THROXBOSIS Sergamon
RESEARCH 16; 26~26h Press Ltd.1979. Printed
BRIEF
in Great
Britain
COMMUNICATION
RELEASE OF PLASMINOGEN ACTIVATOR BY ACETYLCHOLINE FROM THE ISOLATED PERFUSED PIG EAR Hans-Peter Kliicking Institute of Pharmacology and Toxicology, Medical Academy Erfurt, DDR-506 Erfurt, GDR
(Received 25.9.1978; in revised form 13.3.1979. Accepted by Editor Z.S. Latallo)
INTRODUCTION In a previous paper the effect of adrenergic substances on the activator release from the isolated perfused pig ear has been described (1). This communication is concerned with the release of plasminogen activator by cholinergic substances. MATERIAIS AND METHODS The following substances were used: Acetylcholine hydrochloride (VEB Berlin-Chemie, Berlin); a r pine sulfate VEB Jena harm, (Pharmachim, Sofia); carbachol (Jestryl 0R Jena); physostigmine sulfate (Calbiochem A;, Lucerne P ; pilocarpine hydrochloride (VEB Ankerwerk, Rudolstadt). Perfusion: Activator release was studied at constant perfusion volume in the isolated perfused pig ear /for test design see (I, 2)/. Determination of plasminogen activator activity: Plasminogen activator content was estimated by the fibrinolytic activity appearing during application of the perfusate on plasminogen-containing fibrin-agar plates and converted into Ploug units by means of a urokinase calibration curve (2, 3). The venous perfusate did not sh w lytic activity either on heated or on PAMBA-containing (IO- s M) fibrin plates (4, 5). The fibrinolytic activity of the perfusates was found to be induced by released plasminogen activator and not by plasmin or other proteolytic enzymes (2). RESULTS Acetylcholine at a concentration of IO-5 M causes no significant increase in plasminogen activator release. Measurable activator release is observed at concentrations of IO-4 M. 261
262
RELEASE
OF
PLASWISOGEX
AC'i'TVXfDR
Tal.f6,X0.:j’
An increase in activator release is reached ahen acetylchz~ice and physostigmine (IO-5 31) are given SizIJl;ane3USl;i (Table -7). Among the cholinergic substances acetylcholine, arbachol and pilocarpine, carbachol at a concentration of ?O- 9 M qas found to possess the strongest activator-releasing effect (Table I). TABI;E I Influence
of cholinergic substances in the isolated perfused Concentration in
on activator pig ear
release
(M)
Number of experiments (n)
Acetylcholine
10-5
4
Acetylcholine
1O-4
3
Acetylcholine
10-j
5
Acetylcholine + physostigmine
10’ 5 10-5
4
51 +
22
RESEARCH 16; 26~26h Press Ltd.1979. Printed
BRIEF
in Great
Britain
COMMUNICATION
RELEASE OF PLASMINOGEN ACTIVATOR BY ACETYLCHOLINE FROM THE ISOLATED PERFUSED PIG EAR Hans-Peter Kliicking Institute of Pharmacology and Toxicology, Medical Academy Erfurt, DDR-506 Erfurt, GDR
(Received 25.9.1978; in revised form 13.3.1979. Accepted by Editor Z.S. Latallo)
INTRODUCTION In a previous paper the effect of adrenergic substances on the activator release from the isolated perfused pig ear has been described (1). This communication is concerned with the release of plasminogen activator by cholinergic substances. MATERIAIS AND METHODS The following substances were used: Acetylcholine hydrochloride (VEB Berlin-Chemie, Berlin); a r pine sulfate VEB Jena harm, (Pharmachim, Sofia); carbachol (Jestryl 0R Jena); physostigmine sulfate (Calbiochem A;, Lucerne P ; pilocarpine hydrochloride (VEB Ankerwerk, Rudolstadt). Perfusion: Activator release was studied at constant perfusion volume in the isolated perfused pig ear /for test design see (I, 2)/. Determination of plasminogen activator activity: Plasminogen activator content was estimated by the fibrinolytic activity appearing during application of the perfusate on plasminogen-containing fibrin-agar plates and converted into Ploug units by means of a urokinase calibration curve (2, 3). The venous perfusate did not sh w lytic activity either on heated or on PAMBA-containing (IO- s M) fibrin plates (4, 5). The fibrinolytic activity of the perfusates was found to be induced by released plasminogen activator and not by plasmin or other proteolytic enzymes (2). RESULTS Acetylcholine at a concentration of IO-5 M causes no significant increase in plasminogen activator release. Measurable activator release is observed at concentrations of IO-4 M. 261
262
RELEASE
OF
PLASWISOGEX
AC'i'TVXfDR
Tal.f6,X0.:j’
An increase in activator release is reached ahen acetylchz~ice and physostigmine (IO-5 31) are given SizIJl;ane3USl;i (Table -7). Among the cholinergic substances acetylcholine, arbachol and pilocarpine, carbachol at a concentration of ?O- 9 M qas found to possess the strongest activator-releasing effect (Table I). TABI;E I Influence
of cholinergic substances in the isolated perfused Concentration in
on activator pig ear
release
(M)
Number of experiments (n)
Acetylcholine
10-5
4
Acetylcholine
1O-4
3
Acetylcholine
10-j
5
Acetylcholine + physostigmine
10’ 5 10-5
4
51 +
22
