Effects of minoxidil on coronary collateral flow and acute myocardial injury following experimental coronary artery occlusion

1978 ◽  
Vol 12 (2) ◽  
pp. 120-126 ◽  
Author(s):  
P. RADVANY ◽  
M. A. DAVIS ◽  
J. E. MULLER ◽  
P. R. MAROKO
Keyword(s):  
Coronary Artery ◽  
Myocardial Injury ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Collateral Flow ◽  
Coronary Collateral ◽  
Acute Myocardial Injury ◽  
Coronary Collateral Flow

Bradykinin as an endogenous myocardial protective substance with particular reference to ischemic preconditioning–a brief review of the evidence

1995 ◽  
Vol 73 (7) ◽  
pp. 837-842 ◽  
Author(s):  
James R. Parratt ◽  
Agnes Vegh ◽  
Julius Gy. Papp
Keyword(s):  
Coronary Artery ◽  
Myocardial Ischemia ◽  
Ischemic Preconditioning ◽  
Myocardial Injury ◽  
Ischemic Injury ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Ventricular Pacing ◽  
Acute Myocardial Injury ◽  
Rapid Ventricular Pacing

The present brief review summarizes the evidence for the possibility that endogenously released bradykinin plays a major role in protecting the heart against the consequences of acute myocardial injury. This evidence includes the facts that kinins are generated under myocardial ischemia; that when they are administered, they are cardioprotective (e.g., antiarrhythmic); that drugs that enhance the release of bradykinin from the ischemic heart reduce the ischemic injury and, conversely, drugs that block bradykinin receptors attenuate the reduction in ischemic injury resulting from the release of, or administration of, bradykinin. The possible mechanism of bradykinin in the cardioprotection afforded by ischemic preconditioning is summarized. Ischemic preconditioning can be defined as the marked reduction in the severity of ischemic changes that result from coronary artery occlusion when that occlusion is preceded by brief periods of myocardial ischemia, either regional or global, induced, for example, by complete or partial coronary artery occlusion or by rapid ventricular pacing. The possible mechanisms of cardioprotection elicited by bradykinin (and ischemic preconditioning) are summarized. The most likely is the generation of cyclic GMP within the ischemic myocardium following bradykinin-stimulated nitric oxide generation and release from endothelial cells.Key words: endogenous myocardial protective substances, bradykinin, ischemic preconditioning, cardiac arrhythmias, myocardial ischemia.

Vasomotor activity of moderately well-developed canine coronary collateral circulation

1989 ◽  
Vol 256 (3) ◽  
pp. H890-H897 ◽  
Author(s):  
P. V. Hautamaa ◽  
X. Z. Dai ◽  
D. C. Homans ◽  
R. J. Bache
Keyword(s):  
Coronary Artery ◽  
Angiotensin Ii ◽  
Collateral Circulation ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Collateral Flow ◽  
Retrograde Flow ◽  
Coronary Collateral Circulation ◽  
Coronary Collateral ◽  
Vasomotor Activity

This study examined the ability of moderately well-developed coronary collateral vasculature to undergo vasoconstriction in response to alpha-adrenergic agonists, vasopressin and angiotensin, and vasodilation in response to nitroglycerin. Studies were performed in 20 dogs 4-16 wk after left anterior descending coronary artery occlusion had been produced by an Ameroid constrictor or hollow intravascular plug. Collateral flow was estimated from retrograde flow from the cannulated left anterior descending artery. Tissue flow was measured with microspheres. Agonists were introduced into the left main coronary artery to reach collaterals arising from the left circumflex and septal arteries. Vasopressin and angiotensin II decreased retrograde flow from 22.7 +/- 5.5 to 15.5 +/- 2.7 and from 19.2 +/- 2.8 to 14.3 +/- 1.9 ml/min, respectively (each P less than 0.05). Both agents also significantly decreased tissue flow to normally perfused and collateral dependent myocardium. Neither the selective alpha 1-adrenergic agonist phenylephrine nor the alpha 2-agonist B-HT 933 decreased retrograde flow. Nitroglycerin increased retrograde flow by 63 +/- 27% (P less than 0.01). Thus, although the moderately well-developed coronary collateral circulation is capable of vasoconstriction in response to vasopressin and angiotensin II, these data fail to support a role for alpha-adrenergic mechanisms in modulating collateral flow.

