The coronary and luminal circulations of the myocardium of fishes

There are two routes to supply oxygen to the myocardium of fishes, an oxygen-poor luminal supply and, in some fishes, an additional oxygen-rich coronary circulation. When present in teleost fishes, coronary vessels penetrate the myocardium to differing degrees. Elasmobranchs have coronary vessels throughout the myocardium. The different distributions of the coronary vessels reflect solutions to the problem of oxygen diffusion from the luminal blood to various parts of the heart, especially the outer layers of large ventricles. By examining cardiovascular data derived from in vivo experimental perturbations, such as exercise and environmental hypoxia, and from in vitro studies with perfused hearts, we discuss the extent to which luminal venous blood obviates the need for a coronary circulation and the extent to which the coronary circulation supplements the luminal oxygen supply. The oxygen content of the venous blood surpasses the maximal demand of the working heart and so the likely limitation of the luminal blood is the venous partial pressure of oxygen [Formula: see text] which in part determines the oxygen gradient to the mitochondria. The threshold venous [Formula: see text] is between 6 and 16 torr. Whether the coronary circulation is perfused in all species of fishes under resting conditions is not clear. Experimental data support the idea that there are species differences in the relative dependence on the coronary circulation. Coronary perfusion becomes relatively more important in situations where venous [Formula: see text] decreases and myocardial oxygen demand stays the same or increases, e.g., sustained aerobic exercise, environmental hypoxia, and the recovery period after exercise. Observations in vivo and in vitro support the idea that the pressure-generating potential of the heart, as opposed to the potential for flow output, is much more sensitive to changes in coronary blood flow. Coronary blood flow is more likely to be controlled through modulation of a large coronary vasodilatory reserve than through variations in perfusion pressure. Studies on coronary vasoactivity in fishes are limited; nonetheless, species differences are apparent.

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Coronary smooth muscle reactivity to muscarinic stimulation after ischemia-reperfusion in porcine myocardial infarction

Journal of Applied Physiology ◽

10.1152/japplphysiol.00119.2003 ◽

2003 ◽

Vol 95 (1) ◽

pp. 81-88 ◽

Cited By ~ 7

Author(s):

Antonio Rodríguez-Sinovas ◽

Josep Bis ◽

Inocencio Anivarro ◽

Javier de la Torre ◽

Antoni Bayés-Genís ◽

...

Keyword(s):

Blood Flow ◽

Smooth Muscle ◽

Coronary Artery ◽

Coronary Blood Flow ◽

Ischemia Reperfusion ◽

Left Ventricular ◽

Severe Left Ventricular Dysfunction ◽

Coronary Smooth Muscle

This study tested whether ischemia-reperfusion alters coronary smooth muscle reactivity to vasoconstrictor stimuli such as those elicited by an adventitial stimulation with methacholine. In vitro studies were performed to assess the reactivity of endothelium-denuded infarct-related coronary arteries to methacholine ( n = 18). In addition, the vasoconstrictor effects of adventitial application of methacholine to left anterior descending (LAD) coronary artery was assessed in vivo in pigs submitted to 2 h of LAD occlusion followed by reperfusion ( n = 12), LAD deendothelization ( n = 11), or a sham operation ( n = 6). Endothelial-dependent vasodilator capacity of infarct-related LAD was assessed by intracoronary injection of bradykinin ( n = 13). In vitro, smooth muscle reactivity to methacholine was unaffected by ischemia-reperfusion. In vivo, baseline methacholine administration induced a transient and reversible drop in coronary blood flow (9.6 ± 4.6 to 1.9 ± 2.6 ml/min, P < 0.01), accompanied by severe left ventricular dysfunction. After ischemia-reperfusion, methacholine induced a prolonged and severe coronary blood flow drop (9.7 ± 7.0 to 3.4 ± 3.9 ml/min), with a significant delay in recovery ( P < 0.001). Endothelial denudation mimics in part the effects of methacholine after ischemia-reperfusion, and intracoronary bradykinin confirmed the existence of endothelial dysfunction. Infarct-related epicardial coronary artery shows a delayed recovery after vasoconstrictor stimuli, because of appropriate smooth muscle reactivity and impairment of endothelial-dependent vasodilator capacity.

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Blood flow in the ovary and adjacent structures of the non-pregnant sheep

Acta Endocrinologica ◽

10.1530/acta.0.1030259 ◽

1983 ◽

Vol 103 (2) ◽

pp. 259-265 ◽

Cited By ~ 7

Author(s):

P. O. Janson ◽

D. Williams ◽

O. M. Petrucco ◽

F. Amato ◽

R. F. Seamark ◽

...

