Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CORONARY VESSELS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed1985

Plasminogen activator activity of cultured endothelial cells derived from canine coronary vessel and human umbilical artery and vein.

The present study was undertaken to determine which cells participate in plasminogen activator (PA) release from the vascular wall. Canine coronary vessel was confirmed to release PA when various agents were administered in perfusion experiments. Endothelial cells from the coronary vessel were then isolated and cultured for 2 days. PA activity was observed in lysates of the cultured cells, and the medium used for the cultivation was found to contain little PA activity. This suggests that the endothelial cells participate in PA release from the vascular wall. In addition, the PA synthesis was also studied in cultured endothelial cells from human umbilical artery and vein. Both contained little PA activity, indicating that vascular endothelial cells may vary in PA synthesis and release according to the vessel.

Animals↗
PubMed1991

The variable extent of jeopardized myocardium in patients with single vessel coronary artery disease: quantification by thallium-201 single photon emission computed tomography.

To assess the extent of jeopardized myocardium in patients with single vessel coronary artery disease of variable severity and location, quantitative exercise thallium-201 single photon emission computed tomography was performed in 158 consecutive patients with angiographically proved single vessel coronary artery disease. The extent of abnormal left ventricular perfusion was quantified from computer-generated polar maps of three-dimensional myocardial radioactivity. Patients with only a moderate (51% to 69%) stenosis tended to have a small perfusion defect irrespective of the coronary artery involved. Whereas a perfusion defect measuring greater than or equal to 10% of the left ventricle was found in 78% of patients with no prior infarction and severe (greater than or equal to 70%) stenosis, this was observed in only 24% of patients with moderate stenosis. Perfusion defect size increased with increasing severity of stenosis for the entire group without infarction and for those with left anterior descending, right and circumflex coronary artery stenosis. However, the correlation between stenosis severity and perfusion defect size was at best only modest (r = 0.38, p = 0.0001). The left anterior descending artery was shown to be the most important of the three coronary arteries for providing left ventricular perfusion. Proximal stenosis of this artery produced a perfusion defect approximately twice as large as that found in patients with a proximal right or circumflex artery stenosis. However, marked heterogeneity in perfusion defect size existed among all three vessels despite comparable stenosis severity. This was most apparent for the left anterior descending coronary artery, where mid vessel stenosis commonly produced a perfusion defect similar in size to that found in proximally stenosed vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMed2005

[The role of superoxide anions in regulation of coronary vessel tone and myocardial contractile function in changed redox-state of the myocardium].

The study relates to the character of tirone effect (chemical trap of superoxide--anions) on regulation of coronary vessel tone and myocardial contractile function in normal and changed cell redox-state of coronary and cardiac vessels. The experiments were performed in 64 female Wistar rats (180-320 g). The coronary blood flow and myocardial contractile junction were studied in isolated heart preparations. To determine the role of superoxide-anions in regulation of coronary vessel tone, tirone was added to the perfusion solution (4,5-dihydroxy-1,3-benzene disulfonic acid, 10 mm, Sigma USA). Preliminary injection of N-acetyl-L-cysteine evoked a 16 % increase, whereas injection of L-buthionine-(S,R)-sulfoximine reduced concentration of nonprotein thiol group in the myocardium and erythrocytes of experimental animals by 37%. The influence of superoxide anions on the cardiac vessel tone and myocardial contractile function was due to nitric monoxide participation the concentration of which increased in binding of superoxide anions and was directly dependent on concentration of sulfhydrilis groups in the cardiac cells. The oxygen active forms and cellular redox-state seem to play an important role in the regulation mechanisms of the coronary vessel tone and myocardial contractile function.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗
PubMed1993

Chronic carbon monoxide exposure in young rats alters coronary vessel growth.

