Spasm in Arterial Grafts in Coronary Artery Bypass Grafting Surgery

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Spasm in Arterial Grafts in Coronary Artery Bypass Grafting Surgery Guo-Wei He, MD, DSc, David P. Taggart, MD, FRCS The Annals of Thoracic Surgery Volume 101, Issue 3, Pages 1222-1229 (March 2016) DOI: 10.1016/j.athoracsur.2015.09.071 Copyright © 2016 The Society of Thoracic Surgeons Terms and Conditions

Fig 1 Schema of molecular mechanisms of smooth muscle contraction that may lead to spasm and the role of intact endothelium in prevention of spasm. In the vascular smooth muscle, contraction is the summation of myosin light chain kinase (MLCK) and myosin light chain phosphatase (MLCP) activity. Calcium influx through calcium channels located in the membrane (voltage-operated channel [VOC] and receptor-operated channel [ROC]) and release from intracellular stores in the sarcoplasmic reticulum (SR) through phospholipase C (PLC)-mediated hydrolysis of phosphatidyl inositol bisphosphate, yielding inositol triphosphate (IP3), result in an increase in intracellular calcium. The intracellular calcium interacts with calmodulin, forming a calcium-calmodulin complex, which activates MLCK to phosphorylate the myosin light chain, allowing for the close interaction of actin and myosin filaments for force generation. A number of vasoconstrictors, such as α-adrenoceptor (α) agonists, thromboxane A2 (TXA2), and endothelin-1 (ET), stimulate G-protein coupled receptors (GPCRs), which directly open the ROC causing calcium influx, or through the production of second messengers such as IP3, causing release of stored calcium. Contraction can also be mediated through a calcium-sensitization mechanism. Rho-kinase becomes activated by means of the activated RhoA protein (RhoA GTP), and subsequently phosphorylates MLCP, rendering the enzyme inactive and incapable of dephosphorylating the myosin light chain. In an intact endothelium, spasm of the vessel may be prevented by spontaneous (basal) release of a number of endothelium-derived relaxing factors, such as nitric oxide (NO), prostacyclin (PGI2), and endothelium-derived hyperpolarizing factor (EDHF), to balance the vasoconstriction and vasorelaxation in arterial grafts. Importantly, when the endothelium is intact, vasoconstrictors not only cause contraction but also stimulate receptors located on the cellular membrane of the endothelium and cause an increase of the intracellular calcium concentration that, as a second messenger, mediates release of endothelium-derived relaxing factors (NO, PGI2, and EDHF), which through different mechanisms reduce the intracellular calcium concentration in the smooth muscle cell and cause relaxation. (ACh = acetylcholine; α2 = α2-adrenoceptors; AII = angiotensin II receptors; ATII = angiotensin II; ETB = endothelin-1B receptors; FP = PGF2α receptors; His = histamine; H2 = histamine receptors; K+ = potassium; MO = methoxamine; M2 = muscarinic receptors; NE = norepinephrine; PE = phenylephrine; S1D = 5-hydroxytryptamine1D receptors; TP = thromboxane-prostanoid receptors; 5HT = 5-hydroxytryptamine.) The Annals of Thoracic Surgery 2016 101, 1222-1229DOI: (10.1016/j.athoracsur.2015.09.071) Copyright © 2016 The Society of Thoracic Surgeons Terms and Conditions