Effect of arteriolar dilation on coronary artery diameter distal to coronary stenoses

1985 ◽  
Vol 249 (5) ◽  
pp. H981-H988 ◽  
Author(s):  
J. S. Schwartz ◽  
R. J. Bache
Keyword(s):  
Regression Analysis ◽  
Coronary Artery ◽  
Coronary Occlusion ◽  
Circumflex Coronary Artery ◽  
Intracoronary Injection ◽  
Open Chest ◽  
Close Relationship ◽  
Coronary Artery Diameter ◽  
Coronary Stenoses ◽  
Chronically Instrumented Dogs

Previous studies have suggested that worsening hemodynamic severity of coronary stenoses in response to distal arteriolar dilation may be related to dilation of the normal epicardial artery adjacent to the stenosis resulting in increasing percent stenosis. To test this hypothesis we used sonomicrometry to continuously measure external circumflex coronary artery diameter distal to snare stenoses of varying severity in 19 open-chest dogs and 5 awake, chronically instrumented dogs. Arteriolar dilation produced by release of a transient coronary occlusion or by intracoronary injection of adenosine caused a decrease in circumflex coronary diameter distal to the stenosis. Regression analysis showed that circumflex diameter and pressure distal to the stenosis were directly related (mean r: transient occlusion, 0.86 +/- 0.04; adenosine, 0.97 +/- 0.01). The close relationship between pressure and diameter suggests that the decrease in diameter in response to arteriolar dilation was a passive effect. Passive coronary narrowing distal to a stenosis suggests that a similar effect may occur within a compliant stenosis, thus partly explaining the increase in severity of compliant stenoses in response to arteriolar dilation.

Contrasting ischemic contraction patterns by zone and layer in canine myocardium

1982 ◽  
Vol 243 (6) ◽  
pp. H852-H855 ◽  
Author(s):  
S. Hattori ◽  
W. S. Weintraub ◽  
J. B. Agarwal ◽  
M. M. Bodenheimer ◽  
V. S. Banka ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Left Ventricle ◽  
Fiber Orientation ◽  
Coronary Occlusion ◽  
Short Axis ◽  
Circumflex Coronary Artery ◽  
Left Circumflex Coronary Artery ◽  
Close Relationship ◽  
Canine Myocardium

The effect of graded coronary occlusion on myocardial shortening in different zones of the left ventricle is not clear. Therefore, in 15 dogs ultrasonic crystals were used to evaluate the effect of graded coronary occlusion on subendocardial and subepicardial contraction in both the left anterior descending coronary artery (LAD) and left circumflex coronary artery (Circ) distributions. Subepicardial shortening was evaluated along both the long and short axes. In the LAD zones, segment shortening decreased in parallel in the subendocardium and subepicardium. In the circumflex zone subendocardial and subepicardial long axis shortening fell off in parallel, while subepicardial short axis shortening fell off more rapidly. Thus there is a close relationship between endocardial and epicardial segment shortening following graded coronary occlusion. In the circumflex zone, however, fiber orientation may affect the measurement of segment motion.

Effect of coronary occlusion on arrhythmias and conduction in the ovine heart

1983 ◽  
Vol 245 (1) ◽  
pp. H82-H89 ◽  
Author(s):  
D. E. Euler ◽  
J. F. Spear ◽  
E. N. Moore
Keyword(s):  
Ventricular Tachycardia ◽  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Electrical Activity ◽  
Coronary Occlusion ◽  
Circumflex Coronary Artery ◽  
Pentobarbital Sodium ◽  
Normal Zone ◽  
Ventricular Tachycardia And Fibrillation ◽  
Observation Period

The proximal left circumflex coronary artery was occluded for 1 h in 16 open-chest sheep anesthetized with pentobarbital sodium. Epicardial conduction was monitored at three or four sites within the ischemic zone and one site in the normal zone. Eight of the sheep developed ventricular fibrillation within the first 15 min of occlusion; the remaining sheep survived the 1-h observation period. In the sheep that developed spontaneous ventricular fibrillation, the circumflex perfused a significantly greater amount of the left ventricle (44 +/- 3 vs. 39 +/- 3%; P = 0.008). The occurrence of spontaneous ventricular fibrillation was invariably preceded by a period of sustained (0.5-4 min) ventricular tachycardia. Six of the surviving sheep developed episodes of sustained (2-10 min) tachycardia that were self-terminating. The ischemic zone electrograms showed continuous fractionated electrical activity during both self-terminating tachycardias and tachycardias ending in fibrillation. The continuous epicardial electrical activity did not appear to cause the tachycardias but rather occurred as a result of the tachycardias. The genesis of ventricular tachycardia and fibrillation in this model may involve mechanisms different from ischemia-induced ventricular tachycardia and fibrillation in canine and porcine hearts.

