scholarly journals Involvement of Ischemia-driven 5LPOX-RvE1-ChemR23 axis in the resolution of post-CABG inflammation in Coronary Arteries

2021 ◽  
Author(s):  
Finosh Thankam ◽  
Victoria E. D. Wilson ◽  
Mohamed M Radwan ◽  
Aleem Siddique ◽  
Devendra K Agrawal
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Western Blot ◽  
Coronary Arteries ◽  
Protein Level ◽  
Lipid Mediators ◽  
The Other ◽  
Histomorphometric Analysis ◽  
Tissue Architecture ◽  
Expression Status

Abstract Aims: Expression status of pro-resolving lipid mediators (PLM) and receptors in the post-CABG coronary arteries are largely unknown. Here, we aim to investigate the expression of PLMs in the atherosclerotic post-CABG swine LAD compared to without CABG (LAD-AS), and in isolated coronary artery smooth muscle cells (CASMCs) cultured under ischemia. Methodology: The arteries of interest were harvested from post-CABG atherosclerotic swine and the histomorphology and the expression status of key PLM mediators were quantified using immunostaining. SMCs were cultured under ischemia and confirmed the expression on PLM mediators at transcript and protein level.Results: The histomorphometric analysis revealed considerable alterations in the tissue architecture in LAD-CABG and LAD-AS arteries compared to control. PLM synthetic enzyme 5LPOX was significantly upregulated in LAD-CABG and LAD-AS whereas the other mediators including 12LPOX, 15LPOX, COX2, ChemR23, GPCR18, GPCR120 were decreased in LAD-CABG than control. LPOX enzymes and PLM receptors were upregulated in ischemic CASMCs with respect to control. Western blot showed the upregulation of 5LPOX, and ChemR23. Additionally, higher level of RvE1 was observed in ischemic control CASMCs which was decreased following reperfusion. Conclusion: These findings suggest that the CASMCs withstand the ischemia-triggered proinflammatory episodes by increasing the secretion of RvE1 mediated through 5LPOX and ChemR23 signaling.

scholarly journals Myorelaxant Effect of the Dysphania ambrosioides Essential Oil on Sus scrofa domesticus Coronary Artery and Its Toxicity in the Drosophila melanogaster Model

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 2041
Author(s):  
Luiz Jardelino de Lacerda Neto ◽  
Andreza Guedes Barbosa Ramos ◽  
Renata Evaristo Rodrigues da Silva ◽  
Luís Pereira-de-Morais ◽  
Fernanda Maria Silva ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Essential Oil ◽  
Coronary Arteries ◽  
Sus Scrofa ◽  
Ex Vivo ◽  
Alternative Methods ◽  
Major Constituent ◽  
Sus Scrofa Domesticus

Purpose: Alternative methods for the use of animals in research have gained increasing importance, due to assessments evaluating the real need for their use and the development of legislation that regulates the subject. The principle of the 3R’s (replacement, reduction and refinement) has been an important reference, such that in vitro, ex vivo and cord replacement methods have achieved a prominent place in research. Methods: Therefore, due to successful results from studies developed with these methods, the present study aimed to evaluate the myorelaxant effect of the Dysphania ambrosioides essential oil (EODa) using a Sus scrofa domesticus coronary artery model, and the toxicity of both the Dysphania ambrosioides essential oil and its major constituent, α-terpinene, against Drosophila melanogaster in toxicity and negative geotaxis assays. Results: The EODa relaxed the smooth muscle of swine coronary arteries precontracted with K+ and 5-HT in assays using Sus scrofa domesticus coronary arteries. The toxicity results presented LC50 values of 1.546 mg/mL and 2.282 mg/mL for the EODa and α-terpinene, respectively, thus showing the EODa and α-terpinene presented toxicity to these dipterans, with the EODa being more toxic. Conclusions: Moreover, the results reveal the possibility of using the EODa in vascular disease studies since it promoted the relaxation of the Sus scrofa domesticus coronary smooth muscle.