Temporal relation between neutrophil accumulation and myocardial reperfusion injury

1988 ◽  
Vol 255 (5) ◽  
pp. H1060-H1068 ◽  
Author(s):  
E. F. Smith ◽  
J. W. Egan ◽  
P. J. Bugelski ◽  
L. M. Hillegass ◽  
D. E. Hill ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Reperfusion Injury ◽  
Time Course ◽  
Myocardial Injury ◽  
Inflammatory Cells ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Neutrophil Accumulation ◽  
Cell Responses ◽  
Significant Linear Correlation

Infiltration of polymorphonuclear leukocytes (PMN) is associated with the progression of myocardial infarction and reperfusion injury. However, little is known about the time course of cellular infiltration. To investigate this issue, rats were subjected to 30 min of coronary artery occlusion followed by reperfusion for less than or equal to 96 h. Myocardial injury was determined by measuring the depletion of myocardial creatine phosphokinase activity, and PMN infiltration was assessed by measuring myeloperoxidase (MPO) activity. MPO activity increased from 0.7 U/g tissue in non-operated animals, to a peak of 6.7 +/- 0.8 and 6.4 +/- 1.4 U/g at 6 and 24 h after coronary artery reperfusion, respectively. MPO activity decreased to 3.3 +/- 0.8 U/g at 48 h and 1.1 +/- 0.4 U/g at 96 h, suggesting diminished PMN accumulation. Histological examination confirmed the accumulation and resolution of PMN over the 96-h period. At 24 h, there was a significant linear correlation between infarct size and MPO activity, whereas at 96 h no relationship was found. These data indicate that PMN infiltration occurs early in response to reperfusion injury and persists for only 24 h after initiation of reperfusion. These findings suggest that attempts to moderate inflammatory cell responses to myocardial injury should be administered early after coronary artery reperfusion to limit the accumulation of potentially deleterious inflammatory cells.

Early time course of myocardial electrical impedance during acute coronary artery occlusion in pigs, dogs, and humans

2005 ◽  
Vol 99 (4) ◽  
pp. 1576-1581 ◽  
Author(s):  
Carlos L. del Rio ◽  
Patrick I. McConnell ◽  
Bradley D. Clymer ◽  
Roger Dzwonczyk ◽  
Robert E. Michler ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Time Course ◽  
Electrical Impedance ◽  
Early Time ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Acute Ischemia ◽  
Collateral Flow ◽  
Total Occlusion ◽  
Interspecies Differences

Changes in myocardial electrical impedance (MEI) and physiological end points have been correlated during acute ischemia. However, the importance of MEI's early time course is not clear. This study evaluates such significance, by comparing the temporal behavior of MEI during acute total occlusion of the left anterior descending coronary artery in anesthetized humans, dogs, and pigs. Here, interspecies differences in three MEI parameters (baseline, time to plateau onset, and plateau value normalized by baseline) were evaluated using Kruskal-Wallis ANOVA and post hoc tests ( P < 0.05). Noteworthy differences in the MEI time to plateau onset were observed: In dogs, MEI ischemic plateau was reached after 46.3 min (SD 12.9) min of occlusion, a significantly longer period compared with that of pigs and humans [4.7 (SD 1.2) and 4.1 min (SD 1.9), respectively]. However, no differences could be observed between both animal species regarding the normalized MEI ischemic plateau value (15.3% (SD 4.7) in pigs, vs. 19.6% (SD 2.6) in dogs). For all studied MEI parameters, only swine values resembled those of humans. The severity of myocardial supply ischemia, resulting from coronary artery occlusion, is known to be dependent on collateral flow. Thus, because dogs possess a well-developed collateral system (unlike humans or pigs), they have shown superior resistance to occlusion of a coronary artery. Here, the early MEI time course after left anterior descending coronary artery occlusion, represented by the time required to reach ischemic plateau, was proven to reflect such interspecies differences.