The goal of this study was to determine whether chronic monoxide exposure in the developing heart produces long-lasting coronary vasculature alterations. One-day-old male rat pups were exposed to 500 ppm CO continuously for 30 d, while littermate controls remained in room air (AIR). At 61 and 110 d of age hearts were removed, perfusion fixed, x-rayed, and processed for analysis of coronary vessel architecture. Body weight (BW) and heart weight (HW) increased with age; the ratio of HW/BW decreased. There were no differences in HW and ventricular dimensions at either age due to prior CO exposure. Morphometric analysis of the fixed hearts from CO-exposed and AIR rats revealed no significant individual group differences in the number of small (27-114 microns) or larger (> 114 microns) vessels in any heart region. The septum (S) in CO rats was an exception: There were more small veins at 61 d of age and more larger veins at 110 d of age. There was a significant increase in the number of small arteries at both ages in the CO rats across all heart regions, and in the smaller veins at 61 d of age. The large vessels in the S at 61 d of age had a significantly greater diameter in CO compared to AIR rats. This was also true for the large arteries in the S and right ventricle (RV) of the 110-d-old rats. Taking all heart regions together, the large arteries in CO rats were larger than in AIR rats. Previous CO exposure significantly increased large artery and total cross-sectional area in the S and RV at 61 d of age, and in RV at 110 d of age. Total cross-sectional area of veins in the S was also increased. Taking all heart regions together, CO significantly increased small artery cross-sectional area at 61 d of age, and small, large, and total artery cross-sectional area at 110 d of age. With one exception (small veins, 110 d of age), there was no effect of CO on vein cross-sectional area. These changes resulted in the percentage of total cross-sectional area contributed by the larger vessels being increased. Pathological examination showed nothing abnormal. The results suggest profound and persistent changes in coronary vessel architecture following chronic neonatal CO exposure.

Analysis of Variance↗
PubMed1991

Severity of single-vessel coronary arterial stenosis and duration of angina as determinants of recruitable collateral vessels during balloon angioplasty occlusion.

To determine the factors that influence the presence of collateral vessels during coronary occlusion, we performed standardized contrast injection of the contralateral coronary artery in 58 consecutive patients, without previous myocardial infarction, undergoing percutaneous transluminal coronary angioplasty for 1-vessel disease (left anterior descending artery in 45, right coronary artery: in 10 and left circumflex artery in 3). The presence of collateral vessels during coronary occlusion, defined as partial or complete epicardial opacification by collateral vessels of the vessel dilated, was related to clinical, angiographic and electrocardiographic parameters. The angiographic appearance of collateral vessels during balloon inflation showed a weak, although statistically significant, correlation to the percent diameter stenosis before angioplasty (r = 0.28; p = 0.03) and the duration of angina (r = 0.37; p = 0.004). By combining lesion severity with the duration of angina, collateral vessels during coronary occlusion were particularly related to a lesion severity greater than or equal to 70% and duration of angina greater than or equal to 3 months (p less than 0.001). Furthermore, the presence of collateral vessels was associated with an absence of ST-segment shift (greater than or equal to 1 mm) during 1 minute of coronary occlusion (p less than 0.001).

Angina Pectoris↗
PubMed1997

Percutaneous transluminal coronary angioplasty versus medical therapy for stable angina pectoris: outcomes for patients with double-vessel versus single-vessel coronary artery disease in a Veterans Affairs Cooperative randomized trial. Veterans Affairs ACME InvestigatorS.

OBJECTIVES: This study sought to assess outcomes of men with double-vessel coronary artery disease randomly assigned to treatment by percutaneous transluminal coronary angioplasty (PTCA) or medical therapy, compared with previously reported outcomes for men with single-vessel disease. BACKGROUND: We previously reported that PTCA provides better symptom relief and treadmill performance than medical therapy for men with stable angina pectoris due to single-vessel disease. Whether this advantage applies to patients with double-vessel disease is unknown. METHODS: Male patients (n = 328) with stable angina pectoris and ischemia on treadmill testing were randomly assigned to PTCA or medical therapy; 101 patients had double-vessel disease, and 227 had single-vessel disease. Symptoms, treadmill performance, quality of life score, coronary stenosis and myocardial perfusion were compared at baseline and at 6 months. Patients were followed up for up to 6 years and underwent additional treadmill testing 2 to 3 years after randomization. RESULTS: PTCA-treated and medically treated patients with double-vessel disease experienced comparable improvement in exercise duration (+1.2 vs. +1.3 min, respectively, p = 0.89), freedom from angina (53% and 36%, respectively, p = 0.09) and improvement of overall quality of life score (+1.3 vs. +4.4, respectively, p = 0.32) at 6 months compared with baseline. This contrasts with greater advantages favoring PTCA by these criteria in patients with single-vessel disease (p = 0.0001 to 0.02). Trends present at 6 months persisted at late follow-up. Patients undergoing double-vessel dilation had less complete initial revascularization (45% vs. 83%) and greater average stenosis of worst lesions at 6 months (74% vs. 56%). Likewise, patients with double-vessel disease showed less improved myocardial perfusion imaging (59% vs. 75%). CONCLUSIONS: PTCA is beneficial in male patients with double-vessel disease; however, we cannot demonstrate the same advantage over medical therapy seen in similar patients with single-vessel disease. Less complete revascularization and greater restenosis for patients having multiple dilations would account for these findings. Alternatively, a type 2 error might be operative. Technical advances since completion of this trial might improve these outcomes. These findings warrant further investigation in a larger trial.