Smooth muscles from spastic coronary artery segments show hypercontractility to histamine

1990 ◽  
Vol 259 (1) ◽  
pp. H9-H13 ◽  
Author(s):  
S. Satoh ◽  
H. Tomoike ◽  
W. Mitsuoka ◽  
S. Egashira ◽  
H. Tagawa ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Muscle Fibers ◽  
Coronary Spasm ◽  
Smooth Muscles ◽  
Bolus Administration ◽  
Luminal Diameter ◽  
Endothelial Denudation ◽  
Significant Difference

An animal model of coronary spasm was produced in Gottingen miniature pigs by a selective endothelial denudation of the coronary artery. Five months after the denudation, intracoronary bolus administration of 10 micrograms/kg histamine reduced the luminal diameter angiographically by 57 +/- 16 and 17 +/- 10% (P less than 0.01) in the previously denuded and contralateral control coronary arteries. Muscle fibers of 0.08–0.1 mm wide were prepared from circumferential bundles of the medial smooth muscle in the spastic and nonspastic coronary arteries. Upward shifts of either dose-tonic contraction relationships in Ca2(+)-containing solution or dose-monophasic contraction relationships in Ca2(+)-free solution were noted in muscle fibers taken from the spastic site compared with those from the nonspastic site with no difference between the mean effective dose values. After skinning the muscle fibers with saponin, there was no significant difference in the Ca2+ concentration-tension relationships between the two fibers. These findings suggest that an increased number of histaminergic receptors and/or augmentation of signal transduction, but not Ca2+ sensitivity of the contractile proteins in the medial smooth muscle cells, cause histamine-induced coronary hypercontraction.

Extracellular calcium-dependent and -independent effects of adenosine in bovine coronary artery

1990 ◽  
Vol 68 (5) ◽  
pp. 608-613 ◽  
Author(s):  
Mudumbi V. Ramagopal ◽  
S. Jamal Mustafa
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Extracellular Calcium ◽  
Free Medium ◽  
Response Curves ◽  
Coronary Smooth Muscle ◽  
Calcium Dependent ◽  
Relaxation Responses ◽  
The Right

Adenosine relaxes the coronary arteries of various species through A2 receptors. The aim of the present investigation was to evaluate the relaxing effects of adenosine in relation to the role of calcium in bovine coronary arteries by studying the vasodilatory effect of adenosine in normal and calcium-free medium and on calcium-45 efflux into calcium-free medium. Acetylcholine (ACh) and norepinephrine (NE) were used to induce tone in coronary artery rings. Adenosine, 5′-(N-ethylcarboxamido)adenosine (NECA), and N6-(L-phenylisopropyl)adenosine (L-PIA) produced concentration-dependent relaxations of the coronary artery rings. Both in normal and calcium-free medium, the order of potency for adenosine analogs (NECA > L-PIA > adenosine) was similar and 8-phenyltheophylline antagonized the relaxation responses to adenosine and its analogs. Removal of extracellular calcium shifted the concentration–response curves to the right in a parallel fashion, slowed the rate of relaxation, and in NE contracted rings reduced the maximum responses for adenosine and its analogs. In calcium-free medium, adenosine was without an effect on calcium-45 efflux in the presence of ACh. However, adenosine inhibited the stimulated calcium-45 efflux induced by NE. The data suggest that the vasodilatory action of adenosine in bovine coronary smooth muscle has both extracellular calcium-dependent and -independent components.Key words: adenosine receptors, calcium, coronary circulation, vascular smooth muscle, acetylcholine, norepinephrine.

