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Biomedical subjects

C Lyons

Publications and source records attributed to C Lyons.

48 records · Page 3Linked to original sources
PubMed1982

A possible role of the specialized conduction system in the conversion of ventricular tachycardia to ventricular fibrillation.

Electrode recordings from the right bundle branch, His bundle, and right atrium in a canine preparation enabled us to observe the activation of the ventricular myocardium and the specialized conduction system during the conversion of ventricular tachycardia to ventricular fibrillation. At times when ventricular tachycardia degenerated to ventricular fibrillation, asynchronous activation of the right bundle branch and the ventricular myocardium was frequently noted. Such asynchrony of activation was not seen during the spontaneous conversion of ventricular tachycardia to sinus rhythm. We suggest that this asynchronous activity produces increasing fractionation of ventricular activation fronts, which in turn yields fibrillation.

Animals↗
PubMed1982

Sepsis and pacemaker malfunction.

An unconventional presentation of an elderly man with sepsis and a nonfunctioning permanent cardiac pacemaker is reviewed. Our interpretations of signs of an acute abdomen and laboratory evidence suggestive of acute cholecystitis did not lead to the correct diagnosis. The pacemaker electrode had perforated the myocardium and this event is believed to be secondary to bacterial endocarditis at the electrode tip. The therapeutic implications of this unique case are discussed.

Aged↗
PubMed1981

The isolation of large and small plaque canine distemper viruses which differ in their neurovirulence for hamsters.

Large and small plaque-forming viruses were isolated from the Onderstepoort strain of canine distemper virus (CDV). Small plaque virus, which was released more slowly from infected cells than large plaque virus, readily established persistent infections in Vero cells, whereas large plaque virus required undilute passage to do so. All persistently infected cultures eventually released small plaque virus. No difference was found in the size of polypeptides induced by either plaque-purified viruses or virus released from persistent cultures. Both dilute and undilute passage, large plaque virus produced an acute neurological illness in weanling hamsters. whereas small plaque virus failed to produce any clinical signs of disease for 3 months after inoculation. After this period 50% of the animals infected with small plaque virus showed a general deterioration in their condition and lesions were observed in the brain which resembled those found in cases of large plaque virus infection. Serum-neutralizing antibody titres to CDV rapidly increased after infection with small plaque virus, whereas animals infected with large plaque virus had low or undetectable levels. All hamsters infected with small plaque virus and a small number which survived large plaque virus infection had elevated titres of antibody over a test period of 15 months.

Animals↗
PubMed1980

Site of functional right bundle branch block.

An in vivo canine heart was prepared by utilizing a temporary right heart bypass system to place close bipolar electrodes along the course of the right bundle branch. Activation within the right bundle could be recorded in up to six locations along the right bundle with premature supraventricular stimulation that caused functional right bundle branch block. The loss of activation recordings was found to occur in the proximal 0 to 6 mm. of the right bundle branch in every instance and in nine different preparations.

Action Potentials↗
PubMed1977

Herpesvirus in sensory and autonomic ganglia after eye infection.

In herpesvirus hominis (HVH) infections, virus harbored in the sensory ganglia is now thought to be the main source of recurrent infection at peripheral sites. Experimental HVH infection of the external eye in rabbits produces an acute infection and then latent infection of the trigeminal ganglion. In this study, acute infection of the automatic ganglia serving the eye (superior cervical and ciliary) as well as trigeminal ganglia occurred after HVH inoculation of rabbits' corneas with a herpes type 1 strain (RE). Latent virus infection was detected in the trigeminal ganglion of one of five animals tested six months after initial infection. Since the superior cervical and other autonomic ganglia serving the eye become infected during acute herpes simplex virus infection of the external eye in rabbits, it is possible that these ganglia are also sources of reinfection in recurrent herpetic disease of the eye. Following the initial eye disease with this virus strain, HVH shedding could not be demonstrated even after induction attempts by topically applied epinephrine or systemic use of cyclophosphamide. Thus, establishment of latent HVH infection in the ganglia and chronic shedding of virus into the external eye is not a constant feature of this animal model, but may depend on the specific strain of herpesvirus used.

Animals↗