The Influence of Collateral Flow on the Antegrade and Retrograde Distribution of Cardioplegia in Patients with an Occluded Right Coronary Artery 

1998 ◽  
Vol 89 (5) ◽  
pp. 1099-1107 ◽  
Author(s):  
Solomon Aronson ◽  
Eric Jacobsohn ◽  
Robert Savage ◽  
Mario Albertucci
Keyword(s):  
Coronary Artery ◽  
Right Ventricle ◽  
Right Coronary Artery ◽  
Contrast Echocardiography ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Collateral Flow ◽  
Predictive Values ◽  
Antegrade Cardioplegia ◽  
The Right

Background The predictive value of electrocardiography (ECG) and coronary angiography for cardioplegia distribution in patients with an occluded right coronary artery was evaluated. Methods Coronary angiograms and ECGs were evaluated in 15 patients with right coronary artery occlusion. Prediction of antegrade cardioplegia distribution was based on ECG evidence of infarction and coronary collateral flow determined from the angiogram. Antegrade and retrograde delivery of cardioplegia was directly assessed in all patients by myocardial contrast echocardiography. Intraoperative transesophageal echocardiographic images of the right ventricular free wall, the apex, and the intraventricular septum were recorded while 4 ml of Albunex (Mallinckrodt Medical, St. Louis, MO) was injected into antegrade and retrograde cardioplegic catheters during cardioplegia delivery. The observed (myocardial contrast echocardiography) cardioplegia distribution was compared to the predicted cardioplegia distribution. Sensitivity, specificity, positive predictive values, and negative predictive values were calculated. Results Eighty seven of 90 (97%) segments were analyzed. Angiography and ECG poorly predicted incomplete cardioplegia distribution. Electrocardiography was a better predictor of inadequate cardioplegia distribution to the right ventricle than was angiography. The negative predicted values of cardioplegia distribution ranged from 20 to 50% for the septum and right ventricle, respectively, with ECG criteria and from 0 to 33% for the septum and apex, respectively, with angiographic criteria. Antegrade cardioplegia delivery was distributed to the right ventricle in 31% of patients, despite 100% occlusion of the right coronary artery; whereas retrograde cardioplegia delivery to the right ventricle occurred 20% of the time. Conclusions In the presence of 100% right coronary artery occlusion, retrograde cardioplegia delivery is not often observed and antegrade delivery of cardioplegia to the right ventricle is not easily predicted. The preoperative angiography and ECG are not predictive of coronary collateral circulation and therefore not predictive of cardioplegia distribution to the right ventricle.

Failure of Free Fatty Acids to Influence Degree of Myocardial Injury Following Acute Coronary Artery Occlusion in Pigs

Cardiology ◽  
1974 ◽  
Vol 59 (4) ◽  
pp. 201-212 ◽  
Author(s):  
A.S. Most ◽  
R.J. Capone ◽  
P. Szydlik ◽  
C.A. Bruno ◽  
T.S. DeVona
Keyword(s):  
Fatty Acids ◽  
Coronary Artery ◽  
Free Fatty Acids ◽  
Myocardial Injury ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Influence Degree

Abstract 3341: Human Coronary Collaterals Inversely Correlate with Indices of Ischemic Left Ventricular Diastolic Dysfunction during Coronary Balloon Occlusion.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Stephen P Hoole ◽  
Paul A White ◽  
Patrick M Heck ◽  
Michael O’Sullivan ◽  
Sarah C Clarke ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Diastolic Dysfunction ◽  
Diastolic Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Balloon Occlusion ◽  
Flow Index ◽  
Collateral Flow ◽  
Coronary Collaterals