Exercise training restores adenosine-induced relaxation in coronary arteries distal to chronic occlusion

2000 ◽  
Vol 278 (6) ◽  
pp. H1984-H1992 ◽  
Author(s):  
Cristine L. Heaps ◽  
Michael Sturek ◽  
Julie A. Rapps ◽  
M. Harold Laughlin ◽  
Janet L. Parker
Keyword(s):  
Coronary Artery ◽  
Exercise Training ◽  
Sodium Nitroprusside ◽  
Coronary Arteries ◽  
Coronary Occlusion ◽  
Circumflex Coronary Artery ◽  
Miniature Swine ◽  
Chronic Occlusion ◽  
Chronic Coronary Occlusion ◽  
Camp And Cgmp

We previously reported that canine collateral-dependent coronary arteries exhibit impaired relaxation to adenosine but not sodium nitroprusside. In contrast, exercise training enhances adenosine sensitivity of normal porcine coronary arteries. These results stimulated the hypothesis that chronic coronary occlusion and exercise training produce differential effects on cAMP- versus cGMP-mediated relaxation. To test this hypothesis, Ameroid occluders were surgically placed around the proximal left circumflex coronary artery (LCx) of female Yucatan miniature swine 8 wk before initiating sedentary or exercise training (treadmill run, 16 wk) protocols. Relaxation to the cAMP-dependent vasodilators adenosine (10− 7 to 10− 3 M) and isoproterenol (3 × 10− 8 to 3 × 10− 5 M) were impaired in collateral-dependent LCx versus nonoccluded left anterior descending (LAD) arterial rings isolated from sedentary but not exercise-trained pigs. Furthermore, adenosine-mediated reductions in simultaneous tension and myoplasmic free Ca2+ were impaired in LCx versus LAD arteries isolated from sedentary but not exercise-trained pigs. In contrast, relaxation in response to the cAMP-dependent vasodilator forskolin (10− 9 to 10− 5 M) and the cGMP-dependent vasodilator sodium nitroprusside (10− 9 to 10− 4 M) was not different in LCx versus LAD arteries of sedentary or exercise-trained animals. These data suggest that chronic occlusion impairs receptor-dependent, cAMP-mediated relaxation; receptor-independent cAMP- and cGMP-mediated relaxation were unimpaired. Importantly, exercise training restores cAMP-mediated relaxation of collateral-dependent coronary arteries.

Creatine kinase and phosphorylase in cardiac lymph: coronary occlusion and reperfusion

1985 ◽  
Vol 248 (3) ◽  
pp. H350-H359 ◽  
Author(s):  
L. H. Michael ◽  
J. R. Hunt ◽  
D. Weilbaecher ◽  
M. B. Perryman ◽  
R. Roberts ◽  
...  
Keyword(s):  
Cell Death ◽  
Creatine Kinase ◽  
Coronary Artery ◽  
Glycogen Phosphorylase ◽  
Coronary Occlusion ◽  
Cell Injury ◽  
Myocardial Cell ◽  
Circumflex Coronary Artery ◽  
Ischemic Tissue ◽  
Control State

Cardiac lymph, collected from conscious dogs, was monitored for glycogen phosphorylase and creatine kinase (CK) enzymatic activity during control state, circumflex coronary artery (CFX) occlusion, and reperfusion. CFX occlusions, lasting for intervals as short as 10 min, initiated a release of phosphorylase and CK into the cardiac lymph, which was immediately observed during reperfusion of the ischemic tissue. Blood plasma levels did not appear for several hours. In the absence of reperfusion, the appearance of enzymes in cardiac lymph was delayed and peaked later. Glycogen phosphorylase and CK entered the lymph in greater quantities with reperfusion as the length of occlusion was increased. Histological examination of multiple sections of the reperfused hearts showed infarcts in hearts where CFX occlusions lasted 20 min or longer; occlusions of 10-15 min showed evidence of cell injury and death in two hearts and no definable infarct in the majority. Ischemic intervals of short duration release functionally active glycogen phosphorylase and CK, which reflect changes in myocardial cell egress of macromolecules and/or cell death.

