Coronary sinus occlusion enhances coronary collateral flow and reduces subendocardial ischemia

2001 ◽  
Vol 280 (3) ◽  
pp. H1361-H1367 ◽  
Author(s):  
Akira Ido ◽  
Naoyuki Hasebe ◽  
Hironobu Matsuhashi ◽  
Kenjiro Kikuchi
Keyword(s):  
Blood Flow ◽  
Coronary Sinus ◽  
Regional Myocardial Blood Flow ◽  
Collateral Flow ◽  
Vasomotor Tone ◽  
Coronary Collateral ◽  
Intramyocardial Pressure ◽  
Ischemic Region ◽  
Coronary Collateral Flow ◽  
Anesthetized Dogs

On the hypothesis that coronary sinus occlusion (CSO) may reduce myocardial ischemia, we examined the effects of CSO on coronary collateral blood flow and on the distribution of regional myocardial blood flow (RMBF) in dogs. Thirty-eight anesthetized dogs underwent occlusion of the left anterior descending coronary artery with or without CSO and intact vasomotor tone. We measured RMBF and intramyocardial pressure (IMP) in the subendocardium (Endo) and subepicardium (Epi) separately. With intact vasomotor tone, CSO during ischemia significantly increased RMBF in the ischemic region (IR), particularly in Endo from 0.17 ± 0.03 to 0.33 ± 0.05 ml · min−1· g−1( P < 0.05), and increased the Endo/Epi from 0.59 ± 0.10 to 1.15 ± 0.15 ( P < 0.01). These effects of CSO were partially abolished by adenosine. However, the Endo/Epi was still increased from 0.90 ± 0.13 to 2.09 ± 0.30 ( P < 0.01). The changes in RMBF in IR were significantly correlated with the peak CS pressure during CSO. The Endo/Epi of IMP in IR was significantly decreased during CSO. In conclusion, CSO potentially enhances coronary collateral flow, and preserves the ischemic myocardium, especially in Endo.

Influence of cardiac contraction and coronary vasomotor tone on regional myocardial blood flow

1994 ◽  
Vol 266 (6) ◽  
pp. H2542-H2553 ◽  
Author(s):  
R. E. Austin ◽  
N. G. Smedira ◽  
T. M. Squiers ◽  
J. I. Hoffman
Keyword(s):  
Blood Flow ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Regional Myocardial Blood Flow ◽  
Vasomotor Tone ◽  
Coronary Pressure ◽  
Regional Flow ◽  
Anesthetized Dogs ◽  
Coronary Tone ◽  
Regional Myocardial Blood

We analyzed patterns of left ventricular perfusion in arrested hearts without coronary tone and in the same hearts while beating with and without coronary tone. We used microspheres in anesthetized dogs to measure blood flow in 384 regions (averaging 140 mg wet wt) from the subendocardium, midwall, and subepicardium before and during intracoronary infusions of adenosine (beating without tone) or lidocaine and adenosine (arrest without tone). Mean coronary pressure was held constant at 80 mmHg. Changes in regional flow with arrest (vs. beating without tone) were surprisingly variable (range -28 to +124%) and exhibited substantial within-layer heterogeneity, suggesting that local differences in contractility, stresses, or strains limit maximum coronary flow. Regional flows in beating hearts with tone did not correlate with flows in the same hearts without tone, beating or not (r2 < or = 0.03; not significant). Flow patterns during beating with tone also demonstrated significantly shorter (i.e., the distance at which autocorrelation has decreased to 0.5) within-layer spatial autocorrelations as well as a complete loss of radial flow correlation (e.g., between corresponding subendocardial and subepicardial regions; r2 = 0.01). Thus neither coronary anatomy (assessed during arrest without tone) nor the mechanical effects of contraction (beating without tone) appear to influence myocardial perfusion when vasomotor tone is present.

Effects of cardiac contraction and coronary sinus pressure elevation on collateral circulation

1996 ◽  
Vol 271 (4) ◽  
pp. H1433-H1440 ◽  
Author(s):  
M. Sato ◽  
T. Saito ◽  
M. Mitsugi ◽  
S. Saitoh ◽  
T. Niitsuma ◽  
...  
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Coronary Sinus ◽  
Cardiac Contraction ◽  
Regional Myocardial Blood Flow ◽  
Coronary Perfusion ◽  
Collateral Flow ◽  
Pressure Elevation ◽  
Regional Myocardial Blood ◽  
Sinus Pressure