Adrenergic beta-Antagonists↗
PubMed1991

[Angina due to anatomical anomalies and to functional changes in the epicardial coronary vessels].

Myocardial ischemia with normal coronary arteries can be due to anatomic or functional reasons. The more severe congenital coronary anomalies in the adulthood are the origin of the left main of the left coronary artery from the right aortic sinus, with a course between the aorta and the pulmonary trunk, and the origin of the left main from the pulmonary trunk. Both these anomalies can cause sudden death, usually associated with physical exertion. The coronary vasomotion of epicardial vessels depends on the interaction of several neurohumoral substances. We report the hemodynamic, angiographic and stress test data of 30 patients affected by chest pain, with myocardial ischemia and normal coronary arteries. In 8 patients the response of epicardial coronary arteries to intracoronary infusion of acetylcholine was evaluated.

Acetylcholine↗
PubMed1994

Impaired left ventricular function, one- or two-vessel coronary artery disease, and severe ischemia: outcome with medical therapy versus revascularization.

OBJECTIVE: To determine whether patients with impaired left ventricular function and one- or two-vessel coronary artery disease who manifest severe ischemia during exercise radionuclide angiography have a lower rate of subsequent cardiac events when initial management is revascularization rather than medical therapy. DESIGN: During a median follow-up of 100 months, we compared the outcome between 37 patients who underwent a revascularization procedure and 22 who received medical therapy at the Mayo Clinic between September 1980 and December 1985. MATERIAL AND METHODS: The revascularization therapy consisted of coronary artery bypass grafting in 31 patients and coronary angioplasty in 6. Overall survival and survival free of initial cardiac events were compared statistically for the medically and surgically treated patients. RESULTS: Eleven deaths occurred in the patients who received medical therapy and 9 in the revascularization group. Five-year overall survival was 58% in the medically treated patients versus 84% in the revascularization group. A significant association was noted between type of treatment and overall survival (adjusted chi 2 = 6.20; P = 0.013). Twenty patients had initial cardiac events--7 in the medically treated group (3 cardiac deaths and 4 nonfatal myocardial infarctions) and 13 in the revascularization group (3 cardiac deaths, 3 out-of-hospital cardiac arrests, and 7 nonfatal myocardial infarctions). Survival free of cardiac events at 5 years was 72% in the medically treated patients and 66% in those who underwent revascularization. No association was detected between type of treatment and survival free of cardiac events. CONCLUSION: These nonrandomized data suggest that overall survival for patients with one- or two-vessel coronary artery disease, impaired left ventricular function, and severe exercise-induced ischemia may be improved by revascularization, but the subsequent cardiac event rates are not.

Aged↗
PubMed2001

Changes in coronary vessel resistance during postischemic reperfusion and effectiveness of nitroglycerin.

