Effects of sustained leukotriene D4 administration of myocardial contractility and coronary flow

1984 ◽  
Vol 28 (5) ◽  
pp. 673-674 ◽  
Author(s):  
Robert E. Goldstein ◽  
David Ezra ◽  
Gordon Letts
1985 ◽  
Vol 249 (3) ◽  
pp. H698-H702 ◽  
Author(s):  
D. Ezra ◽  
G. Feuerstein ◽  
J. F. Czaja ◽  
F. R. Laurindo ◽  
C. K. Finton ◽  
...  

Coronary blood flow (CBF) and myocardial contractility decrease markedly in response to intracoronary administration of leukotriene D4 (LTD4). With steady infusion, however, both CBF and contractility escape, approaching preinfusion values despite ongoing LTD4 administration. To clarify the mechanism of this escape, we reinfused plasma from the coronary vein draining the myocardial area receiving LTD4. Introducing this plasma into a coronary artery caused a marked rise in coronary flow for the duration of the plasma infusion. Coronary flow reduction with vasopressin or mechanical occlusion matching that caused by LTD4 failed to elicit vasodilator production. Thus a unique coronary vasodilator factor is induced by LTD4. Whole blood or platelet-rich plasma incubated with LTD4 in vitro produced the same pattern of coronary dilation on intracoronary infusion; LTD4 incubation with platelet-poor plasma failed to elicit a vasodilation. The vasodilator factor is stable and is not potassium, a prostaglandin, catecholamine, histamine, serotonin, adenosine, adenosine diphosphate, or platelet-activating factor. Production of this leukotriene-induced vasodilator factor may account for the escape from LTD4-induced coronary constriction.


2001 ◽  
Vol 33 (6) ◽  
pp. A75
Author(s):  
H.K. Maués ◽  
W.C. Pádua Filho ◽  
M. Faraj ◽  
H. Junqueira Neves ◽  
E.S. Gomes ◽  
...  

1973 ◽  
Vol 51 (2) ◽  
pp. 61-67 ◽  
Author(s):  
G. M. Tremblay ◽  
J. de Champlain ◽  
R. A. Nadeau

The effects of d,l-propranolol, d-propranolol, l-propranolol, and sotalol on myocardial contractility and vascular coronary resistance (V.C.R.) were studied on isolated perfused rat and guinea pig hearts, using a modified Langendorff technique. Left ventricular intracavitary pressure (L.V.P.) and maximum dp/dt were depressed by d,l-propranolol and d-propranolol but not by sotalol and l-propranolol. At constant coronary flow, perfusion pressure was decreased to 40% of control values by d,l-propranolol and d-propranolol but perfusion pressure remained unchanged with l-propranolol and increased with sotalol. The drop in V.C.R. following d,l-propranolol and d-propranolol preceded the fall of L.V.P. and occurred in fibrillating hearts as well. The same effect was obtained in noradrenaline-depleted hearts following pretreatment with 6-OH-dopamine. These observations suggest that d,l-propranolol has a coronary vasodilator action unrelated to its adrenergic-receptor blocking properties, and which appears specifically to be an effect of its dextro-isomer.


1998 ◽  
Vol 35 (5) ◽  
pp. 825
Author(s):  
Mi Gyeong Lee ◽  
You Seong Jeong ◽  
Myoung Hoon Kong ◽  
Suk Min Yoon ◽  
Young Seok Choi ◽  
...  

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