Proximal Renal Tubular Acidosis Associated with Glycogen Storage Disease, Type 9

ABSTRACT. A 21/2-year-old Japanese boy with glycogen storage disease, type 9, developed proximal renal tubular acidosis (RTA). The RTA significantly improved in response to cornstarch therapy, implying a direct causal relationship between subtle metabolic derangements in glycogen storage disease, type 9, and proximal RTA.     

Cerulein-induced Pancreatic Polypeptide Secretion

Intramuscular administration of cerulein caused an abrupt rise in plasma pancreatic polypeptide (PP) in normal subjects. Pretreatment by atropine tended to lower the basal plasma PP level and significantly blunted the cerulein-induced PP secretion. It appears, therefore, that PP secretion induced by cerulein is under vagal control. In addition, in normal subjects, a gallbladder series first revealed a well-filled gallbladder of normal size and shape, which then contracted most strongly after a cerulein injection at a time corresponding exactly with the peak plasma PP levels produced by the cerulein. Since exogenous PP is known to cause a relaxation of the gallbladder, it is possible that endogenous PP plays an important role in gallbladder motility.     

Termination of Ventricular Tachycardia by an Implantable Atrial Pacemaker and External Pacemaker Activator

An atrial pacemaker was implanted in a patient who had dilated cardiomyopathy, sinus node dysfunction, and drug-resistant ventricular tachycardia (VT). VT episodes were terminated by atrial overdrive pacing using an implanted pacemaker and a newly developed hand-held external programmer/transmitter. Although successful cases of termination of intractable VT by ventricular pacing have recently been reported, the ventricular method might increase the risk of accelerating VT. Atrial overdrive pacing is a safer method since it minimizes the possibility of tachycardia acceleration and, combined with antiarrhythmic drugs, it appeared to be a unique and useful approach for the treatment of drug-resistant VT.     

Optimal Pacemaker Sensing with Respect to Amplitude and Slew Rate of Intracardiac Electrograms: Theoretical Analysis by Computer Simulation

The optimal amplitude and slew rate of intracardiac electrograms for pacemaker sensing Here examined on a theoretical basis by computer simulation. The simulation was based on the concept that it is the voltage at the position of the pacing electrode in an electrical field of a moving electrical dipole. By changing the distance between the electrode and the myocardium and the moving velocity of the electrical dipole, simulated ECGs with arbitrary amplitudes and slew rates were generated by the computer and fed to a bandpass filter. This filter was equivalent to those assembled in some models of permanent pacemakers and had a center pass-band frequency of 50 Hz and a Q of 1.0. The outputs of the filter were measured. The results showed that, for pacemaker sensing, simulated intracardiac electrograms with high amplitude should have high slew rates and those with low amplitudes should have low slew rates, although the absolute values depend on the characteristics of the bandpass filter and the sensing threshold of the pacemaker.     

INDUCTION OF SIALYL LEWISX ON THE SURFACE OF CULTURED RAT VASCULAR ENDOTHELIAL CELLS AND CARDIAC MYOCYTES BY HYPOXIA/REOXYGENATION IN VITRO

Neutrophils adhere to and roll on vascular endothelial cells (VECs) through interaction of selectins and their carbohydrate ligands in the early stages of inflammation; this adhesion is then later strengthened through interaction of integrins on neutrophils with intercellular adhesion molecule-1 (ICAM-1) on endothelial cells. Recent, as yet unpublished studies showed that myocardial ischaemia/reperfusion caused rapid expression of sialyl Lewis^X (SLe^X), one of the carbohydrate ligands of selectins, on VECs and cardiac myocytes and that an anti-SLe^X monoclonal antibody (MAb) significantly reduced myocardial reperfusion injury in vivo . In the present study, to investigate whether or not ischaemia/reperfusion itself can induce the expression of SLe^X on VECs and cardiac myocytes, the expression of SLe^X on cultured rat VECs and cardiac myocytes was examined by treatment with hypoxia/reoxygenation in vitro , because ischaemia/reperfusion stimuli may partly be due to hypoxia/reoxygenation. The expression of SLe^X was induced rapidly and temporarily on the surface of cultured rat cardiac myocytes and VECs by hypoxia/reoxygenation in vitro . This strongly suggests that the expression of SLe^X on the surface of myocardial cells is induced initially and directly by ischaemia/reperfusion, which results in the rolling attachment of neutrophils in the early stages of myocardial reperfusion injury.     

Early Afterdepolarizations in a Patient with Idiopathic Monomorphic Right Ventricular Tachycardia

To identify the role of afterdepolarizations in the induction of idiopathic monomorphic right ventricular tachycardia (VT), monophasic action potentials (MAPs) were recorded in a patient with this type of VT. The VT had a left bundle branch block configuration and inferior axis, and originated in the right ventricular outflow tract (RVOT). MAPs were recorded with a contact electrode at the origin of the VT, as well as other ventricular sites. The VT was induced by the intravenous administration of isoproterenol and/or rapid ventricular pacing and was preceded by short-long-short sequences of RR intervals. Early afterdepolarizations (EADs) in MAPs were recorded at the origin of VT (RVOT), but not recorded at other ventricular sites. These data suggest that catecholamine sensitive triggered activity seems to be the mechanism of idiopathic monomorphic right VT and EADs can be recorded in association with the occurrence of this type of VT.