OBJECTIVE: Microvascular incompetence after ischemia and reperfusion may compromise the normal postischemic coronary perfusion and additionally jeopardize the recovery of the myocytes. We investigated whether such a form of acute endothelial dysfunction occurs in the routine operative setting despite the use of protective measures. For this purpose, we measured pressure-flow relations in the coronary vasculature during heart operations before and after ischemia and after reperfusion and their reaction to the nitric oxide donor nitroglycerin. METHODS: Forty-eight patients with a low risk profile scheduled for routine coronary artery bypass surgery were included. During normothermic extracorporeal circulation, the fibrillating heart was completely excluded from bypass by clamping of the ascending aorta and snaring of the caval veins. It was relieved of blood by opening the right atrium and venting the left atrium and ventricle to avoid distention. The coronary vessels were perfused under controlled flow, and the perfusion pressures were monitored. This protocol was performed in 24 patients before and immediately after ischemia and after a reperfusion period. RESULTS: Compared with the preischemic control, vascular resistance was decreased by 17% (P <.003) immediately after ischemia but increased again by 46% (P <.0001) during an average of 25 minutes of reperfusion and, even more important, by 23% (P <.028) in comparison with the preischemic values. In two groups of 12 patients, nitroglycerin was added to the perfusate either in a dosage of 3 microg. kg. min(-1) or as a bolus injection of 2 mg. Low-dose nitroglycerin did not reduce the elevated postreperfusion resistances significantly, but bolus injection did (P <.0002). Coronary vessel resistance increased during reperfusion in particular in patients with a history of hypertension. CONCLUSION: Coronary vasoconstriction during postischemic reperfusion is regularly present in the routine operative setting in cardiac surgery, despite myocardial protection measures. The amount of vasoconstriction varies considerably and is particularly increased in patients with hypertension. The nitric oxide donor nitroglycerin can normalize the elevated resistances, but only in high dosages. This demonstrates a preserved ability of vascular smooth muscle to relax. The phenomenon had no sequelae in our low-risk patients having elective operations. However, it may gain significance in the case of severe left heart hypertrophy and in patients at risk with both a postoperative low-output syndrome and reduced mean arterial pressures during reperfusion.

Aged↗
PubMed1993

Effect of phencyclidine on contraction of porcine coronary vessel strips.

Classic muscular contraction experiment was used to study the effect of phencyclidine (Phe) on spiral strips of porcine coronary vessels. It showed that Phe and its analogs: 1-[1-(2-thienyl)cyclohexyl] piperidine (TCP), (+)-5-methyl-10, 11-dihydro-5H-dibenzo [a,d] cyclohepten-5, 10-imine maleatel (dizocilpine maleate) and sigma receptor ligand N-allyl-N-normetazocine (SKF10047) all exhibited a concentration-dependent contraction of porcine coronary vessel strips. Phe had no effect on the electrically stimulated contraction of the spiral strips. Dextromethorphan (Dex), a Phe receptor antagonist, and haloperidol (Hal), a sigma receptor antagonist, partially antagonized and suppressed the actions of Phe in a non-competitive manner. These results suggested that Phe, TCP, dizocilpine maleate, and (+), (-)-SKF10047 cause contraction through Phe and sigma opioid receptors.

Animals↗
PubMed1997

Acetylcholine-induced vasoconstrictor response of coronary vessels in rats: a possible contribution of M2 muscarinic receptor activation.

A mechanism by which acetylcholine (ACh) may elicit vasoconstrictor response in coronary vessels was studied in rat hearts perfused at a constant flow rate. In spontaneously beating hearts, bolus injections of ACh and carbachol (CCh) produced biphasic changes in coronary perfusion pressure (CPP): a transient increase at the initial period followed by a sustained decrease. In KCl-arrested hearts, ACh and CCh produced a monophasic increase in CPP, which was attenuated by either removal of endothelial cells by saponin or cyclooxygenase inhibition by diclofenac sodium. In the spontaneously beating heart, ACh-induced vasoconstriction was almost abolished by atropine (0.1 microM) and was markedly attenuated by an M2 antagonist, methoctramine (0.1 microM), but not by an M1 antagonist, pirenzepine (1 microM). Arecaidine propargyl ester (APE), an M2 agonist, produced coronary artery constriction which was attenuated by methoctramine (0.1 microM) but not by pirenzepine (0.1 microM) in both spontaneously beating and KCl-arrested hearts. McN-A-343, an M1 agonist, increased CPP in both beating and KCl-arrested hearts, but to a lesser degree than APE. These results suggest that the release of vasoconstrictor prostaglandins from endothelial cells contributes to the vasoconstrictor response to ACh in perfused rat coronary vessels, and the response to ACh appears to be mediated, in part, via the M2 subtype of muscarinic receptors.