Reactive dilation and late-hyperemic constriction of epicardial coronary artery after short coronary occlusion

1986 ◽  
Vol 251 (3) ◽  
pp. H554-H561
Author(s):  
H. Yamamoto ◽  
H. Tomoike ◽  
K. Hisano ◽  
T. Inoue ◽  
M. Mohri ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Coronary Blood Flow ◽  
Coronary Occlusion ◽  
Reactive Hyperemia ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Epicardial Coronary Artery ◽  
Dependent Change ◽  
Coronary Artery Diameter

Coronary blood flow and epicardial coronary artery diameter were simultaneously measured by an electromagnetic or Doppler flow probe and a pair of ultrasonic crystals, respectively, during reactive hyperemia in conscious dogs. Reactive dilation appeared after the full appearance of reactive hyperemia and lasted for a period of 4-20 times the duration of the coronary occlusion. beta-Receptor blockade (propranolol, 1 mg/kg iv) attenuated both the reactive hyperemia in volume by 21-22% (P less than 0.01) and dilative responses of the epicardial coronary diameter by 27-28% (P less than 0.01), despite a nonsignificant attenuation of the resting or peak hyperemic coronary blood flow. When coronary blood flow was held constant during reperfusion, by an occluder distal to the ultrasonic crystals, the reactive dilation disappeared. A peculiar reactive constriction was noted when coronary occlusion was performed proximal to the site of the ultrasonic crystals. Appearance of this constriction was at 149 and 385 s after the release of 5 and 60 s of coronary occlusion, respectively. This late reactive constriction disappeared after pretreatment with alpha- (phentolamine, 1 mg/kg iv) and/or alpha- + beta-blockade, but not with beta-blockade alone, and it was not observed when the coronary diameter was measured proximal to the occluder. Thus reactive dilation of the epicardial coronary artery derives from an increase in coronary flow and is reduced by propranolol via a reduction in the hyperemic flow, suggesting a flow-dependent change in the diameter of the epicardial coronary artery. Reactive constriction is a local phenomenon following marked reduction in the coronary diameter and is abolished by alpha-adrenergic blockade with phentolamine.

Origin of atrial coving in canine phasic coronary artery blood flow

1986 ◽  
Vol 251 (4) ◽  
pp. H774-H778
Author(s):  
P. A. McHale ◽  
J. C. Greenfield
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Coronary Flow ◽  
Diastolic Pressure ◽  
Artery Blood Flow ◽  
Circumflex Coronary Artery ◽  
Left Circumflex Coronary Artery ◽  
Open Chest ◽  
Transient Decrease ◽  
Atrial Contraction

The transient decrease in left circumflex coronary artery blood flow during atrial contraction (atrial coves) was examined in open-chest, heart-blocked dogs. Prominent atrial coves were observed in left circumflex flow during both diastole and systole as a result of the asynchrony of atrial and ventricular contractions. In eight open-chest dogs, atrial contractions decreased diastolic circumflex coronary flow by 0.016 +/- 0.002 ml and systolic flow by 0.014 +/- 0.001 ml compared with diastolic and systolic intervals during which no atrial contractions occurred. The diastolic and systolic flow reductions in this vessel were not significantly different (P greater than 0.14). In five of the eight dogs no diastolic atrial coves were observed in left anterior descending coronary flow, and only minimal diastolic coving was present in the remaining three dogs; no systolic coves were present in this vessel in any of the eight dogs. In five additional open-chest dogs, brief inflation of a balloon in the left atrium produced elevations of left ventricular diastolic pressure comparable to those produced by atrial contraction. Only minimal atrial coves were associated with these balloon inflations. These data are consistent with the hypothesis that atrial contraction limits flow through the atrial blood vessels and results in a transient decrease in flow in the atrial arteries that arise from the left circumflex coronary artery. Although increases in ventricular diastolic pressure may be partially responsible for the appearance of atrial coves in the left circumflex coronary artery, mechanical contraction of the atrial musculature appears to be of significant importance.

