Coronary Vascular Resistance and ST-Segment Changes during Coronary Microvascular Spasm

2001 ◽  
Vol 61 (2) ◽  
pp. 227-229
Author(s):  
Masashi Horimoto ◽  
Mitsunori Kamigaki ◽  
Takashi Takenaka ◽  
Hitoki Inoue ◽  
Keiichi Igarashi
Keyword(s):  
Vascular Resistance ◽  
Coronary Vascular Resistance ◽  
St Segment ◽  
Microvascular Spasm

scholarly journals Acetylcholine- and ergonovine-induced coronary microvascular spasm reflected by increased coronary vascular resistance and myocardial lactate production

2000 ◽  
Vol 23 (3) ◽  
pp. 221-225 ◽  
Author(s):  
Masashi Horimoto ◽  
Keiich Igarashi ◽  
Takashi Takenaka ◽  
Hitoki Inoue ◽  
Kohko Yamazaki ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Lactate Production ◽  
Coronary Vascular Resistance ◽  
Microvascular Spasm

Catapres (ST-155)-induced changes in coronary vascular resistance

1970 ◽  
Vol 4 (4) ◽  
pp. 457-465 ◽  
Author(s):  
W. G. Nayler ◽  
I. McInnes ◽  
J. Stone ◽  
V. Carson ◽  
T. E. Lowe
Keyword(s):  
Vascular Resistance ◽  
Coronary Vascular Resistance ◽  
Induced Changes

Effects of contrast media on coronary vascular resistance during coronary arteriography in dogs

1982 ◽  
Vol 394 (S1) ◽  
pp. R16-R16
Author(s):  
R. Schräder ◽  
D. Baller ◽  
A. Hoeft ◽  
H. Korb ◽  
Ph. A. Schnabel ◽  
...  
Keyword(s):  
Contrast Media ◽  
Vascular Resistance ◽  
Coronary Arteriography ◽  
Coronary Vascular Resistance

scholarly journals The effect of coronary inflow pressure on coronary vascular resistance in the isolated dog heart.

1984 ◽  
Vol 54 (6) ◽  
pp. 760-772 ◽  
Author(s):  
F L Hanley ◽  
L M Messina ◽  
M T Grattan ◽  
I E Hoffman
Keyword(s):  
Vascular Resistance ◽  
Coronary Vascular Resistance ◽  
Dog Heart ◽  
Isolated Dog Heart

scholarly journals Bidirectional Control of Coronary Vascular Resistance by Eicosanoids via a Novel GPCR

2021 ◽  
Author(s):  
Nabil Alkayed ◽  
Zhiping Cao ◽  
Zu Yuan Qian ◽  
Shanthi Nagarajan ◽  
Carmen Methner ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Vascular Resistance ◽  
Muscle Cell ◽  
Cell Receptor ◽  
Zinc Ion ◽  
Coronary Vascular Resistance ◽  
Wild Type ◽  
Acid Metabolites ◽  
G Protein Coupled

Abstract Arachidonic acid metabolites epoxyeicosatrienoates (EETs) and hydroxyeicosatetraenoates (HETEs) are important regulators of myocardial blood flow and coronary vascular resistance (CVR), but their mechanisms of action are not fully understood. We identified G protein-coupled receptor 39 (GPR39) as a microvascular smooth muscle cell (mVSMC) receptor antagonistically regulated by two endogenous eicosanoids: 15-HETE, which stimulates GPR39 to increase mVSMC intracellular calcium and augment microvascular CVR, and 14,15-EET, which inhibits these actions. Furthermore, zinc ion acts as an allosteric modulator of GPR39 to potentiate the efficacy of the two ligands. Finally, GPR39 knockout mice are protected from myocardial ischemia compared to wild-type littermates. Our findings will have a major impact on understanding the roles of eicosanoids in cardiovascular physiology and disease, and provide an opportunity for the development of novel GPR39-targeting therapies for cardiovascular disease. One Sentence Summary: GPR39 is a microvascular smooth muscle cell receptor regulated by two vasoactive eicosanoids with opposing actions.

Glutathione enhances endothelium-mediated control of coronary vascular resistance via a ROS- and NO intermediate-dependent mechanism

2012 ◽  
Vol 113 (2) ◽  
pp. 246-254 ◽  
Author(s):  
Andrew S. Levy ◽  
Chris Vigna ◽  
James W. E. Rush
Keyword(s):  
Vascular Resistance ◽  
Dose Response ◽  
Vascular Function ◽  
Soluble Guanylate Cyclase ◽  
Threshold Concentration ◽  
Coronary Vascular Resistance ◽  
Sprague Dawley ◽  
Response Curves ◽  
Physiological Relevance ◽  
Dependent Mechanism

