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Notes: Abstract— [2-14C]Propionate injected into rats was metabolized into [14C]glucose and 14C-labelled aspartate, glutamate, glutamine and alanine. The results are consistent with the conversion of propionate into succinate and the oxidation of succinate into oxaloacetate, the precursor of labelled amino acids and the substrate for gluconeogenesis.The ratio of the specific radioactivity of glutamine to glutamate was greater than 1 during the 30 min period in the brain, indicating that propionate taken up by the brain was metabolized mainly in the ‘small glutamate compartment’ in the brain. The results, therefore, support the previous conclusion (Gaitonde, 1975) that the labelling of amino acids by [14C]propionate formed from [U-14C〉]-threonine in thiamin-deficient rats was metabolized in the ‘large glutamate compartment’ of the brain.The specific radioactivity ratio of glutamine to glutamate in the liver was less than 1 during the 10 min period but greater than 1 at 30min. These findings which gave evidence against metabolic compartments of glutamate in the liver, were interpreted as indicative of the entry of blood-borne [14C]glutamine synthesized in other tissues, e.g. brain. The labelling of amino acids when compared to that after injection of [U-14C]glucose showed that [2-14C]propionate was quantitatively a better source of amino acids in the liver. The concentration of some amino acids in the brain and liver was less in the adult than in the young rats, except for alanine and glutathione, where the liver content was more than double that in the adult.

Notes: Implantable Atrial Defibrillators. Due to the limited efficacy of antiarrhythmic drugs for atrial fibrillation, several nonpharmacologic therapeutic options have evolved. One of these is an implantable atrial defibrillator. Recent studies have shown that internal atrial defibrillation is feasible with relatively low energies. To date, the optimal electrode configuration involves large surface area catheters in the right atrium and coronary sinus. In humans, atrial defibrillation can generally be achieved with 〈 2 J using this electrode configuration and a biphasic shock waveform. For shocks 〈 5 J, there is no significant pathological damage to the atria or coronary sinus. Further investigation is needed to guarantee that atrial defibrillation shocks do not provoke ventricular arrhythmias. Preliminary data suggest that atrial defibrillation shocks synchronized to R waves that are not closely coupled are safe. In addition, the shocks are well tolerated if the shock energy is 〈 1.5 J. With additional studies to confirm the safety of implantable atrial defibrillators, further reduce shock energy, and improve patient tolerance, an implantable atrial defibrillator can become an acceptable therapy for patients with symptomatic, paroxysmal atrial fibrillation.

Notes: Limited information is available regardIng potential adverse Interactions between transvenous nonthoracotomy cardioverter defibrillators and pacemakers. We describe our experience with 37 patients who have undergone successful Implantation of both a transvenous defibrillator and pacemaker. The patients’mean age was 64 ± 12,9 years. Thirty-three were male and four were female. The mean LVEF wos 30.8%±11.8%, The indications for pacemaker implantation included sick sinus syndrome in 13 patients, complete heart block in 15 patients, sinus brady-cardia secondary to medications In 8 patients, and neurocardlogenlc syncope In 1 patient. The Indications for Insertion of a defibrillator Included medically refractory VT in 27 patients and sudden cardiac death in 10 patients. Twenty-three patients received an Endotak lead and 14 patients received o Transvene lead. Eighteen patients had a pacemaker prior to an ICD, 14 patients had an ICD prior to a pacemaker, and 4 patients had both devices placed simultaneously. Interaction was evaluated at Implant of the second device and 1–3 days after both devices were placed. Detection of VF/VT was analyzed during asynchronous pacing (DOO/VOO) with maximum pacing output. In addition, in six patients, DFT was determined before and after pacemaker implantation. In 14 patients (38%), device interactions that could not always be optimally corrected were observed. In five patients, the pacemaker was reset to the “noise reversion” mode after high energy ICD discharge, Oversensing of atrial pacemaker stimuli resulted in inappropriate ICD firings in four patients. This wos observed only with a specific device ond could not be prevented by atriol leod repositioning in two of them, but required reprogramming of the pacemaker to the VVImode. An increase in DFT was observed in five patients who had a pacemaker implanted after on ICD. Compared with previously published studies, a greater frequency of tronsvenous ICD and pacemaker Interactions were observed. Considering that almost 50% of the patients already have o pacemaker ot the time of ICD Implant, the ovalloblllty of deflbrlllotors with dual chamber pocing capability will not eliminate the potential for this problem.