Keyword(s):

Blood Flow ◽

Venous Blood ◽

Vascular Pedicle ◽

Venous Flow ◽

Adjacent Structures ◽

Pregnant Sheep ◽

Rapid Changes ◽

Capillary Bed

Abstract. Blood flow to the ovary, vascular pedicle and oviduct was measured in anaesthetized non-cycling and cycling ewes by timed collection of ovarian venous blood. The degree of arterio-venous shunting across the ovary and pedicle was estimated both in vivo and in vitro by perfusing the tissues with 15 ± 5 μm radioactive microspheres. The mean ovarian blood flow in non-cycling animals was 1.9 ml/min, which was 51% of blood flow in the ovarian vein. In cycling animals ovarian blood flow at midcycle was 2.9 ml/min (66% of ovarian venous flow) in non-luteal ovaries and 4.3 ml/min (79% of venous flow) in luteal ovaries. The degree of arterio-venous shunting was low in all stages of the cycle (1.0–2.6% across ovary + pedicle). The degree of shunting was also found to be very small in vitro (0.007–1.38%) in both non-luteal and luteal ovaries. A considerable number of microspheres was entrapped in the vascular pedicle of the ovary indicating the presence of an extensive capillary bed. There was an inverse relationship between blood flow in the ovary and flow in the vascular pedicle. Alterations in distribution of blood flow between the ovary and adjacent structures supplied by the ovarian artery may be of functional significance in allowing rapid changes in ovarian blood flow. The results of the present study indicate that changes in ovarian blood flow during the oestrous cycle are not caused by an action on arteriovenous shunt vessels.

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Functional contribution of P2Y1receptors to the control of coronary blood flow

Journal of Applied Physiology ◽

10.1152/japplphysiol.00946.2011 ◽

2011 ◽

Vol 111 (6) ◽

pp. 1744-1750 ◽

Cited By ~ 19

Author(s):

Shawn B. Bender ◽

Zachary C. Berwick ◽

M. Harold Laughlin ◽

Johnathan D. Tune

Keyword(s):

Nitric Oxide ◽

Blood Flow ◽

Coronary Blood Flow ◽

Coronary Vasodilation ◽

Pressure Flow ◽

Coronary Pressure ◽

Mrs 2179 ◽

Dependent Mechanism

Activation of ADP-sensitive P2Y1receptors has been proposed as an integral step in the putative “nucleotide axis” regulating coronary blood flow. However, the specific mechanism(s) and overall contribution of P2Y1receptors to the control of coronary blood flow have not been clearly defined. Using vertically integrative studies in isolated coronary arterioles and open-chest anesthetized dogs, we examined the hypothesis that P2Y1receptors induce coronary vasodilation via an endothelium-dependent mechanism and contribute to coronary pressure-flow autoregulation and/or ischemic coronary vasodilation. Immunohistochemistry revealed P2Y1receptor expression in coronary arteriolar endothelial and vascular smooth muscle cells. The ADP analog 2-methylthio-ADP induced arteriolar dilation in vitro and in vivo that was abolished by the selective P2Y1antagonist MRS-2179 and the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester. MRS-2179 did not alter baseline coronary flow in vivo but significantly attenuated coronary vasodilation to ATP in vitro and in vivo and the nonhydrolyzable ATP analog ATPγS in vitro. Coronary blood flow responses to alterations in coronary perfusion pressure (40–100 mmHg) or to a brief 15-s coronary artery occlusion were unaffected by MRS-2179. Our data reveal that P2Y1receptors are functionally expressed in the coronary circulation and that activation produces coronary vasodilation via an endothelium/nitric oxide-dependent mechanism. Although these receptors represent a critical component of purinergic coronary vasodilation, our findings indicate that P2Y1receptor activation is not required for coronary pressure-flow autoregulation or reactive hyperemia.

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Coronary vascular sympathetic beta-receptor innervation

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.230.6.1569 ◽

1976 ◽

Vol 230 (6) ◽

pp. 1569-1576 ◽

Cited By ~ 53

Author(s):

FN Hamilton ◽

EO Feigl

Keyword(s):

