Document Detail


Myocardial contractile effects of L-arginine in the human allograft.
MedLine Citation:
PMID:  9137232     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: In the present study, we investigated, in transplant recipients, whether L-arginine (L-arg) potentiates the myocardial contractile effects of receptor-mediated coronary endothelial stimulation. Moreover, because inducible nitric oxide synthase (iNOS) is frequently expressed in transplanted myocardium, we also performed intracoronary infusion of L-arg in the absence of receptor-mediated coronary endothelial stimulation to investigate whether similar left ventricular (LV) contractile effects could be induced by providing more substrate for iNOS. BACKGROUND: Nitric oxide (NO), released from coronary endothelium after receptor-mediated stimulation by substance P (SP), affects vascular smooth muscle tone and modulates LV contractile performance. L-arg augments receptor-mediated endothelium-dependent coronary vasodilation in transplant recipients by increasing substrate availability for endothelial NO production. METHODS: Sixteen transplant recipients were studied at the time of annual coronary angiography. In eight transplant recipients, microtip LV pressures were recorded before and during intracoronary (IC) SP (20 pmol/min) and after the addition of IC L-arg (160 mumol/min) to IC SP. In eight transplant recipients, microtip LV pressures were recorded before and during IC L-arg (160 mumol/min) alone, and in six of these patients, endomyocardial biopsy samples were obtained to detect the expression of iNOS gene by reverse transcription-polymerase chain reaction. RESULTS: Addition of IC L-arg to IC SP induced a fall (mean +/- SEM) in LV peak systolic pressure (-16 +/- 4 mm Hg), which was larger (p < 0.01) than that observed during IC SP (-7 +/- 2 mm Hg). During IC L-arg alone, there was no change in LV peak systolic pressure despite the presence of iNOS mRNA in five of the six biopsy samples. CONCLUSIONS: In transplant recipients, L-arg potentiates the paracrine myocardial contractile effects of receptor-mediated coronary endothelial stimulation, probably by providing more substrate for endothelial NO production. Despite the myocardial expression of iNOS gene, L-arg alone fails to elicit similar contractile effects.
Authors:
W J Paulus; S Kästner; M Vanderheyden; A M Shah; H Drexler
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  29     ISSN:  0735-1097     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  1997 May 
Date Detail:
Created Date:  1997-06-03     Completed Date:  1997-06-03     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1332-8     Citation Subset:  AIM; IM    
Affiliation:
Cardiovascular Center, O.L.V. Ziekenhuis, Aalst, Belgium.
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MeSH Terms
Descriptor/Qualifier:
Arginine / pharmacology*
Coronary Angiography
Endothelium, Vascular / metabolism*,  physiology
Female
Heart Catheterization
Heart Transplantation / physiology*
Humans
Infusions, Intra-Arterial
Male
Middle Aged
Myocardial Contraction / drug effects*
Nitric Oxide / biosynthesis,  physiology*
Nitric Oxide Synthase / biosynthesis,  physiology*
Polymerase Chain Reaction
RNA, Messenger / genetics
Substance P / pharmacology
Ventricular Function, Left / drug effects
Ventricular Pressure / drug effects
Chemical
Reg. No./Substance:
0/RNA, Messenger; 10102-43-9/Nitric Oxide; 33507-63-0/Substance P; 74-79-3/Arginine; EC 1.14.13.39/Nitric Oxide Synthase

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