and cryocoagulation offers a curative treatment of VT associated with arrhythmogenic right ventricular dysplasia and yields excellent long-term results when the VT origin is well identified in the right ventricle.
This study evaluated the effect of stimulating the central nervous system (CNS) with neostigmine, an inhibitor of acetylcholinesterase, on the blood lactate concentration in fed rats and in rats fasted for 48 hours. After the rat was anesthetized with pentobarbital, neostigmine was stereotaxically injected into the third cerebral ventricle. In fed rats, the central injection of neostigmine significantly increased the blood lactate level, while concomitantly increasing plasma glucagon, epinephrine and norepinephrine concentrations. Constant infusion of somatostatin throughout the experiments, to inhibit glucagon secretion from the pancreas, did not affect alterations in blood lactate by central injection of neostigmine. In adreno-medullated rats, CNS-stimulation by neostigmine still increased plasma norepinephrine significantly, however, the alteration in blood lactate was only one-third of that in intact rats. Intraperitoneal propranolol, but not phentolamine, prevented the rise in lactate. Neostigmine increased lactate in fasted rats as well as in fed rats. We conclude that in anesthetized rats, stimulation of the CNS by neostigmine increases blood lactate mainly through circulating epinephrine and partially through circulating norepinephrine or direct sympathetic nervous stimulation; glucagon does not appear to be involved in the increase in blood lactate.
To investigate whether the efficacy of intraoperative laser ablation therapy is affected by myocardial blood perfusion, we irradiated 11 canine hearts through the epicardium with a Nd:YAG laser (10, 20, and 30 J/mm2) using air as the medium. Compared coagulated myocardial depth, width, and volume obtained in the red beating heart was compared with those in the white nonbeating heart infused with 0 degrees C saline (cardioplegic model) via the coronary artery. Histologically, the macro- and microscopical findings were very similar. At each level of energy, the width and volume of red myocardium coagulated were significantly larger than those of white myocardium (P < 0.01). At 30 J/mm2, the depth of coagulation of red myocardium was significantly larger than that of white myocardium (P < 0.01). The coagulated volume of the white myocardium was about 60% of that of the red myocardium. Nd:YAG laser energy was absorbed by blood (red color = hemoglobin), and more energy was transferred in the higher temperature myocardium. During intraoperative Nd:YAG laser ablation, the presence of blood perfusion in cardiac tissue is thought to be an important factor affecting safe irradiation.
BACKGROUND: The mechanism of ventricular tachycardia (VT) after correction of tetralogy of Fallot (TF) is poorly understood. The purpose of this study was to examine the histopathology of the arrhythmogenic area detected by intraoperative mapping. METHODS AND RESULTS: The patients were three men who underwent radical surgery for TF at age 3, 3, or 5 years, respectively. VT developed at 8, 9, or 11 years, respectively, after surgery, and shock developed during VT in every case. The ECG revealed monomorphic VT in two cases and polymorphic VT in one case. Induction of VT resulted in a wide left-axis deviation-pattern QRS with cycle lengths varying between 260 and 330 milliseconds. The VT origin was identified at the right ventricular outflow tract (RVOT). A radical operation was performed with the patient under cardiopulmonary bypass. On epicardial mapping, delayed activation of the RVOT was recorded during sinus rhythm, and clockwise circus movement of the macroreentry current during VT on the right ventricular free wall was documented in each case. The VTs were treated successfully by surgical resection and cryoablation of the myocardium. In every patient, histology of the myocardial specimens showed degeneration, adiposis, fibrosis, inflammatory cell infiltration, and scattered myocyte islets. These lesions corresponded anatomically to the area of myocardium in which delayed activation was evident during epicardial mapping. CONCLUSIONS: The results of this study indicate that patients with VT after radical correction of the TF have abnormal histopathological findings at the site of the prior right ventriculotomy scar. These lesions were noted within the region of delayed activation found during epicardial mapping and were found to be a part of the reentrant circuit.
