Biomedical subjects
Publications and source records attributed to T H Phan.
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AGN 2979 [3-(3-methoxyphenyl)-3-(3-dimethylaminopropyl)-4, 4-dimethylpiperidine-2,6-dione] blocked the increase in tryptophan hydroxylase activity that occurred when slices of brainstem were exposed to a depolarizing medium or to agents that mobilize intracellular pools of calcium, but it had no effect on the activity of enzyme prepared from slices of brainstem incubated in control medium. AGN 2979 also blocked the calcium-calmodulin-dependent activation of tryptophan hydroxylase that was seen when supernatant preparations of the enzyme were exposed to phosphorylating conditions but not the activation induced by calcium-dependent proteases that was triggered by millimolar calcium concentrations. An identical pattern of inhibition has been found with the antipsychotic drugs, haloperidol and fluphenazine [Boadle-Biber, Biochem. Pharmac. 31, 2495 (1982)]. The sensitivity to the same inhibitors of both the activation of tryptophan hydroxylase produced by pretreatment of brainstem slices and that induced by incubation of supernatant preparations of enzyme under phosphorylating conditions suggests involvement of a common mechanism of enzyme activation in response to these different treatments.
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110 point cartography was carried out over the ventricular pericardium during sinus rhythm (SR) and during ventricular tachycardia (VT) in four patients whose infarctions were 15 days, 4 months, 4 years and 7 years previously, and in whom electrocardiographic investigation had suggested a ventricular reentry phenomenon. The macroscopical appearances of the heart at operation suggested that the infarct was situated along the left side in two cases, and in or along the septum in two others. Cartography in sinus rhythm showed that the onset of ventricular activity was compatable with a site of origin in the node/bundle of His. Cartography during VT showed up the epicentre of the abnormal impulses which were always situated outside the exit points and dependent upon the node/bundle of His system as demonstrated by cartography in sinus rhythm. Moreover, in at least two cases this was found to lie outside the infarcted area, in portions of the myocardium which could be considered as healthy. In one case it was found to lie along the anterior interventricular groove, facing the septal infarct. In two cases the arrhythmia will not recur, one having achieved this status bu simple ventriculotomy. The failures are reported in relation to the extent of the lesion anatomically, which may cause disorientation of the surgical approach, and make the results difficult to interpret.
Ventricular pericardial cartography in sinus rhythm (SR) and during ventricular tachycardia (VT) in four cases of myocardial infarction has yielded additional information in the study of conduction disorders in myocardial ischaemia: 1. The significant slowing of activity in SR as well as in VT is demonstrated by this direct method. It is associated with a diminution in amplitude of the pericardial potentials in the zones affected by the ischaemia; 2. Cartography during VT accentuates or reveals disorders of conduction which are slight or latent in SR; 3. Disorders of intra-ventricular conduction are found to be related either to segmental blocks on the branches of the bundle of His, or as focal blocks (peri-infarct block) on the left side, whose nature can be shown up even during VT; 4. Secondary activation of the myocardial fiber found to be related either to segmental blocks on the bundle of His during VT is demonstrated.