Blood Flow ◽

Coronary Blood Flow ◽

Oxygen Tension ◽

Coronary Sinus ◽

Stellate Ganglion ◽

Coronary Vessels ◽

Coronary Perfusion ◽

Receptor Blockade ◽

Langendorff Preparation ◽

Beta 2

Recent studies indicate that coronary vessels have alpha- and beta-2-adrenergic receptors and that the alpha receptors are functionally innervated. We studied whether the beta-2-vasodilator receptors are functionally innervated, using a dog in situ modified Langendorff preparation with constant coronary perfusion pressure. The beating, nonworking heart and systemic circulation were supported with a pump oxygenator. Stimulation of the left stellate ganglion increased coronary blood flow and decreased coronary sinus oxygen tension from prestimulation control values. After beta-1-receptor blockade (practolol, 10 mg/kg), stellate stimulation decreased coronary blood flow and decreased coronary sinus oxygen tension from prestimulation control values, revealing alpha-receptor vasoconstriction. After the addition of alpha-receptor blockade (Dibozane, 5 mg/kg), stellate stimulation increased coronary blood flow and coronary sinus oxygen tension a small amount from prestimulation values. Finally, after the addition of beta-2-receptor blockade (propranolol, 2 mg/kg), stellate stimulation increased flow and coronary sinus oxygen tension slightly from prestimulation control values. Direct intracoronary injections of isoproterenol, norepinephrine, and epinephrine gave results consistent with the presence of beta-1 myocardial receptors and alpha and beta-2 coronary receptors. We conclude that there is little functional innervation of coronary vascular beta-2 receptors. Intracoronary injections of isoproterenol and epinephrine activated beta-2-receptor coronary vasodilation after beta-1-receptor blockade, but norepinephrine did not.

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Aortic distensibility is associated with both resting and hyperemic coronary blood flow

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00067.2019 ◽

2019 ◽

Vol 317 (4) ◽

pp. H811-H819 ◽

Cited By ~ 3

Author(s):

Adam J. Nelson ◽

Rishi Puri ◽

Stephen J. Nicholls ◽

Benjamin K. Dundon ◽

James D. Richardson ◽

...

Keyword(s):

Blood Flow ◽

Cardiac Magnetic Resonance ◽

Magnetic Resonance ◽

Coronary Blood Flow ◽

Large Body ◽

Aortic Distensibility ◽

Coronary Perfusion ◽

Large Artery ◽

Descending Aorta

A large body of evidence demonstrates an independent association between arterial stiffness and prospective risk of cardiovascular events. A reduction in coronary perfusion is presumed to underscore this association; however, studies confirming this are lacking. This study compared invasive measures of coronary blood flow (CBF) with cardiac magnetic resonance (CMR)-derived aortic distensibility (AD). Following coronary angiography, a Doppler FloWire and infusion microcatheter were advanced into the study vessel. Average peak velocity (APV) was acquired at baseline and following intracoronary adenosine to derive coronary flow velocity reserve (CFVR = hyperemic APV/resting APV) and CBF [π × (diameter)2 × APV × 0.125]. Following angiography, patients underwent CMR to evaluate distensibility at the ascending aorta (AA), proximal descending aorta (PDA) and distal descending aorta (DDA). Fifteen participants (53 ± 13 yr) with minor epicardial disease (maximum stenosis <30%) were enrolled. Resting CBF was 44.1 ± 11.9 mL/min, hyperemic CBF was 143.8 ± 37.4 mL/min, and CFVR was 3.15 ± 0.48. AD was 3.89 ± 1.72·10−3mmHg−1 at the AA, 4.08 ± 1.80·10−3mmHg−1 at the PDA, and 4.42 ± 1.67·10−3mmHg−1 at the DDA. All levels of distensibility correlated with resting CBF ( R2 = 0.350–0.373, P < 0.05), hyperemic CBF ( R2 = 0.453–0.464, P < 0.01), and CFVR ( R2 = 0.442–0.511, P < 0.01). This study demonstrates that hyperemic and, to a lesser extent resting CBF, are significantly associated with measures of aortic stiffness in patients with only minor angiographic disease. These findings provide further in vivo support for the observed prognostic capacity of large artery function in cardiovascular event prediction. NEW & NOTEWORTHY Cardiac magnetic resonance-derived aortic distensibility is associated with invasive measures of coronary blood flow. Large artery function is more strongly correlated with hyperemic than resting blood flow. Increased stiffness may represent a potential target for novel antianginal medications.

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H2O2increases sheep tracheal blood flow, permeability, and vascular response to luminal capsaicin

Journal of Applied Physiology ◽

10.1152/jappl.1997.82.2.621 ◽

1997 ◽

Vol 82 (2) ◽

pp. 621-631 ◽

Cited By ~ 2

Author(s):

U. M. Wells ◽

S. Duneclift ◽

J. G. Widdicombe

Keyword(s):