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Between November 1973 and March 1993, 454 patients underwent surgical division of an accessory pathway. The surgical and electrophysiologic data for 15 of these patients who underwent concomitant operation for acquired valvular heart disease were examined. This subgroup consisted of 10 male and 5 female patients whose ages ranged from 11 to 62 years (mean 51.6 +/- 9.7 years). The primary surgical indication was congestive heart failure in all cases; a concomitant history of cardiopulmonary resuscitation was present in two cases. Nine of these patients had mitral valve disease, three had aortic valve disease, two had combined aortic and mitral valve disease, and one had tricuspid valve disease. The surgical technique used for the treatment of Wolff-Parkinson-White syndrome included (1) an endocardial approach with the use of cardioplegic arrest, (2) a sharp dissection of the involved valve anulus, and (3) cryoablation. Concomitant surgical treatments of valvular heart disease included open mitral commissurotomy in five cases, mitral valve replacement in four cases, aortic valve replacement in three cases, aortic valve replacement with mitral valve commissurotomy in two cases, and tricuspid valvuloplasty (De Vega technique) in one case. Other concomitant surgical procedures included tricuspid annuloplasty with atrialized right ventricle and replacement of the ascending aorta in one case and left ventricular myectomy for hypertrophic obstructive cardiomyopathy in one case. No early deaths occurred. A successful disappearance of the delta wave and episodes of recurrent tachycardia were achieved in all 15 patients. Long-term surgical follow-up, averaging 86.2 +/- 54.8 months also demonstrated no late instances or recurrence of either a delta wave or tachycardia.
A twenty eight year-old man with anomalous pulmonary venous drainage from the right lung to the inferior vena cava (scimitar syndrome) underwent surgical treatment. We have successfully modified the surgical technique that consists of using the anterior wall of the right atrium, to form a tunnel that will divert the anomalous pulmonary vein to the left atrium. After rerouting of the anomalous pulmonary vein, the anterior wall of the right atrium was reconstructed with a polytetrafluoroethylene patch. To our knowledge, this is the first time this technique has been used to correct this syndrome.
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Aortic root infection remains a challenging problem in the surgical treatment of both native and prosthetic valve endocarditis. Between 1980 and 1991, 73 patients with active aortic valve endocarditis and paravalvular infection underwent operation. Indications for operation included congestive heart failure and uncontrolled sepsis. Aortic root abscesses were located in the noncoronary anulus or in the aorticomitral junction in 45% of cases, followed by the subannular interventricular septum in 23%. Two patients had an aorticoatrial fistula, seven an interventricular septal defect. Total or partial left ventricular-aortic dehiscence was observed in 27 patients. All patients underwent aortic valve replacement, nine with simultaneous mitral valve operations. Two of the latter required patch reconstruction of the destroyed aorticomitral septum with double valve replacement. Reconstruction of the aortic base was possible in 16 patients, whereas in 12 total replacement of the aortic root was necessary. In one patient, supracoronary aortic valve replacement was used. Recently, topical application of antibiotics in fibrin sealant was used in 25 patients. The operative mortality rate was 21% and correlated to preoperative uncontrolled sepsis and the presence of extensive root destruction. Operation for active endocarditis of the aortic root requires radical, individualized techniques and results in an acceptable operative and long-term risk. The use of an antibiotic fibrin compound appears to be a useful prophylactic tool to prevent postoperative residual endocarditis.
Between 3/91 and 3/93 twenty-nine patients (pts.) with a mean age of 55 years (30-68) underwent CABG (including 3 reoperation) using inferior epigastric artery (IEA) in addition to internal thoracic artery and saphenous vein graft. IEAs were harvested as pedicles with a mean length of 12.2 cm (7.5-17). Overall distal anastomoses were performed 3.2 per patients. And a mean of 2.3 anastomoses were completed as an arterial graft. IEA grafts were applied to left anterior descending artery in 10, diagonal branch in 15, in marginal branches in 2 and right coronary artery in 2. Mean cardiopulmonary bypass time amounted to 103 minutes and operation procedures were completed in 258 minutes (mean). Aortic cross clamp time of 48 minutes were required. One patient was died of cerebral accident 23 days postoperatively. Except for two abdominal wall infection no wound healing problems occurred. One reexploration for bleeding were necessary. Postoperative angiography revealed patent IEA grafts in 12 of 13 patients (92%). We concluded that the application of IEAs for CABG is available as a third arterial graft and with respect to intraoperative management and perioperative complications use of IEA combined with ITAs appears suited or superior to the use of the right gastroepiploic artery.
The role of prostaglandins in the secretion of inhibin and oestradiol-17 beta was examined in immature female rats treated with equine chorionic gonadotrophin. Administration of prostaglandin (PG) F2 alpha to animals whose serum and ovarian levels of inhibin and oestradiol-17 beta had been suppressed by indomethacin given 24 h after equine chorionic gonadotrophin prevented the inhibition or restored the levels to normal. Initiation of PGF2 alpha replacement immediately after treatment with indomethacin was more effective. The results are consistent with the hypothesis that PGs play a regulatory role in the synthesis and secretion of inhibin and oestradiol-17 beta by the rat ovary.