Isolated human coronary arteries in response to vasoconstrictor substances

1983 ◽  
Vol 245 (6) ◽  
pp. H937-H941 ◽  
Author(s):  
N. Toda
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Muscarinic Receptors ◽  
Coronary Arteries ◽  
Distal Portion ◽  
Alpha Adrenoceptors ◽  
Prostaglandin F2 Alpha ◽  
Arterial Contraction ◽  
Human Arteries ◽  
Contraction And Relaxation

In helical strips of human epicardial coronary arteries, norepinephrine produced a concentration-related contraction; the contractions relative to those induced by 30 mM K+ were greater in the proximal portion of the arteries than in the distal portion. The amine-induced contraction was suppressed by treatment with phentolamine. Acetylcholine contracted human coronary arteries but, in contrast, relaxed the monkey coronary arteries (both freshly excised and cadaver) previously contracted with prostaglandin F2 alpha. Both the contraction and relaxation induced by acetylcholine were suppressed by atropine. Removal of the endothelium abolished the relaxation of monkey arteries but did not significantly alter the contraction of human arteries. Human coronary arteries responded to histamine with contractions, which were reversed to relaxations following treatment with chlorpheniramine. It is concluded that, as far as the portions of human coronary arteries used in the present study are concerned, the arterial contraction mediated via alpha-adrenoceptors is inversely related to the distance from the coronary artery orifice. Acetylcholine produces contractions of human coronary arteries, possibly due to activation of muscarinic receptors on smooth muscle cells. Histamine-induced contractions appear to be mediated via H1-receptors.

scholarly journals Intimal Estrogen Receptor (ER)β, But Not ERα Expression, Is Correlated with Coronary Calcification and Atherosclerosis in Pre- and Postmenopausal Women

2006 ◽  
Vol 91 (7) ◽  
pp. 2713-2720 ◽  
Author(s):  
Rose C. Christian ◽  
Peter Y. Liu ◽  
Sean Harrington ◽  
Ming Ruan ◽  
Virginia M. Miller ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Postmenopausal Women ◽  
Coronary Arteries ◽  
Smooth Muscle Actin ◽  
Premenopausal Women ◽  
Calcium Content ◽  
Coronary Calcification ◽  
Calcium Deposition ◽  
Plaque Area

Abstract Background: Controversy exists over the association of estrogen and cardiovascular disease. Estrogen receptors (ERs) α and β are expressed in the endothelial cells and vascular smooth muscle cells (VSMCs) of many arteries, but the relative importance of ERα or ERβ in mediating the vascular response to estrogens is not well defined, particularly in humans. We have shown previously that postmenopausal women receiving hormone therapy (HT) had lower mean coronary artery calcium, plaque area, and calcium-to-plaque ratio compared with untreated women. In this study, we examined coronary artery ERα and ERβ expression in pre- and postmenopausal women as a function of plaque area, calcium area, calcium-to-plaque ratio, and estrogen status. Methods: Coronary arteries were obtained at autopsy from a total of 55 women: nine premenopausal women, 13 postmenopausal women on HT and 33 untreated postmenopausal women (non-HT). Coronary calcification was quantified by contact microradiography, and atherosclerotic plaque area was measured histologically. Coronary artery cross-sections were immunostained for ERα and ERβ, and the amount of receptors was estimated semiquantitatively in each arterial wall layer (intima, adventitia, and media). Double immunofluorescence was used to colocalize ERα and ERβ with smooth muscle actin, a marker of VSMCs. Results: ERβ and ERα were expressed in all artery wall layers, but most avidly in the media (P = 0.001), and colocalized with VSMCs. ERβ expression exceeded ERα expression in all wall layers (P < 0.001) and was adjacent to areas of calcium deposition. ERβ expression in the intimal layer correlated with calcium content, plaque area, and calcium-to-plaque ratio (all P < 0.01) and tended to be greater in non-HT than in HT women (P = 0.06). ERα expression did not vary significantly among groups, nor did it correlate with calcium content, plaque area or calcium-to-plaque ratio. Expression of ERα but not ERβ declined with age (P < 0.01) in HT women only. Age had no effect on ERα or ERβ expression in non-HT or premenopausal women. Conclusions: ERβ is the predominant ER in human coronary arteries and correlates with coronary calcification, a marker of severe atherosclerosis. Increased ERβ expression is linked to advanced atherosclerosis and calcification independent of age or hormone status. Future pharmacogenetic studies that target this receptor are needed to confirm causality.