The purpose of this investigation was to determine the effects of acute physiological GSH administration on endothelium-mediated reduction in coronary vascular resistance (CVR) using isolated perfused Sprague-Dawley rat hearts. A dose-response curve to GSH was conducted to determine a threshold concentration of GSH. We demonstrate that 30 μM GSH was sufficient to reduce CVR, and maximal dilation was achieved with 1 mM. In subsequent experiments, GSH was administered at concentrations of 0 [control (CON)], 1 μM, or 10 μM (GSH10), and dose-response curves to the endothelial agonist bradykinin (BK) were constructed. These GSH concentrations were chosen because of the physiological relevance and because the effects of GSH on BK action could be assessed independent of baseline differences in CVR. Sensitivity to BK (EC50) was enhanced in GSH10 vs. CON ( P < 0.05). This enhancement remained in the presence of nitric oxide (NO) synthase inhibition l-ωnitro-l-arginine (lNAME) and/or soluble guanylate cyclase (sGC) inhibition. Treatment with 4-hydroxy (2,2,6,6-tetramethylpiperidin-1-yl)oxyl (TEMPOL) enhanced the sensitivity to BK in CON, similar to the effects of GSH10 and GSH10 + TEMPOL. However, the GSH10-dependent enhancement of EC50 observed in the presence of lNAME did not occur in the presence of lNAME + TEMPOL or in the presence of lNAME + sGC inhibition and NO scavenging. Collectively, these results suggest that GSH enhances BK-mediated dilation and reduction in CVR through an antioxidant-dependent mechanism that involves a NO intermediate but is unrelated to acute production of NO and GC-dependent effects of NO. These results suggest a mechanism whereby physiologically relevant levels of GSH modulate the endogenous reactive oxygen species and NO control of endothelium-dependent coronary vascular function.

Effect of K ATP + channel inhibition on total and regional vascular resistance in guinea pig pregnancy

1998 ◽  
Vol 275 (2) ◽  
pp. H680-H688 ◽  
Author(s):  
Linda Keyes ◽  
David M. Rodman ◽  
Douglas Curran-Everett ◽  
Kenneth Morris ◽  
Lorna G. Moore
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Guinea Pig ◽  
Vascular Resistance ◽  
Coronary Vascular Resistance ◽  
Ang Ii ◽  
Channel Activity ◽  
Vasoconstrictor Response ◽  
Regional Vascular Resistance

Decreased vascular resistance and vasoconstrictor response during pregnancy enables an increase in cardiac output and regional blood flow to the uterine circulation. We sought to determine whether inhibition of vascular smooth muscle ATP-sensitive potassium ([Formula: see text]) channel activity during pregnancy increased systemic and/or regional vascular resistance and resistance response to ANG II. A total of 32 catheterized, awake, pregnant or nonpregnant guinea pigs were treated with either the [Formula: see text]channel inhibitor glibenclamide (3.5 mg/kg) or vehicle (DMSO) ( n = 8/group). In nonpregnant and pregnant animals, glibenclamide raised blood pressure and systemic, uterine, and coronary vascular resistance, diminishing cardiac output and organ blood flow. Glibenclamide produced a greater rise in coronary vascular resistance in the pregnant than nonpregnant groups and increased renal and cerebral vascular resistance in the pregnant animals only. ANG II infusion raised blood pressure and systemic and renal vascular resistance and lowered cardiac output and renal blood flow in vehicle-treated animals. Glibenclamide augmented ANG II-induced systemic vasoconstriction in the nonpregnant and pregnant groups and the rise in uteroplacental vascular resistance in the pregnant animals. We concluded that [Formula: see text] channel activity likely modulates systemic, uterine, and coronary vascular resistance and opposes ANG II-induced systemic vasoconstriction in nonpregnant and pregnant guinea pigs. Pregnancy augments[Formula: see text] channel activity in the uterine, coronary, renal, and cerebral vascular beds and the uteroplacental circulation during ANG II infusion. Thus increased[Formula: see text] channel activity appears to influence regional control of vascular resistance during guinea pig pregnancy but cannot account for the characteristic decrease in systemic vascular resistance and ANG II-induced systemic vasoconstrictor response.

Relationships between adenosine and coronary resistance in conscious exercising dogs

1982 ◽  
Vol 242 (1) ◽  
pp. H24-H29 ◽  
Author(s):  
J. E. McKenzie ◽  
R. P. Steffen ◽  
F. J. Haddy
Keyword(s):  
Vascular Resistance ◽  
Coronary Sinus ◽  
Treadmill Exercise ◽  
Coronary Vascular Resistance ◽  
Adenosine Concentration ◽  
Myocardial Hypoxia ◽  
Lactate Uptake ◽  
Plasma Adenosine ◽  
Coronary Sinus Blood ◽  
Pyruvate Ratio

The relation between myocardial adenosine content, coronary sinus plasma concentration, and coronary vascular resistance was studied in conscious dogs during rest or treadmill exercise. Exercise at 5 mi/h for 7 min on a 20% slope had a significant threefold increase in cardiac work over that of dogs at rest. Exercise increased myocardial adenosine content from 1.35 +/- 0.54 to 8.18 +/- 0.60 nmol/g and decreased coronary vascular resistance from 1.07 +/- 0.13 to 0.69 +/- 0.08 mmHg.ml-1.min.100 g; the former correlated negatively with the latter (r = -0.74, P less than 0.01). The adenosine concentration in coronary sinus plasma increased from 108 +/- 16 to 184 +/- 18 nmol/l plasma and correlated negatively with coronary vascular resistance (r = -0.83, P less than 0.01). Myocardial adenosine content correlated positively with coronary sinus plasma adenosine concentration (r = 0.77, P less than 0.05). Low myocardial lactate content, continued lactate uptake, lack of change in the lactate-pyruvate ratio, and stable coronary sinus oxygen tension values indicated no myocardial hypoxia. These findings demonstrate the release of adenosine into coronary sinus blood and show significant correlations between myocardial adenosine content, coronary sinus adenosine concentration, and coronary vascular resistance during physiological exercise in the dog. The results support the hypothesis that adenosine regulates coronary blood flow during increased metabolic activity.

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