Document Detail


Blood cardioplegia enhanced with nitric oxide donor SPM-5185 counteracts postischemic endothelial and ventricular dysfunction.
MedLine Citation:
PMID:  7776679     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study tested the hypothesis that enhancement of blood cardioplegia with the nitric oxide donor agent SPM-5185 inhibits postischemic left ventricular and coronary endothelial dysfunction. Eighteen anesthetized dogs supported by total vented bypass were subjected to 30 minutes of normothermic ischemia followed by 4 degrees C multidose blood cardioplegia. Hearts received either standard blood cardioplegia (vehicle group; n = 6), blood cardioplegia with 1 mumol/L SPM-5185 (low-dose group; n = 6), or 10 mumol/L SPM-5185 (high-dose group; n = 6). After 60 minutes of cardioplegic arrest, the heart was reperfused for a total of 60 minutes, first in the beating empty state for 30 minutes and then after discontinuation of bypass for 30 minutes. Baseline and postischemic left ventricular function was assessed by the slope of the end-systolic pressure-volume (impedance catheter) relation. Postischemic end-systolic pressure-volume relation was depressed by 53.7% of preischemic values in the vehicle group (from 8.2 +/- 1.0 to 3.8 +/- 0.3 mm Hg/ml) and by 33.7% (from 9.2 +/- 1.1 to 6.1 +/- 0.5 mm Hg/ml) in the low-dose group. In contrast, there was complete postischemic functional recovery in the high-dose group (from 7.6 +/- 1.1 to 7.2 +/- 1.2 mm Hg/ml). In coronary arteries isolated from these hearts, endothelium-dependent maximal relaxation to acetylcholine was impaired by 27% in the vehicle group and by 18% in the low-dose group, whereas the high-dose group showed complete endothelium-dependent relaxation. Myeloperoxidase activity, an index of neutrophil accumulation in postischemic myocardium, was elevated in the vehicle and low-dose groups (3.36 +/- 0.58 and 2.56 +/- 0.68 U/100 mg tissue) but was significantly reduced in the high-dose group to 1.27 +/- 0.45 U/100 mg tissue. We conclude that inclusion of 10 mumol/L nitric oxide donor SPM-5185 in blood cardioplegia improves postischemic ventricular performance and endothelial function in ischemically injured hearts, possibly via inhibition of neutrophil-mediated damage.
Authors:
K Nakanishi; Z Q Zhao; J Vinten-Johansen; D A Hudspeth; D S McGee; J W Hammon
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of thoracic and cardiovascular surgery     Volume:  109     ISSN:  0022-5223     ISO Abbreviation:  J. Thorac. Cardiovasc. Surg.     Publication Date:  1995 Jun 
Date Detail:
Created Date:  1995-07-07     Completed Date:  1995-07-07     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0376343     Medline TA:  J Thorac Cardiovasc Surg     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1146-54     Citation Subset:  AIM; IM    
Affiliation:
Department of Cardiothoracic Surgery, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, N.C., USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood*
Cardioplegic Solutions*
Coronary Vessels / physiology
Creatine Kinase / blood
Dipeptides / administration & dosage,  pharmacology*
Dogs
Endothelium, Vascular / physiology*
Female
Heart Arrest, Induced / methods
Male
Myocardial Reperfusion*
Myocardial Reperfusion Injury / prevention & control*
Myocardium / enzymology
Nitric Oxide / physiology
Peroxidase / metabolism
Time Factors
Ventricular Dysfunction, Left / prevention & control*
Grant Support
ID/Acronym/Agency:
HL46179/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Cardioplegic Solutions; 0/Dipeptides; 10102-43-9/Nitric Oxide; 139146-66-0/N-nitratopivaloyl-S-(N'-acetylalanyl)-cysteine ethyl ester; EC 1.11.1.7/Peroxidase; EC 2.7.3.2/Creatine Kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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