Comparison of hypoxia-induced contraction in human, monkey, and dog coronary arteries

1992 ◽  
Vol 262 (3) ◽  
pp. H678-H683 ◽  
Author(s):  
N. Toda ◽  
T. Matsumoto ◽  
K. Yoshida
Keyword(s):  
Superoxide Dismutase ◽  
Coronary Artery ◽  
Receptor Antagonist ◽  
Coronary Arteries ◽  
Superoxide Anion ◽  
The Other ◽  
Human Coronary Artery ◽  
Synthesis Inhibitor ◽  
Other Hand

In monkey coronary artery strips contracted with prostaglandin (PG) F2 alpha or K+, exchange of entire N2 for O2 in the gas aerating the bathing media produced a contraction. Endothelium denudation did not alter the response. Aspirin, indomethacin, and ONO 3708, a PG receptor antagonist, markedly inhibited the hypoxia-induced contraction, whereas superoxide dismutase and OKY 046, a thromboxane (Tx) A2 synthesis inhibitor, were ineffective. Diltiazem depressed the contraction. Hypoxia increased the release of PGE2 but not 6-keto-PGF1 alpha and TxB2. Contractions induced by hypoxia of human coronary artery strips were also independent of the endothelium but were suppressed by indomethacin and diltiazem. On the other hand, dog coronary artery contractions induced by hypoxia were attenuated by endothelium denudation but were not influenced by indomethacin. It may be concluded that the hypoxia-induced contraction of monkey and human epicardial coronary arteries is associated with vasoconstrictor PGs released from subendothelial tissues; however, TxA2 and superoxide anion are not involved. The dog coronary artery contraction appears to be elicited by substance(s), other than cyclooxygenase products, released from the endothelium.

Canine arteries release two different endothelium-derived relaxing factors

1989 ◽  
Vol 257 (1) ◽  
pp. H330-H333 ◽  
Author(s):  
U. Hoeffner ◽  
M. Feletou ◽  
N. A. Flavahan ◽  
P. M. Vanhoutte
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Vascular Smooth Muscle ◽  
Coronary Arteries ◽  
Relaxing Factor ◽  
Prostaglandin F2 Alpha ◽  
Donor Artery ◽  
Canine Coronary Artery ◽  
Endothelium Derived Relaxing Factor

Experiments were designed to analyze the effects of ouabain on the response of vascular smooth muscle to endothelium-derived relaxing factors released under basal conditions and on stimulation with acetylcholine or bradykinin. Bioassay rings of canine coronary artery (without endothelium) were superfused with perfusate from canine left circumflex coronary arteries with endothelium (donor arteries). During contractions of the bioassay ring evoked by prostaglandin F2 alpha, the relaxations caused by endothelium-derived relaxing factor(s), released under basal conditions or on exposure of the endothelial cells of the donor artery to maximally effective concentrations of acetylcholine, were reduced by incubation of the bioassay ring with ouabain. However, the relaxations evoked by infusion of bradykinin were not altered by incubation of the bioassay rings with ouabain. These experiments demonstrate the release of two endothelium-derived relaxing factors that can be distinguished using ouabain.

Coronary Intimal Thickening Begins in Fetuses and Progresses in Pediatric Population and Adolescents to Atherosclerosis

Angiology ◽  
2019 ◽  
Vol 71 (1) ◽  
pp. 62-69 ◽  
Author(s):  
Roberto Guerri-Guttenberg ◽  
Rocío Castilla ◽  
Gabriel Cao ◽  
Francisco Azzato ◽  
Giuseppe Ambrosio ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Pediatric Population ◽  
Elastic Membrane ◽  
Lipid Deposition ◽  
Intimal Thickening ◽  
Histomorphometric Analysis ◽  
Young Population ◽  
The Right ◽  
Immunohistochemical Studies

