Functional anatomical site of intramural collaterals in dogs

1990 ◽  
Vol 259 (3) ◽  
pp. H706-H711 ◽  
Author(s):  
K. W. Scheel ◽  
G. Daulat ◽  
S. E. Williams

The objectives of the present study were to determine quantitatively whether the retrograde flow measurement reflects the total flow from collateral vessels or overestimates or underestimates collateral flow, and to determine the functional anatomical origin of intramural collaterals in the native dog heart. In an isolated heart preparation, three experimental procedures were used. 1) The left circumflex coronary artery was embolized with microspheres of different sizes; then retrograde flows and the peripheral coronary pressures were measured. 2) Epicardial collaterals were cauterized, and retrograde flows were measured before and after cautery. 3) Epicardial collaterals were cauterized followed by embolization of the circumflex coronary artery with different size spheres. We found that 1) the retrograde flow measurement underestimates the total collateral flow to the circumflex coronary artery by approximately 25%, 2) intramural collateral flow constitutes 58 +/- 3.5% of the retrograde flow measurement, 3) the antegrade component of blood flow that is not measured during a retrograde flow measurement is from the intramural collateral circulation, and 4) the functional site of origin of intramural collaterals is greater than 25 microns but less than 80 microns in diameter. We conclude that, in our preparation, retrograde flow underestimates total collateral flow, and that intramural collateral flow is a major component of retrograde flow in the native dog heart.

1993 ◽  
Vol 264 (2) ◽  
pp. H408-H412
Author(s):  
K. W. Scheel ◽  
H. Mass ◽  
S. E. Williams

The purpose of the present investigation was to determine the pressure-flow (PF) relationship of intramural collaterals and to determine whether their characteristics differ significantly from those of the total collateral network, defined as the epicardial plus intramural collateral network. Because a significant portion of the collateral flow is diverted away from the retrograde flow measurement, we embolized the coronary vessel on which the retrograde flow was measured with spheres of various sizes until the retrograde flow was maximized and retrograde flow diversion blocked. The PF relationship was obtained before and after the epicardial collaterals were cauterized to determine the characteristics of the total and intramural collateral network. PF data for the collateral circulations were obtained by changing the inflow pressure to all coronary vessels simultaneously and by measuring the retrograde flow while maintaining the retrograde outflow pressure at 0 mmHg. The PF characteristics of the total and intramural collateral circulations could be fitted by either a second-degree polynomial or linear equation. In both cases the pressure intercept crossed the origin of the axes. The average contribution of intramural collaterals to total retrograde flow was 58 +/- 5%. We conclude that the PF characteristics of intramural collaterals parallel those of the total collateral circulation.


1993 ◽  
Vol 264 (2) ◽  
pp. H567-H572 ◽  
Author(s):  
J. Altman ◽  
D. Dulas ◽  
T. Pavek ◽  
D. D. Laxson ◽  
D. C. Homans ◽  
...  

This study examined responses of coronary collateral blood flow to endothelial-dependent vasodilators. Studies were performed in 13 dogs 4-6 mo after embolic occlusion of the left anterior descending coronary artery (LAD). Collateral flow was determined as the sum of retrograde flow from the cannulated LAD, and continuing tissue flow was measured with microspheres administered during the retrograde flow collection. Agonists were introduced into the left main coronary artery to reach collaterals arising from the left coronary arterial system. The endothelial-dependent vasodilators acetylcholine and bradykinin caused 21 +/- 7 and 25 +/- 8% increases of collateral flow, respectively (each P < 0.05). This was not different from the 28 +/- 8% increase in collateral flow produced by nitroglycerin. To determine whether vasodilator prostaglandins contributed to the increased collateral flow, studies were performed after cyclooxygenase blockade with indomethacin (5 mg/kg iv). Indomethacin caused a 30 +/- 9% decrease of retrograde flow during basal conditions but did not blunt the maximum collateral flow rates produced by acetylcholine, bradykinin, or nitroglycerin. These data demonstrate intact endothelial-dependent vasodilator mechanisms in the well-developed coronary collateral circulation.


1965 ◽  
Vol 208 (1) ◽  
pp. 144-148 ◽  
Author(s):  
Matthew N. Levy ◽  
Moris Chansky

The extent and distribution of the collateral circulation to the ventricular myocardium which develops after partial constriction of the left circumflex coronary artery for 1 week were investigated by means of the Rb86-clearance technic. Interarterial communications were distinguished from anastomoses occurring at lower levels of the vascular tree by comparing the Rb86 clearances obtained while the retrograde-flow tubing was clamped with clearances obtained while the tubing was patent. In the central region of the ischemic myocardium, there was a two- to threefold increase in the total collateral flow after coronary artery narrowing. The collateral vessels to this region were predominantly interarterial communications. The data suggested, however, that non-interarterial anastomoses to the central zones must also have proliferated. In the marginal zones of the ischemic region, the predominant communications were non-interarterial.