Controlled coronary sinus occlusion was shown to retard necrosis of ischemic myocardium. To elucidate this mechanism, regional myocardial blood flow measurement was performed with and without coronary sinus pressure elevation to 30 mmHg (CS30). Colored microspheres were injected into left and right coronary arteries after coronary perfusion of the left anterior descending (LAD) coronary artery was stopped in seven isolated canine hearts with induced atrioventricular block, either paced at 120 beats/min by direct right ventricular stimulation [beating heart (B)] or during asystole induced by stopping pacing [nonbeating heart (NB)]. Regional myocardial blood flow in the LAD perfused area in the control state in the NB with normal coronary sinus pressure (NB-CScont; 0.27 +/- 0.13 ml.min-1.g-1, means +/- SE) was significantly greater than those in B-CScont (0.19 +/- 0.09 ml.min-1.g-1; P < 0.05) and in NB with CS30 (NB-CS30; 0.19 +/- 0.09 ml.min-1.g-1; P < 0.05). Regional myocardial blood flow of the LAD area in B with CS30 (B-CS30; 0.23 +/- 0.10 ml.min-1.g-1) was significantly greater in comparison with that at B-CScont and NB-CS30 (P < 0.05). The augmentative effect of the LAD area regional myocardial blood flow was observed only in the periphery of the ischemic region but not in its center. Cardiac contraction and CS30 impede regional myocardial blood flow in the ischemic bed independently. The coexistence of these two factors enhances regional myocardial blood flow. In conclusion, coronary sinus pressure elevation in B may participate in augmenting collateral flow.

Distribution of coronary collateral blood flow at different levels of collateral growth in conscious ponies

1992 ◽  
Vol 263 (4) ◽  
pp. H1145-H1153
Author(s):  
R. B. Boatwright ◽  
D. O. Williams ◽  
K. S. Rugh ◽  
R. D. Sarazan ◽  
C. R. Ross ◽  
...  
Keyword(s):  
Blood Flow ◽  
Reactive Hyperemia ◽  
Regional Myocardial Blood Flow ◽  
Collateral Blood Flow ◽  
Coronary Collateral ◽  
Ischemic Region ◽  
Myocardial Layers ◽  
Collateral Growth ◽  
Collective Resistance ◽  
In Series

Coronary collateral growth was stimulated in chronically instrumented conscious ponies by a previously validated intermittent coronary occlusion method. Changes in regional myocardial function (sonomicrometry) and reactive hyperemia (Doppler method) were used to monitor collateral growth and to program measurements of regional myocardial blood flow (microsphere method). A serial analysis of the transmural and lateral distributions of collateral blood flow was performed at the native and three superimposed levels of collateral growth. Results in nine animals undergoing an average of 553 +/- 188 brief coronary occlusions over 68 +/- 18 days demonstrated that as collateral conductance increased, the perfusion field within the ischemic region increased from the epicardium to the endocardium but not from the lateral edges to the center of the ischemic region. The findings are consistent with an analog model consisting of interarterial collaterals whose collective resistance is in series with arteriolar resistance of the recipient artery. No special protection of deeper myocardial layers by a subendocardial plexus or intramural collaterals was noted. Instead, the findings suggest that coronary extravascular compressive forces play a more important role than the transmural location of collaterals in determining the volume and spatial distribution of collateral blood flow during collateral growth in the pony.

Myocardial and total body extractions of radiorubidium in anesthetized dogs

1975 ◽  
Vol 38 (1) ◽  
pp. 31-32 ◽  
Author(s):  
H. F. Downey ◽  
F. A. Bashour ◽  
P. E. Parker ◽  
C. A. Bashour ◽  
C. S. Rutherford
Keyword(s):  
Blood Flow ◽  
Individual Differences ◽  
Pulmonary Artery ◽  
Coronary Sinus ◽  
Confidence Level ◽  
Rapid Decline ◽  
Arterial Concentration ◽  
Anesthetized Dogs ◽  
Total Body ◽  
Uptake Method

Myocardium (EM) and average total body (ETB) extractions of 86-Rb were determined in 24 anesthetized, open-chest dogs. Blood from the coronary sinus and from the pulmonary artery reflected the uptake of 86-Rb by myocardium and the total body, respectively, and extractions were computed from the relative arteriovenous differences (A-V/A). While the arterial concentration of 86-Rb was constant, EM varied from 0.66 plus or minus .02 (SE) at 2–2.5 min to 0.65 plus or minus 0.02 at 5–5.5 min, and ETB varied from 0.63 plus or minus 0.01 to 0.58 plus or minus 0.01 over the same interval. Mean extractions were similar statistically at 2–2.5 min, but individual differences as great as 30% were encountered at the 95% confidence level. After 3 min of 86-Rb administration, EM significantly exceeded ETB (P is less than 0.05) due to the more rapid decline with time of ETB. The similarity of the early extractions of 86-Rb by myocardium and by the total body supports, in general, the use of the radiorubidium uptake method for measuring coronary blood flow. However, the administration of the indicator should be brief, and rather large errors in individual estimates must be anticipated.