Acetylcholine↗
PubMed2004

Role of vasa vasorum in transendothelial solute transport in the coronary vessel wall: a study with cryostatic micro-CT.

Using cryostatic microscopic computed tomography (micro-CT), we sought to determine the role of coronary vasa vasorum (VV) in transendothelial solute transport in arteries with normal and increased permeability due to high plasma cholesterol levels. In 6-mo-old pigs on a normal (n=23) and 2% high cholesterol (HC) diet (n=8), 2-cm segments of the proximal left anterior descending coronary arteries were removed in vivo after a selective injection of X-ray contrast solution. Harvesting of the specimens occurred at 0, 15, 25, 35, or 45 s after completion of the contrast injection. Specimens were snap frozen and scanned in our cryostatic micro-CT. The spatial distribution of contrast in the coronary artery wall was quantified using the CT images. Right coronary arteries were infused with Microfil to determine VV density (VV/mm2) and the cumulative lumen surface area (mm2/mm3). Transendothelial diffusion of contrast into the coronary vessel wall is a dynamic process starting at both the subintima and the adventitia. The subintimal opacification moves as a wave toward the adventitia, whereas the adventitial wave resolves. The coronary vessel wall in animals on a HC diet shows higher opacification than in normal coronary arteries without an increase of VV total luminal surface area. The loss of endothelial integrity in hypercholesterolemia significantly alters VV solute washin to, and washout from, the coronary artery wall.

Animals↗
PubMed1998

Long-term L-arginine supplementation improves small-vessel coronary endothelial function in humans.

BACKGROUND: Coronary endothelial dysfunction is characterized by an imbalance between endothelium-derived vasodilating and vasoconstricting factors and coronary vasoconstriction in response to the endothelium-dependent vasodilator acetylcholine. Thus, the present double-blind, randomized study was designed to test the hypothesis that long-term, 6-month supplementation of L-arginine, the precursor of the endothelium-derived vasodilator NO, reverses coronary endothelial dysfunction to acetylcholine in humans with nonobstructive coronary artery disease. METHODS AND RESULTS: Twenty-six patients without significant coronary artery disease on coronary angiography and intravascular ultrasound were blindly randomized to either oral L-arginine or placebo, 3 g TID. Endothelium-dependent coronary blood flow reserve to acetylcholine (10(-6) to 10(-4) mol/L) was assessed at baseline and after 6 months of therapy. There was no difference between the two study groups in clinical characteristics or in the coronary blood flow in the response to acetylcholine at baseline. After 6 months, the coronary blood flow in response to acetylcholine in the subjects who were taking L-arginine increased compared with the placebo group (149 +/- 20% versus 6 +/- 9%, P < 0.05). This was associated with a decrease in plasma endothelin concentrations and an improvement in patients' symptoms scores in the L-arginine treatment group compared with the placebo group. CONCLUSIONS: Long-term oral L-arginine supplementation for 6 months in humans improves coronary small-vessel endothelial function in association with a significant improvement in symptoms and a decrease in plasma endothelin concentrations. This study proposes a role for L-arginine as a therapeutic option for patients with coronary endothelial dysfunction and nonobstructive coronary artery disease.

Adult↗
PubMed1990

Simple method to produce acute heart failure by coronary vessel embolization in closed chest rats with microspheres.

Changes in left ventricle (LV) function, systemic, and regional hemodynamics as a result of coronary artery embolization by 15 microns microspheres were studied in rats. Selective coronary embolization was produced by injection of microspheres during ascending aorta occlusion animals by using an "L"-shaped wire in closed chest animals. Maximal developed LV systolic pressure (LVSPmax) was determined during ascending aorta occlusion. Coronary embolization evoked reductions in LVSPmax and +dP/dtmax and then decreased in basal LVSP, dP/dtmax, dP/dtmax/P, with a parallel increase in LV end-diastolic pressure (LVEDP). The number of microspheres accumulating in the heart following coronary embolization was about 40% of the total amount of the injected microspheres (300,000-400,000). In conscious rats 48 hr after coronary vessel embolization (in LV myocardium 100,003 +/- 4,334 microspheres per gram) the cardiac index, mean arterial pressure, -dP/dtmax and stroke volume were reduced by 35.6%, 20%, 17.2%, and 26.7%, respectively, when compared with sham-operated rats. LVEDP was increased by 40%, when compared with sham-operated rats. These results show that in this rat model of coronary vessel embolization heart failure develops. The model created may be used for the studies of pathophysiology of acute heart failure as well as for screening new compounds potentially effective in heart failure.

