Myocardial enzymatic and morphologic changes by tyramine-relea sed catecholamines in the rat

Myocardial enzymatic and morphologic changes by tyramine-relea sed catecholamines in the rat

POTASSIUM-ION and A. J. Williams. Street, MOVEMENTS Cardiothoracic Landan, WIN 2DX, It is now generally capable of generating membrane, gradient ...

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POTASSIUM-ION and A. J. Williams. Street,

MOVEMENTS Cardiothoracic

Landan,

WIN

2DX,

It is now generally capable of generating membrane, gradient using

safranine

On

the

Dissipation

of the

the

suggest

that

’Influx

movement

ENZYMATIC

logy, y. An

II Naples;+

IN

K’ 7.2)

Generat-

net efflux reaction

either

mitochondria

is

concentration potentials

mitochondria.

by

to rapid release and medium K+

the

ct

animals

was

ed

multiple

from medium.

net efflux reaction.

an uncoupler

of mitochondrial concentrations.

is caused

by

K+, We

changes

of the

significant at in

in the

a

tyramine

on

the

serum

msrked studies

ern,

transverse

CK

MB-CK

male

tubules

that were

rats

depletion

ultrastructural

tindings.

was

observed

tyramine the

hours mitochondria, variously

inta

receiv

creatinkinase

drug

in was

after

reach-

injection.

decrease by

inju-

Myocardial

serum

levels after

Na-

in

activity(CK) and

tour

myocardial

chloridrate.

hour

depletion showed

of

Sprague-Dawley of

Pa-

of Rome,Rome,

catecholamines

basis

treated

Medical

University

evaluating

progressive

rats

W.De of

Surgery, University

creatinkinase

fourth

Geigy-

TYRAMINE-RELEA

Institute

tissue,

significant the

the most structural and

of

cardiac

rise peak

Accordingly content

levels

BY

and

M.Chiariello,

endogenous

Th us

Council

CHANGES

at

of

changes, of

Research

A.Genovese,

aiming

documented

homogenate

Medical

Medicine and of Pathology,

performed,

isoenzyme(MB-CK)

the

RAT.

release

dose were

the

MORPHOLOGIC

study

by

al

in

potential

led

M.Condorelli.

of

experimental

lesions

from

THE

and

Faculty Institute

induced

ing

a chemical membrane

potential dropped and K+ chelator EGTA reversed this

cardiac

grants

A.Modesti+

ry

A

in

AND

CATECHOLAMINES

Alfieri,

in

membrane calciun

membrane

of K’

MYOCARDIAL

ples, ltal

fluxes

transport system inner mitochondrial

potential. supported by Basel).

tho

the of the

with

substrate stopped 2mM Hepes (pH

of medium oxygen between mitochondrial

(This work was Jubilthrms-Stiftung,

SED

electron across the

to K+net

respiration-generated

or total depletion in equilibration net

potential

addition

(FCCP) resulting membrane

a mitochondrial gradient

with a respiratory in a 250mM sucrose

of Ca2’ The

C.A. Gehring 2, Beaumont

England.

related

potential suspended

induction

MITOCHONDRIA. University of London,

of a membrane potential together We have estimated transmitochondrial

and

recommenced.

CARDIAC Institute,

accepted that an electrochemical

consisting of protons.

ing a membrane mitochondria

IN

CK

achieved, tyramine. myofibrillar

affected,

myocardiwith Ultra patt