METHODS: Eighty-three patients with hepatocellular carcinoma (HCC) were treated with curative surgical resection during the past 8 years. RESULTS: No operative deaths occurred. The cumulative recurrence rates after resection at the ends of years 1, 2, and 3 were 37.0%, 57.1%, and 71.6%, respectively. After adjusting the imbalance in clinical factors among patients by using a Cox proportional-hazards model, it was shown that multiplicity, histologic classification, and absence of antibody to hepatitis C virus were associated significantly with recurrence after resection. The size of the tumor did not affect the incidence of recurrence. Thirty-eight of 41 patients with intrahepatic tumor recurrence had undergone at least one of the following three therapies against HCC: surgical reresection, percutaneous ethanol injection (PEI), and transcatheter arterial embolization (TAE). The most significant factor affecting the survival time of patients with tumor recurrence was the total number of tumor nodules at the time of recurrence. Although surgery and PEI were thought to be more effective treatments than TAE in prolonging life, multivariate analysis showed that they were not significant factors of survival time because choices in the method of treatment were correlated closely with the number of cancer nodules. A 65.3% 5-year survival rate from the time of first surgery was accomplished through vigorous therapy when tumors recurred. CONCLUSION: In conclusion, despite the high recurrence rate after resection of HCC, the use of multiple therapies can achieve increased survival rates.
We investigated the effects of intrahypothalamic or hippocampal injection of GABA receptor agonists on hyperglycemia induced by hippocampal neostigmine. Prior to the injection of neostigmine (50 nmol) into the hippocampus (HPC), muscimol (0.01-1 nmol) or baclofen (1 nmol) was injected into the bilateral ventromedial hypothalamus (VMH). Muscimol suppressed the hyperglycemia in a dose-dependent manner, but baclofen affected it only minimally. In contrast, neither hippocampal muscimol (1 or 2.5 nmol) nor baclofen (1 nmol) suppressed the hippocampal neostigmine-dependent hyperglycemia. Intrahypothalamic muscimol (1 nmol) also decreased the changes in hepatic venous plasma glucagon and epinephrine significantly. These results indicate that intrahypothalamic muscimol suppresses hyperglycemia caused by cholinergic neurons originating from the HPC, indicating existence of the location specificity.
We investigated the relationship between histamine and muscarinic cholinergic neurons in central nervous system (CNS)-mediated glucose regulation in anesthetized fed rats. The injection of pyrilamine (5 x 10(-7) mol) into the third cerebral ventricle suppressed the hyperglycemia induced by intraventricular injection of histamine (5 x 10(-7) mol). Ranitidine (5 x 10(-7) mol), however, did not suppress this hyperglycemia. The injection of atropine (5 x 10(-9)-5 x 10(-7) mol) into the third cerebral ventricle suppressed the histamine-induced hyperglycemia in a dose-dependent manner. These findings suggest that histamine induction of CNS-mediated hyperglycemia involves neuronal transmission not only via H1 receptors but also, at least in part, by muscarinic cholinergic neurons.
We investigated the effect of GABA receptor agonists on the central nervous system (CNS)-mediated hyperglycemia induced by neostigmine or histamine in anesthetized fed rats. The injection of muscimol, GABAA receptor agonist (1, 2.5 nmol) into the third cerebral ventricle suppressed the hyperglycemia induced by intraventricular injection of neostigmine (1 x 10(-8) mol) or histamine (5 x 10(-7) mol). Baclofen, GABAB receptor agonist (1, 2.5 nmol), however, did not suppress these hyperglycemia. Neither muscimol nor baclofen (2.5 nmol) affected plasma glucose levels. These findings suggest that activation of GABAA receptor in the CNS suppresses the hyperglycemia induced by the stimulation of cholinoceptive neuron or histaminergic neuron, but activation of GABAB receptor does not affect them.
We previously reported that injection of PGF2 alpha into the third cerebral ventricle produces hyperglycemia and hyperthermia associated with catecholamine secretion in anesthetized rats. We have also studied the potency of catecholamine secretion induced by injecting PGE2 or PGF2 alpha into the third cerebral ventricle and the effect of the GABA-selective agonist, muscimol, on the catecholamine secretion induced by PGE2 or PGF2 alpha. Administration of 50 micrograms of PGE2 into the third cerebral ventricle increased norepinephrine secretion to a greater extent than the same dose of PGF2 alpha, whereas the latter increased epinephrine secretion to a greater degree. These effects paralleled the potencies of the hyperglycemic and hyperthermic effects of PGF2 alpha and PGE2, respectively. Simultaneous injection of 2.5 nmol of muscimol into the third cerebral ventricle with 50 micrograms of PGF2 alpha or PGE2 completely suppressed epinephrine and norepinephrine secretion induced by PGF2 alpha or PGE2. These findings suggest that central PGF2 alpha and PGE2 stimulate epinephrine and norepinephrine secretion with different potencies, and that brain GABAA receptors suppress catecholamine secretion induced by PGF2 alpha or PGE2.