Notes: During testing of a CPI model 1715 ICD, an apparent sensing abnormality was noted following shock delivery for VF. Close inspection of the recording prior to the defib-rillation attempt revealed that the surface leads spontaneously lost 848 ms of data while the event marker was unaffected. Computer simulations revealed that an inadequate buffer size for the ampHfied (surface ECC) data was the likely source of data loss. It is important to recognize tbat a discordance between surface leads and event marker may represent an abnormality in tlie data acquisition system and simulate an ICD or lead malfunction.

Notes: Although changes in autonomic tone affect ventricular defibrillation, little is known about the effect of increased parasympathetic or sympathetic tone on the atrial defbrillation threshold. Methods: To evaluate the effect of reflexly increased parasympathetic and increase α- and β-adrenergic tone on the atrial defibrillation threshold (ADFT), atrial fibrillation was induced in 14 patients. ADFTs, right atrial refractory period (RARP), and monophasic action potential duration (MAPD) were determined before and after autonomic intervention. ADFTs were determined with a step-up protocol using 3/3-ms biphasic shocks delivered through decapolar catheters in the right atrial appendage and coronary sinus. Two groups were studied. Group I (N = 8) had ADFTs determined at baseline, after receiving phenylephrine (PE), and with PE plus atropine (A). Group 2 (N = 6) had ADFTs determined at baseline and after receiving isoproterenol (ISO). Results: Group I: PE significantly increased sinus cycle length (SR-CL) compared to baseline (742 ± 123 to 922 ± 233 ms) without significantly changing RARP, MAPD, or ADFT (2.3 ± 1.3 J vs 2.3 ± 0.8 J). With PE + A, SR-CL significantly decreased (529 ± 100 ms vs 742 ± 123 ms) and MAPD shortened (231 ± 41 ms vs 279 ± 49 ms) without altering RARP or ADFT (1.94 ± 0.9 J vs 2.25 ± 1.25 J). Group 2: ISO decreased SR-CL (486 ± 77 ms vs 755 ± 184 ms) and MAPD (169 ± 37 ms vs 226 + 58 ms) but not RARP or ADFT (2.25 ± 1.21 J vs 2.33 ± 1.75 J). Conclusions: Increasing parasympathetic, α-, or β-adrenergic tone does not affect the ADFT despite causing significant electrophysiological changes in the atria.

Notes: We report a 51-year-old man with severe ischemia cardiomyopathy and heart failure in whom incessant bigeminal ventricular ectopy failed to generate a detectable arterial pressure. This created a mechanical bradycardia despite an adequate electrical heart rate. Dual chamber pacing increased the effective heart rate and allowed discontinuation of an intraaortic balloon pump from which the patient could not otherwise be weaned.

Notes: Whether the presence of abnormal PR before selective slow pathway ablation for AV node reentrant tachycardia increased the risk of complete heart block remains controversial. We report our experience in seven patients with prolonged PR intervals undergoing catheter ablation for AV reentry tachycardia. Their mean age was 66 ± 12 years; four patients were female and three were male. RF ablation was performed using an anatomically guided stepwise approach. In six patients, common type AV node reentry was induced and uncommon type was observed in the remaining patient. In all seven patients, successful selective slow pathway ablation was associated with no occurrence of complete heart block and was followed by shortening of the AH interval in five patients. In all seven patients, successful ablation was achieved at anterior sites (M1 in two patients and M2 in five patients). Despite AH shortening after ablation, the 1:1 AV conduction was prolonged after elimination of the slow pathway, excluding either sympathetic tone activation or parasympathetic denervation. In conclusion, selective slow pathway ablation can be performed safely in the majority of patients with prolonged PR interval before the procedure. Because successful ablation is achieved at anterior sites in most patients, careful selection and monitoring of catheter position is required.

Notes: CTL-TIL lines have been developed from tumour infiltrating lymphocytes (TIL) from the ascites of patients with ovarian carcinoma, and used to investigate whether common tumour antigens are expressed on allogeneic ovarian tumours epithelial tumour lines derived from colon and pancreatic carcinoma. Three CTL lines expressed preferential cytolytic activity against autologous tumour cells and against certain allogeneic ovarian tumour cells that shared HLA-A2 molecules. Analysis of the target specificity of these CTL lines indicated that they also lysed human colon and pancreatic tumour lines sharing HLA-A2. CTL-TIL clones isolated from these lines were found to lyse HLA-A2+ ovarian, colon and pancreatic tumours, and to recognize clonally distributed common epitopes on pancreas and colon tumour clones. These results indicate that shared tumour antigens can he found among tumours of common epithelial cell origin. These results indicate a novel class of T-cell-definable tumour antigens recognized by tumour-reactive CTL on human tumours and may be significant for understanding of cellular immunity in ovarian cancer, identification of CTL-defined tumour antigens and future adoptive specific immunotherapeutic approaches in ovarian cancer.