1991 ◽  
Vol 261 (4) ◽  
pp. H1019-H1025 ◽  
Author(s):  
R. J. Bache ◽  
B. Foreman ◽  
P. V. Hautamaa

The ability of moderately well-developed coronary collateral vessels to undergo vasoconstriction in response to alpha-adrenergic stimulation and to ergonovine was studied. Studies were performed in 15 dogs 4-16 wk after embolic occlusion of the left anterior descending coronary artery had been performed to stimulate collateral vessel growth. Interarterial collateral flow was measured as retrograde flow from the cannulated left anterior descending coronary artery, while microvascular collateral flow was measured as continuing tissue flow determined with radioactive microspheres administered during the retrograde flow collection. Studies were performed after beta-adrenergic blockade with propranolol. Neither cardiac sympathetic nerve stimulation nor alpha 1-adrenergic stimulation with phenylephrine caused significant change in retrograde blood flow or myocardial tissue flow. The selective alpha 2-adrenergic agonist, B-HT 933, decreased tissue flow in the collateral-dependent region but did not significantly alter retrograde flow. Although these data indicate that intramural microvascular collateral communications are capable of vasoconstriction in response to alpha 2-adrenergic stimulation, the larger interarterial collaterals are unresponsive to alpha-adrenergic influences. However, under the conditions of the experiment, adrenergic activity did not appear to influence collateral function, since neither alpha 1-adrenergic blockade with prazosin nor alpha 2-adrenergic blockade with rauwolscine altered collateral flow. Ergonovine, 0.2-0.8 microgram.kg-1.min-1, caused a 22 +/- 4% decrease in retrograde flow (P less than 0.01) but did not alter microvascular collateral flow. Thus, of the agents tested, only ergonovine caused vasoconstriction of the large interarterial coronary collateral vessels.


1984 ◽  
Vol 56 (3) ◽  
pp. 656-665 ◽  
Author(s):  
C. M. Bloor ◽  
F. C. White ◽  
T. M. Sanders

To study the effects of exercise on collateral development in myocardial ischemia, we induced coronary arterial stenosis of the left circumflex coronary artery (LCCA) in 18 of 30 pigs. During that surgery, we identified the coronary bed at risk. Nine of these pigs were then subjected to 5 mo of exercise training on a treadmill. After exercise training, we determined regional collateral and myocardial blood flow using radiolabeled microspheres. At autopsy, all animals had complete occlusion of the LCCA. Infarct size in the exercise-trained pigs was significantly less than in the sedentary pigs (5.9 +/- 1.0 vs. 11.7 +/- 1.0% of the left ventricle). The exercise-trained animals had a greater increase in collateral flow, 35.1 +/- 3.0 vs. 28.7 +/- 4.1 ml X min-1 X 100 g-1, in the noninfarcted jeopardized zone of the LCCA bed. The major findings of the study were the following: 1) chronic coronary artery stenosis progressing to occlusion stimulated development of the collateral circulation and salvaged tissue in the jeopardized myocardium of an animal model with sparse collaterals; 2) development of the collateral circulation and tissue salvage is increased by exercise training; 3) collaterals develop primarily in or near the ischemic zone; and 4) all collateral beds develop a circumferential flow gradient following occlusion.


1989 ◽  
Vol 256 (2) ◽  
pp. H441-H445 ◽  
Author(s):  
K. W. Scheel ◽  
H. Mass ◽  
S. E. Williams

In this study we utilized two methods to investigate the pressure-flow, P-F, relationship of the coronary collateral vessels in a beating, blood-perfused, isolated heart preparation. In the first method (free-flow method), 12 dog hearts were perfused at pressures ranging from 100 to 0 mmHg, whereas the retrograde flow (index of collateral flow) was measured on the circumflex coronary artery, LCA, against atmospheric pressure, first during autoregulation and then after maximum vasodilation. In the second method (back-pressure method), the back pressure to retrograde flow was varied from 0 to 100 mmHg, whereas the perfusion pressure to the remaining vessels was maintained constant at 100 mmHg. This procedure was performed on four hearts with and without embolization of the LCA by 25-microns spheres. The free-flow method demonstrated a linear P-F relationship with an average correlation coefficient, r, of 0.98. The pressure intercept was 1.7 +/- 1.2 mmHg. The back-pressure method yielded a relationship that was more curvilinear with an average pressure intercept of 13 mmHg without embolization and 38 mmHg with embolization. An analog of the coronary and collateral circulation was used to illustrate that, in the back-pressure method, changes in the coronary resistance at low pressures contributed to the nonlinearity of the collateral P-F characteristics and that the network formed between the collateral and coronary resistances was responsible for the higher pressure intercept value.


