Myeloperoxidase enzyme reaction as a marker for neutrophil infiltration into ischemiccanine myocardium

j Mol Cell Cardiol 19 (Supplement III) (1987) 64 ELECTROPHYSIOLOGICAL ANALYSIS OF THE EFFECTS OF CHLOROQUINE ON ATRIAL AND VENTRICULAR MYDCARDIUM. T. Fazekas, J.Gy. Papp, L. Szekeres. Department of Pharmacology, University Medical School, Szeged,Hungary. In earlier studies the authors observed that chloroquine (C), an inhibitor of phospholipase, is capable of preventing arrhythmias seen in ischaemic dog and rat heart 'in situ'. Since C possesses not only antiphospholipase, but also,quinidine-like' activity, the electrophysiological effects of C and quinidine (Q) (5 and tO mg/1) on rabbit heart muscle preparations have been compared with a view to analysing the mechanisms by which C exerts its antidysrhythmic effect. It turned out that, with an incubation time of 60 min, the effects of C in elevating the ventricular electrical threshold and lengthening the effective refractory period were about one-quarter to those of Q. The negative chronotropic effect of C and its depressant action on the atrial and ventricular conduction also proved significantly weaker than those of O. The 'in vitro' 'quinidine-like' electrophysiological effects of C are therefore moderate, which indicates that other factors,including its antiphospholipase activity and protective effect on the myocardial PL-membranes, may play a role in the development of the marked 'in vivo' antiischaemic/antiarrhythmic effects of the drug.

65

ISOPRENALINE INDUCED RELEASE OF ATRIAL NATRIURETIC PEPTIDE-LIKE IMMUNOREACTIVE MATERIAL FROM RAT ATRIUM IN VITRO.

R.

Ferrari,

G.

AgnoletLi,

A.

Rodella,

A.

Cornacchiari, C. Poiesi and A. Albertinl. Chair of

Cardiology and Chair of Chemistry, University of 8rescia, Brescia, I t a l y . We studied

the role of isoprenaline (1) in the mechanism of release of a t r i a l

matriuretic

peptlde-like

immunoreactive material (ANP) measured by RIA, from isolated rat atria. I (from I0 -g M to 10-6 M) induced a dose related transient

increase of peak developed tension.

increase

of

pmol/g/min at the f i r s t minute. dose

Administration of I (10-9 M) caused a sharp and

the rate of release of ANP, from 0.61 § 0.20 (S.E.) pmol/g/min to The preparation also responsed with a release of ANP to

or 10-8 M (from 0.26 + 0.10 pmol/g/min to 0.48 + 0.14 pmol/g/min)

lesser degree (from 0.17 • 0.03 pmol/g/min to 0.21 • 0.03 pmol/g/min). however, group rate

+ 0.21

subsequent

although

to

of

was not followed by a release of ANP, despite the increment in developed tension. release

variation

hipothesia,

of ANP from 1.18 + 0.25 pmol/g/mim to 1.77 ~ 0.36 pmml/g/mim s~ggestimg

In an other

atria

that:

2) i t is independent from the absolute

in tension of the a t r i a l f i b r e s seems to be involved in the release.

To prove

I) dose;

this

which had been previously depolarized with KCI (40 mM) in order to completely

contraction~ where~ exposed to

a

The subsequent dose (10-6 M) of I

of experiments I was administered directly at the dose of 10-6 M and i t induced an increase of

mechanism of release of ANP becomes readily attenuated; the

and of 10-7 M,

0.93 the

I which f a i l e d to induce any increment of the rate of

release

the the 3) last

abolish of

ANP,

suggesting that receptorial stimulation is not involved in the mechanism of release of ANP.

66 MYELOPEROXIDASE ENZYME REACTION AS A MARKER FOR NEUTROPHIL INFILTRATION INTO ISCHEMIC CANINE MYOCARDIUM. V.B. F i e d l e r , E. Bischoff. Bayer AG, Pharma Research Center, Wuppertal, Federal Republic of Germany. I n f i l t r a t i o n of polymorphonuclear n e u t r o p h i l s (PMNs) i n t o ischemic heart may exacerbate myocardial damage upon reperfusion. We used a spectrophotometric assay for a PMNs p e c i f i c enzyme marker, myeloperoxidase (MPO) to assess the PMN migration into expanding inflammatory cardiac lesions. MPO is an enzyme capable of binding hydrogen peroxide causing production of a c t i v a t e d oxygen. The l e f t a n t e r i o r descending (LAD) canine coronary a r t e r y was occluded f o r 90 min and reperfused f o r 5 hrs. A f t e r 90 min of coronary occlusion, tissue MPO a c t i v i t y was 0.18+0.08 u n i t s / l O 0 mg muscle. This a c t i v i t y increased over 5 hrs of reperfusion to 0.66+0.26 units MPO/IO0 mg tissue (p
S.22