Background: Coronary collaterals are thought to reduce myocardial ischemia during coronary artery occlusion. Coronary collaterals, defined angiographically, reduce end diastolic LV dilatation during coronary occlusion. However, counter to a role in reducing ischemia, they appear to be associated with an increase in LV end diastolic pressure. These changes may be explained if coronary collaterals act as an external LV scaffold. We aimed to re-evaluate this relationship by simultaneously measuring coronary collaterals and LV contractility quantitatively. Methods: Ten patients with normal LV function and single vessel coronary disease awaiting PCI were recruited. Collateral flow index, derived by pressure-wire measurement (CFI p = [P distal (occluded) − P venous ] / [P aorta − P venous ]) and change in LV end-diastolic pressure (LVEDP), volume (LVEDV) and Tau, measured by an LV cavity conductance catheter, were recorded simultaneously after 1 minute coronary balloon occlusion. A mean of 5 cardiac cycles was analyzed. Measurements were repeated after a recovery period of 30 minutes. Results: Percentage change in LVEDP and Tau inversely correlated with CFI p (ΔLVEDP vs. CFI p : y = −216.6x +63.4, r = 0.57, p=0.01; ΔTau vs. CFI p : y = −64.1x + 27.8, r = 0.47, p<0.05) (Figure ). There was also an inverse relationship between ΔLVEDV vs. CFI p (y = −8.4x + 1.5, r = 0.35, p = 0.15). Conclusion: Coronary collaterals inversely correlate with LV end diastolic stiffness and dilatation after 1 minute of coronary artery occlusion. This reflects a role in reducing ischemic LV diastolic dysfunction, by providing an alternative blood supply to the LV myocardium, rather than acting as an LV scaffold.

scholarly journals Novel Acute Collateral Flow Index in Patients With Total Coronary Artery Occlusion During ST-Elevation Myocardial Infarction

2012 ◽  
Vol 76 (2) ◽  
pp. 414-422 ◽  
Author(s):  
Simcha R. Meisel ◽  
Michael Shochat ◽  
Aaron Frimerman ◽  
Aya Asif ◽  
David S. Blondheim ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
St Elevation Myocardial Infarction ◽  
Flow Index ◽  
Collateral Flow ◽  
St Elevation

Reactive oxygen species are critical mediators of coronary collateral development in a canine model

2003 ◽  
Vol 285 (4) ◽  
pp. H1582-H1589 ◽  
Author(s):  
Weidong Gu ◽  
Dorothee Weihrauch ◽  
Katsuya Tanaka ◽  
John P. Tessmer ◽  
Paul S. Pagel ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Blood Flow ◽  
Coronary Artery ◽  
Reactive Oxygen ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Oxygen Species ◽  
Collateral Blood Flow ◽  
Collateral Development ◽  
Coronary Collateral

Recent evidence suggests that reactive oxygen species (ROS) promote proliferation and migration of vascular smooth muscle (VSMC) and endothelial cells (EC). We tested the hypothesis that ROS serve as crucial messengers during coronary collateral development. Dogs were subjected to brief (2 min), repetitive coronary artery occlusions (1/h, 8/day, 21 day duration) in the absence (occlusion, n = 8) or presence of N-acetylcysteine (NAC) (occlusion + NAC, n = 8). A sham group ( n = 8) was instrumented identically but received no occlusions. In separate experiments, ROS generation after a single 2-min coronary artery occlusion was assessed with dihydroethidium fluorescence. Coronary collateral blood flow (expressed as a percentage of normal zone flow) was significantly increased (71 ± 7%) in occlusion dogs after 21 days but remained unchanged (13 ± 3%) in sham dogs. Treatment with NAC attenuated increases in collateral blood flow (28 ± 8%). Brief coronary artery occlusion and reperfusion caused ROS production (256 ± 33% of baseline values), which was abolished with NAC (104 ± 12%). Myocardial interstitial fluid produced tube formation and proliferation of VSMC and EC in occlusion but not in NAC-treated or sham dogs. The results indicate that ROS are critical for the development of the coronary collateral circulation.

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