Contribution of endogenous endothelin to large epicardial coronary artery tone in dogs and humans

1999 ◽  
Vol 277 (2) ◽  
pp. H524-H532 ◽  
Author(s):  
Éric Thorin ◽  
Robert Parent ◽  
Zhi Ming ◽  
Michel Lavallée
Keyword(s):  
Coronary Artery ◽  
Coronary Arteries ◽  
Receptor Activation ◽  
Receptor Blockade ◽  
Circumflex Coronary Artery ◽  
No Formation ◽  
Inhibitory Feedback ◽  
Coronary Artery Diameter

Nitric oxide (NO) may normally impair endothelin (ET) activity in epicardial coronary arteries. Lifting this inhibitory feedback could reveal ET-dependent effects involving ETA- and/or ETB-receptor activation. In conscious dogs, the blockade of ETA receptors (intracoronary Ro-61–1790) increased external circumflex coronary artery diameter (CD) (sonomicrometry) by 0.10 ± 0.01 from 3.04 ± 0.12 mm ( P < 0.01) without altering coronary blood flow (Doppler). Similarly, CD increased (0.09 ± 0.01 from 2.91 ± 0.14 mm; P < 0.01) when Ro-61–1790 was given after blockade of NO formation with intracoronary N ω-nitro-l-arginine methyl ester (l-NAME). In contrast, ETB-receptor blockade (intracoronary Ro-46–8443) did not influence baseline CD with and without l-NAME. In vitro, increases in tension caused by N ω-nitro-l-arginine (l-NNA) or PGF2α in arterial rings were reduced by ETA- but not ETB-receptor blockade. ETA-receptor blockade also reduced the increase in tension caused byl-NNA in human coronary arterial rings. Thus ETA receptors, but not ETB receptors, account for ET-dependent constriction in canine epicardial coronary arteries in vivo. ET-dependent effects were independent of the level of NO formation in vitro and in vivo. In human epicardial coronary arterial rings, ETA-receptor blockade also caused significant relaxation.

Interregional Differences in the Systolic and Diastolic Response of Nonischemic Myocardium to Remote Coronary Occlusion 

1999 ◽  
Vol 91 (3) ◽  
pp. 815-815 ◽  
Author(s):  
Stephan C. U. Marsch ◽  
Hernan R. Muñoz ◽  
Serge Dalmas ◽  
Pierre Foëx
Keyword(s):  
Coronary Artery ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Posterior Wall ◽  
Anterior Wall ◽  
Artery Occlusion ◽  
Regional Function ◽  
Circumflex Coronary Artery ◽  
Twofold Increase ◽  
Left Circumflex Coronary Artery

Background Previous work showed a twofold increase in stiffness of nonischemic myocardium at the base during ischemia of the left anterior wall. Whether the diastolic response of nonischemic myocardium to remote ischemia depends on the localization of the ischemic or the nonischemic area is unknown. Methods In dogs with open chests, regional function in ischemic and nonischemic myocardium was assessed (sonomicrometry) before and 5 min after occlusion of the left anterior descending coronary artery (LAD; n = 7) or the left circumflex coronary artery (LCX; n = 7). Results In nonischemic myocardium at the base, left anterior descending and left circumflex coronary artery occlusion both resulted in a twofold increase in chamber stiffness, whereas contractility and peak lengthening rate remained unchanged. In nonischemic myocardium of the posterior wall, left anterior descending coronary artery occlusion resulted in a significant (P&lt;0.05 vs. control, P&lt;0.05 vs. base) increase (mean+/-SD) in chamber stiffness (25+/-6%), contractility (17+/-5%), and peak lengthening rate (28+/-6%). In nonischemic myocardium at the apex, left circumflex coronary artery occlusion resulted in a significant (P&lt;0.05 vs. control, P&lt;0.05 vs. base) increase in chamber stiffness (15+/-5%), contractility (16+/-4%), and peak lengthening rate (19+/-6%). Conclusions Stiffening of remote nonischemic myocardium occurs regardless of the localization of the ischemic and nonischemic area. The systolic and diastolic responses of nonischemic myocardium are not necessarily homogenous but may vary among different regions.

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