1996 ◽  
Vol 271 (2) ◽  
pp. H490-H497 ◽  
Author(s):  
J. W. Kinn ◽  
J. D. Altman ◽  
M. W. Chang ◽  
R. J. Bache

Well-developed coronary collateral vessels contain an abundant muscular media and can undergo active vasomotion. However, early after coronary occlusion, coronary collateral vessels are thin walled with little smooth muscle, suggesting that vasomotor capability might be limited. Consequently, this study determined whether newly developed coronary collateral vessels have active vasomotor activity and whether endothelial function in these newly developed vessels is impaired. Retrograde blood flow was measured as an index of coronary collateral blood flow approximately 2 wk after embolic occlusion of the anterior descending coronary artery of dogs. Agonists were administered into the left main coronary artery to reach collaterals originating from the left coronary system. Baseline retrograde blood flow was 25.1 +/- 2.7 ml/min and increased to 36.7 +/- 3.7 ml/min after nitroglycerin (6 micrograms.kg-1.min-1, P < 0.05). Cyclooxygenase blockade with indomethacin (5 mg/kg i.v.) decreased retrograde collateral blood flow to 16.8 +/- 2.3 ml/min (P <a 0.05). Subsequent administration of acetylcholine increased retrograde flow to 29.4 +/- 3.7 ml/min (P < 0.05), indicating intact endothelium-mediated vasodilation. Inhibition of nitric oxide synthase with NG-nitro-L-arginine further decreased coronary collateral retrograde flow to 12.0 +/- 2.8 ml/min (P < 0.05) and markedly blunted the response to acetylcholine. These findings demonstrate substantial vasomotor capability even early during coronary collateral development and indicate that both nitric oxide and cyclooxygenase-dependent endothelial mechanisms are intact.


2015 ◽  
Vol 26 (4) ◽  
pp. 827-830 ◽  
Author(s):  
Jae Ho Byeon ◽  
Mi-Hyang Jung ◽  
Ho-Joong Youn

AbstractUnilateral pulmonary artery atresia is a rare congenital defect. The affected lung in unilateral pulmonary artery atresia usually receives its blood supply from many collateral vessels including the coronary artery. We report a case of an elderly woman with suspected anginal symptoms who had a coronary artery fistula functioning as a collateral vessel due to unilateral pulmonary artery atresia.


1988 ◽  
Vol 254 (5) ◽  
pp. H855-H861 ◽  
Author(s):  
T. Miura ◽  
S. Yoshida ◽  
O. Iimura ◽  
J. M. Downey

We investigated dobutamine effect on infarct size during permanent coronary artery occlusion in dogs. The coronary artery of closed-chest dog was embolized by a 2.5-mm Teflon bead. Regional flow was measured 8 min after embolization with microspheres and, in drug-treated animals, again 20 min after starting dobutamine infusion (10 micrograms.kg-1.min-1 for 5 h immediately after the first microsphere measurement). The percent of the ischemic region progressing to infarct was determined 48 h later in each animal. Percent necrosis in the control group correlated closely with collateral flow to the epicardial one-third of the ischemic zone normalized against flow to the corresponding layer in the nonischemic zone. This flow should reflect an index of supply (collateral flow) and demand (flow to the nonischemic region determined by autoregulation). Percent necrosis in the drug-treated group did not correlate with normalized collateral flow measurement made before drug infusion, indicating that dobutamine had modified the course of infarction. Percent necrosis correlated well with normalized collateral flow measured during drug infusion, and that relationship was not different from that in the control group. Dobutamine increased infarct size over that expected from the predrug flow measurement in some dogs and reduced it in others. In all cases, however, the drug effect on infarct size was clearly reflected in normalized collateral flow measurement during drug infusion. Percent necrosis correlated with absolute collateral flow but less closely than with the normalized one.(ABSTRACT TRUNCATED AT 250 WORDS)


2000 ◽  
Vol 279 (3) ◽  
pp. H1264-H1273 ◽  
Author(s):  
Serge A. I. P. Trines ◽  
Cornelis J. Slager ◽  
Joost Van der Moer ◽  
Pieter D. Verdouw ◽  
Rob Krams

There is no evidence regarding the effect of stunning on maximization of regional myocardial external work (EW) or efficiency of energy transfer (EET) in relation to regional afterload (end-systolic stress, ςes). To that end, we studied these relationships in both the left anterior descending coronary artery (LADCA) and left circumflex coronary artery regions in anesthetized, open-chest pigs before and after LADCA stunning. In normal myocardium, EET vs. ςes was maximal at 75.4 (69.7–81.0)%, whereas EW vs. ςes was submaximal at 12.0 (6.61–17.3) × 102 J/m3. Increasing ςes increased EW by 18 (10–27)%. Regional myocardial stunning decreased EET (27%) and EW (36%) and caused the myocardium to operate both at maximal EW (EWmax) and at maximal EET (EETmax). EET and EW became also more sensitive to changes in ςes. In the nonstunned region the situation remained unchanged. Combining the data from before and after stunning, both EWmax and EETmax displayed a positive relationship with contractility. In conclusion, the normal regional myocardium operated at maximal EET rather than at maximal EW. Therefore, additional EW could be recruited by increasing regional afterload. After myocardial stunning, the myocardium operated at both maximal EW and maximal EET, at the cost of increased afterload sensitivity. Contractility was a major determinant of this shift.


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