Blood Flow ◽

Venous Blood ◽

Tracer Uptake ◽

T Test ◽

Airway Epithelial ◽

Vascular Response ◽

Epithelial Damage ◽

Afferent Nerve Endings

Wells, U. M., S. Duneclift, and J. G. Widdicombe.H2O2increases sheep tracheal blood flow, permeability, and vascular response to luminal capsaicin. J. Appl. Physiol. 82(2): 621–631, 1997.—Exogenous hydrogen peroxide (H2O2) causes airway epithelial damage in vitro. We have studied the effects of luminal H2O2in the sheep trachea in vivo on tracheal permeability to low-molecular-weight hydrophilic (technetium-99m-labeled diethylenetriamine pentaacetic acid;99mTc-DTPA) and lipophilic ([14C]antipyrine; [14C]AP) tracers and on the tracheal vascular response to luminal capsaicin, which stimulates afferent nerve endings. A tracheal artery was perfused, and tracheal venous blood was collected. H2O2exposure (10 mM) reduced tracheal potential difference (−42.0 ± 6.4 mV) to zero. It increased arterial and venous flows (56.7 ± 6.1 and 57.3 ± 10.0%, respectively; n = 5, P < 0.01, paired t-test) but not tracheal lymph flow (unstimulated flow 5.0 ± 1.2 μl ⋅ min−1⋅ cm−1, n = 4). During H2O2exposure, permeability to99mTc-DTPA increased from −2.6 to −89.7 × 10−7cm/s ( n = 5, P < 0.05), whereas permeability to [14C]AP (−3,312.6 × 10−7cm/s, n = 4) was not altered significantly (−2,565 × 10−7cm/s). Luminal capsaicin (10 μM) increased tracheal blood flow (10.1 ± 4.1%, n = 5) and decreased venous99mTc-DTPA concentration (−19.7 ± 4.0, P < 0.01), and these effects were significantly greater after epithelial damage (28.1 ± 6.0 and −45.7 ± 4.3%, respectively, P < 0.05, unpaired t-test). Thus H2O2increases the penetration of a hydrophilic tracer into tracheal blood and lymph but has less effect on a lipophilic tracer. It also enhances the effects of luminal capsaicin on blood flow and tracer uptake.

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Effect of platelet depletion and inhibition of platelet cyclooxygenase on C5a-mediated myocardial ischemia

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.267.4.h1288 ◽

1994 ◽

Vol 267 (4) ◽

pp. H1288-H1294 ◽

Cited By ~ 1

Author(s):

B. R. Ito ◽

U. Del Balzo

Keyword(s):

Blood Flow ◽

Coronary Artery ◽

Myocardial Ischemia ◽

Coronary Blood Flow ◽

Venous Blood ◽

Arterial Blood ◽

Anaphylatoxin C5a ◽

Integral Role ◽

Measured Flow

Activation of the complement cascade is involved in the myocardial injury resulting from transient ischemia and reperfusion. We previously showed that the complement anaphylatoxin C5a causes myocardial ischemia in vivo, mediated in part via thromboxane (Tx) A2. In the present study, we assess the role of platelets in the C5a-induced myocardial ischemia and Tx release. The left anterior descending coronary artery of anesthetized pigs was perfused with arterial blood at constant pressure and measured flow (coronary blood flow). Segment function (percent segment shortening) was measured with sonomicrometry, and regional coronary venous blood was sampled and assayed for TxB2 (by radioimmunoassay). We found that the C5a-induced decrease in coronary blood flow and percent segment shortening and the release of Tx were indistinguishable whether the left anterior descending coronary artery bed was perfused with normal arterial blood, with arterial blood obtained from animals depleted of platelets (cyclophosphamide, n = 6), or with arterial blood from aspirin-treated animals (n = 9) in which the platelets were unable to produce Tx. These data demonstrate that platelet-derived Tx does not contribute to the C5a-induced myocardial ischemia and Tx release in this model and that these cells do not play an integral role in this phenomenon.

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Effect of caffeine on theophyliine on cerebral blood flow response to brain activation: In vitro and in vivo studies

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/sj.jcbfm.9591524.0198 ◽

2005 ◽

Vol 25 (1_suppl) ◽

pp. S198-S198

Author(s):

Joseph R Meno ◽

Thien-son K Nguyen ◽

Elise M Jensen ◽

G Alexander West ◽

Leonid Groysman ◽

...

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Brain Activation ◽

In Vivo Studies ◽

Blood Flow Response ◽

Flow Response

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Contribution of extravascular compression to reduction of maximal coronary blood flow

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.262.1.h68 ◽

1992 ◽

Vol 262 (1) ◽

pp. H68-H77

Author(s):

F. L. Abel ◽

R. R. Zhao ◽

R. F. Bond

Keyword(s):

Blood Flow ◽

Coronary Blood Flow ◽

Coronary Flow ◽

Perfusion Pressure ◽

Left Ventricular Pressure ◽

Coronary Perfusion Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Coronary Perfusion ◽

Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

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