The prevalence of coronary intimal thickening (IT) was assessed in fetuses and pediatric population. We studied the coronary arteries of 63 hearts obtained from fetuses, infants, children, and adolescents, deceased from noncardiac disease or trauma. Histomorphometric analysis, planimetry, and immunohistochemical studies were conducted. Intimal thickening consisted of proliferation of smooth muscle cells and scarce monocytes embedded in amorphous deposits within the internal elastic membrane (IEM). Intermingled lesions of intimal hyperplasia and parietal nonstenotic plaques were also observed. Intimal thickening was found in 10% of 20 fetuses, in 33.3% of 18 infants, 73.3% of 15 children, and 100% of 10 adolescents. A significant correlation ( r = 0.671, P < 0.001) was found between the extent of IT and age. The IEM was duplicated or interrupted in 43% of patients, showing a positive correlation with the degree of IT ( P = 0.01). Intimal thickening was predominantly found near bifurcation sites in the left anterior descending coronary artery (55.6%) and in zones free of bifurcation in the right coronary artery (75%). In conclusion, the prevalence and extension of IT lesions are higher at older ages within a young population. Intimal thickening may be regarded as the first event occurring in coronary preatherosclerosis, preceding lipid deposition.

Inward rectifier K+ currents in smooth muscle cells from rat coronary arteries: block by Mg2+, Ca2+, and Ba2+

1996 ◽  
Vol 271 (2) ◽  
pp. H696-H705 ◽  
Author(s):  
B. E. Robertson ◽  
A. D. Bonev ◽  
M. T. Nelson
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Coronary Arteries ◽  
Inward Rectifier ◽  
Inward Rectification ◽  
K Channels ◽  
Inward Currents ◽  
K Currents

Inward rectifier K+ channels have been implicated in the control of membrane potential and external K(+)-induced dilations of small coronary arteries. To identify and characterize inward rectifier K+ currents in coronary artery smooth muscle, whole cell K+ currents in smooth muscle cells enzymatically isolated from rat coronary (septal) arteries (diameters, 100-150 microns) were measured in the conventional and perforated configurations of the patch-clamp technique. Ba(2+)-sensitive, whole cell K+ current-voltage relationships exhibited inward rectification. Blockers of Ca(2+)-activated K+ channels (1 mM tetraethylammonium ion), ATP-sensitive K+ channels (10 microM glibenclamide), and voltage-dependent K+ channels (1 mM 4-aminopyridine) in smooth muscle did not affect inward rectifier K+ currents. The nonselective K+ channel inhibitor phencyclidine (100 microM) reduced inward rectifier K+ currents by approximately 50%. External Ba2+ reduced inward currents, with membrane potential hyperpolarization increasing inhibition. The half-inhibition constant for Ba2+ was 2.1 microM at -60 mV, decreasing e-fold for a 25-mV hyperpolarization. External Cs+ also blocked inward rectifier K+ currents, with the half-inhibition constant for Cs+ of 2.9 mM at -60 mV. External Ca2+ and Mg2+ reduced inward rectifier K+ currents. At -60 mV, Ca2+ and Mg2+ (1 mM) reduced inward currents by 33 and 21%, respectively. Inward rectification was not affected by dialysis of the cell's interior with a nominally Ca(2+)- and Mg(2+)-free solution. These findings indicate that inward rectifier K+ channels exist in coronary artery smooth muscle and that Ba2+ may be a useful probe for the functional role of inward rectifier K+ channels in coronary arteries.

Conduit Coronary Artery: Control by Autonomic Nervous System

Physiology ◽  
1991 ◽  
Vol 6 (3) ◽  
pp. 103-107
Author(s):  
M Gerova
Keyword(s):  
Blood Flow ◽  
Nervous System ◽  
Smooth Muscle ◽  
Autonomic Nervous System ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Secondary Effect ◽  
Sympathetic Stimulation ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor

Sympathetic stimulation induces a primary and secondary effect on smooth muscle of conduit coronary arteries. The former causes contraction, mediated by norepinephrine, and the latter, dilatation. The dilatation is due to endothelium-derived relaxing factor released as a consequence of the increased coronary blood flow.

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