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

Effect of Contrast Media on Coronary Vascular Resistance

CHEST Journal ◽  
1999 ◽  
Vol 116 (4) ◽  
pp. 1039-1045 ◽  
Author(s):  
Elisabeth M. Baile ◽  
Peter D. Paré ◽  
Yulia D’yachkova ◽  
Ronald G. Carere
Keyword(s):  
Contrast Media ◽  
Vascular Resistance ◽  
Coronary Vascular Resistance

Contrast Media in Coronary Arteriography: A Review

1978 ◽  
Vol 13 (5) ◽  
pp. 450-459 ◽  
Author(s):  
HARRY W. FISCHER ◽  
KENNETH R. THOMSON
Keyword(s):  
Contrast Media ◽  
Coronary Arteriography

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

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.

Abstract 2017: A Single Bolus Intravenous Administration of Sodium Bicarbonate is Effective in the Prevention of Contrast-Induced Nephropathy in Patients with Renal Insufficiency Undergoing Diagnostic Coronary Arteriography or Elective Percutaneous Coronary Intervention

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Akira Tamura ◽  
Kumie Miyamoto ◽  
Shigeru Naono ◽  
Yoshiyuki Kawano ◽  
Munenori Kotoku ◽  
...  
Keyword(s):  
Renal Insufficiency ◽  
Serum Creatinine ◽  
Contrast Media ◽  
Intravenous Administration ◽  
Coronary Intervention ◽  
Coronary Arteriography ◽  
Single Bolus ◽  
Elective Percutaneous Coronary Intervention ◽  
Intravenous Hydration ◽  
Group B

BACKGROUND: Recent prospective studies have demonstrated that intravenous hydration with sodium bicarbonate (SB) is effective in the prevention of contrast-induced nephropathy (CIN). However, it has not yet been invetigated whether a single bolus intravenous administration of SB immediately before exposure to contrast media can prevent CIN. Accordingly, this prospective, controlled, randomized trial was designed to examine the efficacy of a single bolus administration of SB in the prevention of CIN in patients with renal insufficiency undergoing diagnostic coronary arteriography (CAG) or elective percutaneous coronary intervention (PCI). METHODS: A total of 144 patients with a serum creatinine level of >1.1 mg/dl and <2.0 mg/dl scheduled for diagnostic CAG or elective PCI were enrolled in this study. The patients were randomly assigned to the following 2 groups: standard intravenous hydration with sodium chloride plus a single bolus intravenous administration of SB (20 ml = 20 mEq) 5 min before exposure of contrast media (group A, n = 72) and standard intravenous hydration with sodium chloride alone (group B, n = 72). The primary end point was the development of CIN, defined as an increase of ≥25% or ≥0.5mg in serum creatinine level within 3 days after the procedure. We also evaluated the incidence of adverse clinical events, including acute pulmonary edema, acute renal failure requiring dialysis, and death within the first 7 days after the procedure. RESULTS: There were no significant group differences in age, gender, the frequencies of diabetes mellitus and PCI, serum creatinine at baseline, the volume of contrast media, and drugs administered. The single bolus intravenous administration of SB led to a significant increase in arterial blood pH (7.41 ± 0.04 to 7.43 ± 0.03, p <0.001). The incidence of primary end point was significantly lower in group A than in group B (1.4% vs 12.5%, p = 0.017). The incidence of adverse clinical events did not differ significantly between the 2 groups (0% vs 1.4%). CONCLUSIONS: A single bolus intravenous administration of SB before contrast injection is effective in the prevention of CIN in patients with renal insufficiency undergoing diagnostic CAG or elective PCI.

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.

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