Acute Disease↗
PubMed2005

Increased expression of bradykinin type-1 receptors in endothelium of intramyocardial coronary vessels in human failing hearts.

In experimental animals, bradykinin type-1 receptors (BK-1Rs) are induced during inflammation and ischemia, and, by exerting either cardioprotective or cardiotoxic effects, they may contribute to the pathogenesis of heart failure. Nothing is known about the expression of BK-1Rs in human heart failure. Human heart tissue was obtained from excised hearts of patients undergoing cardiac transplantation (n = 13), due to idiopathic dilated cardiomyopathy (IDC; n = 7) or to coronary heart disease (CHD; n = 6), and from normal hearts (n = 6). The expression of BK-1Rs was analyzed by means of competitive RT-PCR, Western blot analysis, and immunohistochemistry. Expression of BK-1R mRNA was increased in both IDC (2.8-fold) and CHD (2.1-fold) hearts compared with normal hearts. The observed changes were verified at the protein level. Expression of BK-1Rs in failing hearts localized to the endothelium of intramyocardial coronary vessels and correlated with an increased expression of TNF-alpha in the vessel wall. Treatment of human coronary artery endothelial cells with TNF-alpha increases their BK-1R expression. These novel results show that BK-1Rs are induced in the endothelium of intramyocardial coronary vessels in failing human hearts and so may participate in the pathogenesis of heart failure.

Adult↗
PubMed1997

Reduced basal NO-mediated dilation and decreased endothelial NO-synthase expression in coronary vessels of spontaneously hypertensive rats.

Basal vasomotor tone in coronary vessels is, in part, maintained by nitric oxide (NO) production by endothelial constitutive NO synthase (ecNOS). Alteration of coronary circulation observed in left ventricular hypertrophy secondary to hypertension could be associated with a decrease in NO production. The aim of this study was to measure: (1) coronary flow in the Langendorff-perfused heart model at baseline, after maximum vasodilation in response to adenosine (10(-5) M), after endothelium-dependent vasodilation in response to bradykinin (10(-8) M) and after ecNOS inhibition by nitro-L-arginine methyl ester (L-NAME) (10(-4) M); (2) medial thickening of coronary microvessels and perivascular collagen on histological heart sections; and (3) ecNOS expression by immunohistochemical staining in these vessels using 20-week-old spontaneously hypertensive (SHR) and Wistar-Kyoto control rats (WKY). These measurements were determined by computer-directed color analysis. When SHR were compared with WKY rats, we found: (1) a decrease in basal flow (10.1+/-0.6 v 15.3+/-1.2 ml/min/g, n=10, P<0.0001), in maximum flow (15.4+/-0.7 v 24.3+/-1.3 ml/min/g, n=10, P<0.001), in bradykinin-induced flow increment (1.5+/-0.3 v 2.6+/-0.3 ml/min/g, n=5, P<0.05) and in L-NAME-sensitive flow (3.3+/-0.6 v 6.3+/-0.9 ml/min/g, n=7, P<0.05); (2) an increase in medial thickness (9.4+/-0.6 v 5.4+/-0.3 microm, n=8, P<0.001) and in perivascular collagen area (1509+/-311 v 462+/-120 microm2, n=8, P<0.01) of coronary arterioles; and (3) a decrease in ecNOS expression in the endothelium (ecNOS-stained cross-sectional area in arterioles: 40.0+/-9.1 v 84.6+/-9.0 microm2, n=7, P<O.005). These results suggest that in SHR the decrease in basal coronary flow can be related to a structural alteration of the microvessels with an increase of perivascular collagen but also to a decrease in ecNOS expression which might be associated with reduced NO production.

Animals↗