Yutaka Dohi

The evidence of platelet activation in bronchial asthma

The possible involvement of platelets in bronchial asthma was investigated under three different conditions: (1) chronic asthma, (2) bronchial provocation inhaling house dust mite (HDM), and (3) status asthmaticus. Plasma levels of beta-thromboglobulin (beta-TG), platelet factor 4 (PF4), and in part, platelet-activating factor (PAF) were measured. Approximately one third of the subjects with symptomatic or asymptomatic chronic asthma showed an increased level of beta-TG or PF4. Statistically significant differences occurred in beta-TG and PF4 levels only between healthy controls and symptomatic subjects. Five out of six subjects showed no elevation of beta-TG and PF4 during immediate asthmatic response. In two out of nine subjects with status asthmaticus, beta-TG or PF4 was elevated, and statistically significant correlations occurred between the initial level of PAF and that of beta-TG or PF4. Those results suggest that the platelet activation in the circulation is sometimes provoked in asthma, but plasma level of alpha-granule-derived proteins does not reflect the intensity or severity of asthma, and that PAF is likely to be a mediator responsible for the platelet activation.

Intravenous Adenosine Triphosphate Disodium: Its Efficacy and Electrophysiologic Effects on Patients with Paroxysmal Supraventricular Tachycardias

We studied the electrophysiologic effects of intravenous adenosine triphosphate disodium (ATP‐2Na) on 17 patients with paroxysmal supraventricular tachycardias (PSVTs). One patient had sinus node (SN) reentry, two had intraatrial (IA) reentry, 7 patients had AV nodal reentry and seven had atrioventricular reentrant tachycardias (AVRTs) with accessory pathways (APs). ATP‐2Na was injected during ventricular pacing in patients with AV nodal reentry and AVRTs with APs. A bolus injection of ATP‐2Na terminated all the PSVTs within 50 s except for one case of IA reentry (case 2). The sites of block at termination were the atrium in SN reentry and IA reentry, between A and H (AH) or between H and A (HA) in AV nodal reentry, and AH block in all the PSVTs with APs. The sites of action on the patients with AV nodal reentry were both the antegrade and retrograde pathways, while the modes of block were Mobitz type I and type II, respectively. ATP‐2Na during ventricular pacing in patients with AV nodal reentry produced Mobitz type II ventriculoatrial block (VAB) in four of seven cases. ATP‐2Na during ventricular pacing in patients with AVRTs with APs produced changes of atrial activation sequences in two patients, induction of PSVT in two patients, and Mobitz type II VA block in three patients. The former two phenomena suggested a retrograde AV nodal block and raised the possibility of a simple test for retrograde atrial fusion during ventricular pacing in patients with WPW syndrome. Chest discomfort of short duration was most commonly noted after ATP‐2Na administration.

Effects of aprindine on monophasic action potentials

Using a catheter electrode developed by the authors for recording monophasic action potentials (MAPs), the atrial and ventricular MAPs of seven mongrel dogs were simultaneously recorded. The results were used to evaluate the effect of the new antiarrhythmic drug aprindine on MAPs. An electrophysiologic study was also carried out to evaluate the effect of aprindine on the conduction system. Aprindine caused a significant increase in both the AH interval (at a basic cycle length of 400 ms) and the HV interval (at basic cycle lengths of 400 and 500 ms). The effective refractory period increased in both the right atrium and the right ventricle. Although an increase in MAP duration at repolarizations to 90% MAP (MAPD90) was not observed in the right atrium, a significant increase was noted in MAPD90 in the right ventricle. There were no significant changes in the ratio between the effective refractory period and MAPD90 of the right ventricle before and after administration of aprindine. This result suggests that increases in MAPD90 contribute to an increase in the effective refractory period of the right ventricle.

Electrophysiological Effects of Intravenous Disopyramide Phosphate on the Wolff‐Parkinson‐White Syndrome

The effects of a single intravenous infusion of 2mg/kg body weight disopyramide phosphate (DP) on the mode of initialion of reentrant supraventricular tachycardia were assessed in seven patients with Wolff‐Parkinson‐White fWPW) syndrome using bundle of His electrograms and the ventricular extrastimulus method. The delta wave disappeared in three potients after DP. However, retrograde conduction via the accessory pathway persisted even ofter DP administration in all patients. These effects contributed to the induction of reciprocating tachycardia after DP. The retrograde functional refractory period of the His‐Purkinje system (HPS) and the effective refractory period of the accessory pathway were increased in all cases and contributed to the development of reentry HPS. After DP. the zone of reentry HPS widened in four cases (including a newly developed case) and remained unchanged in three cases. Reentrant supraventricular tachycardia zones widened in three cases: these widened reentrant supraventricular tachycardia zones were induced by the widened reentry HPS, that is, reentry HPS was followed by the reentrant supraventricu‐lar tachycardia. This study demonstrates that persistence of retrograde accessory pathway conduction and widened reentry HPS which might be dose‐related after DP could be the retrograde determinants affecting the reentrant supraventricular tachycardia zone. (PACE, Vol. 5, September‐October, 1982)