coronary circulation in acute myocardial ischaemia/reperfusion injury: a target for cardioprotection.
acute coronary syndromes; blood capillaries; cardiac myocytes; cardiac vasculature; Cardioprotection; Coronary circulation; Coronary circulation; CYTOLOGY; edema; endothelium; erythrocytes; HEMORRHAGE; infarction; Ischaemia; ischemia; ischemia; ISCHEMIC preconditioning; leukocytes; MEDICAL sciences; Microvascular obstruction; midventricular obstruction; MYOCARDIAL reperfusion; personal integrity; pharmacology; physiologic reperfusion; PRASUGREL; Reperfusion; reperfusion injury; reperfusion injury; reperfusion therapy
The coronary circulation is both culprit and victim of acute myocardial infarction. The rupture of an epicardial atherosclerotic plaque with superimposed thrombosis causes coronary occlusion, and this occlusion must be removed to induce reperfusion. However, ischaemia and reperfusion cause damage not only in cardiomyocytes but also in the coronary circulation, including microembolization of debris and release of soluble factors from the culprit lesion, impairment of endothelial integrity with subsequently increased permeability and oedema formation, platelet activation and leucocyte adherence, erythrocyte stasis, a shift from vasodilation to vasoconstriction, and ultimately structural damage to the capillaries with eventual no-reflow, microvascular obstruction (MVO), and intramyocardial haemorrhage (IMH). Therefore, the coronary circulation is a valid target for cardioprotection, beyond protection of the cardiomyocyte. Virtually all of the above deleterious endpoints have been demonstrated to be favourably influenced by one or the other mechanical or pharmacological cardioprotective intervention. However, no-reflow is still a serious complication of reperfused myocardial infarction and carries, independently from infarct size, an unfavourable prognosis. MVO and IMH can be diagnosed by modern imaging technologies, but still await an effective therapy. The current review provides an overview of strategies to protect the coronary circulation from acute myocardial ischaemia/reperfusion injury. This article is part of a Cardiovascular Research Spotlight Issue entitled 'Cardioprotection Beyond the Cardiomyocyte', and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.
Hausenloy Derek J; Chilian William; Crea Filippo; Davidson Sean M; Ferdinandy Peter; Garcia-Dorado David; van Royen Niels; Schulz Rainer; Heusch Gerd
Cardiovascular Research
2019
1905-07
<a href="http://doi.org/10.1093/cvr/cvy286" target="_blank" rel="noreferrer noopener">10.1093/cvr/cvy286</a>
Macromolecular transport in canine coronary microvasculature.
*Coronary Circulation; Animals; Biological Transport; Blood Proteins/metabolism; Coronary Disease/metabolism; Dogs; Female; Immunoglobulin G/*metabolism; Immunoglobulin M/*metabolism; Lymph/metabolism; Macromolecular Substances; Male; Microcirculation; Myocardial Reperfusion; Myocardium/metabolism; Osmolar Concentration; Permeability; Reference Values; Serum Albumin/*metabolism
Coronary vascular osmotic reflection coefficients (sigma dS) for total protein, albumin (Alb), immunoglobulin (Ig)G, and IgM were determined in the anesthetized dog. Myocardial lymph was collected from the anterior interventricular lymphatic trunk, and the sigma dS estimated from filtration rate-independent lymph-to-plasma protein concentration ratios (CL/CPS). Lymph flows of at least 12 times base line were needed to produce filtration rate-independent CL/CPS, and these were achieved in 9 of 12 experiments. In these nine experiments, sigma dS for total protein, Alb, IgG, and IgM were, respectively, 0.67 +/- 0.02 (SE), 0.59 +/- 0.05, 0.70 +/- 0.03, and 0.87 +/- 0.01. The data were fitted to a model that showed that transvascular fluid and solute flux could be described by two populations of pores. A large pore system with an equivalent radius of 235 A was responsible for 39% of the transvascular volume flow. A small pore system less than 53 A accounted for the remaining flow. In a second group of experiments (n = 8), 60 min of ischemia decreased the sigma dS to 0.27 +/- 0.03, 0.07 +/- 0.05, 0.22 +/- 0.03, and 0.69 +/- 0.04 for total protein, Alb, IgG, and IgM, respectively. A single population of pores of 220 A could describe the entire transvascular volume flow. These results indicate that coronary vascular protein permeability is moderately high and can be increased significantly by ischemia.
Pilati C F
The American journal of physiology
1990
1990-03
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/ajpheart.1990.258.3.H748" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1990.258.3.H748</a>