Effects of time on volume and distribution of coronary collateral flow

1976 ◽  
Vol 230 (2) ◽  
pp. 279-285 ◽  
Author(s):  
ML Marcus ◽  
RE Kerber ◽  
J Ehrhardt ◽  
FM Abboud
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Coronary Occlusion ◽  
Marked Decrease ◽  
Relative Proportion ◽  
Collateral Flow ◽  
Coronary Vascular Resistance ◽  
Collateral Blood Flow ◽  
Coronary Collateral Flow ◽  
Hemodynamic Measurements

Changes in the volume and distribution of collateral blood flow were studied during the 1st h after coronary occlusion in nine open-chest dogs. Labeled microspheres (7-10 mum) were injected into the left atrium prior to and 20 s, 5 min, and 60 min after acute occlusion of the midcircumflex coronary artery so that myocardial perfusion to small segments of the entire left ventricle could be measured. The segmental perfusions were classified as normally perfused, severely hypoperfused, moderately hypoperfused, and borderline hypoperfused. Standard hemodynamic measurements were obtained and relative coronary vascular resistance to the normally perfused and hypoperfused zones was calculated. The principal conclusions of the study are as follows: 1) during the 1st h after coronary occlusion the collateral flow to the hypoperfused myocardium increases substantially; 2) the increase in collateral flow is distributed fairly evenly to various hypoperfused zones and is associated with a marked decrease in coronary vascular resistance; and 3) as a result of this influx in collateral flow the size of the hypoperfused area decreases and the relative proportion of severely hypoperfused segments within the hypoperfused area decreases.

Influence of coronary collateral flow on coronary diagnostic parameters: An in vitro study

2009 ◽  
Vol 42 (16) ◽  
pp. 2753-2759 ◽  
Author(s):  
Srikara Viswanath Peelukhana ◽  
Lloyd H. Back ◽  
Rupak K. Banerjee
Keyword(s):  
In Vitro Study ◽  
Vitro Study ◽  
Collateral Flow ◽  
Diagnostic Parameters ◽  
Coronary Collateral ◽  
Coronary Collateral Flow

Protamine inhibits coronary collateral development in a canine model of repetitive coronary occlusion

1995 ◽  
Vol 268 (2) ◽  
pp. H720-H728 ◽  
Author(s):  
J. R. Kersten ◽  
P. S. Pagel ◽  
D. C. Warltier
Keyword(s):  
Blood Flow ◽  
Myocardial Ischemia ◽  
Contractile Function ◽  
Regional Myocardial Blood Flow ◽  
Collateral Development ◽  
Coronary Collateral ◽  
Debt Repayment ◽  
Chronic Myocardial Ischemia

Protamine has been demonstrated to inhibit angiogenesis in vitro and in vivo; however, its effect on coronary collateral development has not been examined. The present investigation tested the hypothesis that subcutaneously administered protamine inhibits canine coronary collateral development in response to chronic myocardial ischemia. Dogs underwent daily, repetitive, 2-min, left anterior descending coronary artery (LAD) occlusions for 22 consecutive days. Regional myocardial blood flow (radioactive microspheres), LAD segment shortening, and coronary flow debt repayment were measured in saline-treated (n = 7) and protamine-treated (n = 6) dogs on days 1, 8, 15, and 22. Coronary collateral development in saline-treated dogs was demonstrated by time-dependent significant (P < 0.05) increases in collateral blood flow to ischemic myocardium [day 1 0.10 +/- 0.01 vs. day 22 0.88 +/- 0.05 (SE) ml.min-1.g-1], progressive normalization of myocardial contractile function during LAD occlusion, and successive reduction in flow debt repayment. In contrast, protamine treatment significantly attenuated, increases in collateral perfusion (day 1 0.13 +/- 0.02 vs. day 22 0.36 +/- 0.03 ml.min-1.g-1). Regional contractile dysfunction and postocclusive reactive hyperemic responses were sustained over time in protamine-treated compared with saline-treated dogs. The results demonstrate that protamine inhibits coronary collateral development in response to chronic myocardial ischemia.

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