Coronary Blood Volume Research Articles

Dynamics of coronary adjustment to a change in heart rate in the anaesthetized goat.

1. We have previously shown that steady-state coronary flow during auto-regulation and metabolic rate changes is predicted by a mathematically expressed theory which assigns control of coronary vascular resistance to tissue PO2. Our present purpose was to test the applicability of this theory to the non-steady state as exemplified by a sudden step change in heart rate. 2. The theory predicted that the response time of change of resistance in these circumstances would be slower with constant-flow perfusion of the coronary bed than with constant-pressure perfusion, and that with constant-pressure perfusion only, the rate of adaption of resistance would be dependent on the level of pressure used. 3. These predictions were tested in open-chest goats with cannulation of the left main coronary artery and perfusion with alternately constant pressure or constant flow. Sudden step changes in heart rate were induced by pacing to induce rapid transients in myocardial metabolic rate. 4. The half-time of subsequent change in perfusion pressure-flow ratio, which in the dynamical state is not equal to resistance, was 15.7 +/- 0.4 s (mean +/- S.E.M.), which was statistically shorter than for constant flow (22.2 +/- 0.5 s, P less than 0.001). 5. The half-time of subsequent change in perfusion pressure-flow ratio with constant-pressure perfusion was 14.4 +/- 0.6 s at low pressure and 17.0 +/- 0.6 s at high pressure (P less than 0.001). 6. The results differed from those predicted by the theory, in that the changes described above were preceded by a rapid (5 s) step change in pressure-flow ratio, up with an increase in heart rate and down with a decrease in heart rate. We postulated that this was a mechanical effect due to greater compression of the coronary microvasculature with more frequent contractions. 7. To test this hypothesis, we measured changes in coronary blood volume by integrating the difference between arterial inflow and venous outflow. These experiments showed a decrease in coronary blood volume with heart rate increase and vice versa. 8. Abolition of autoregulation and metabolic regulation was achieved with maximum vasodilatation of the coronary bed with adenosine. A sudden switch in heart rate then produced the initial step change in pressure-flow ratio, but not the subsequent adaptation over 13-25 s. This confirmed that the former effect is attributable to a passive mechanical mechanism.

Evidence of myocardial ischaemia in patients with chest pain syndromes and normal coronary angiograms.

Patients with chest pain syndromes and normal coronary angiograms were studied with a new set of methods that included thermodilution coronary sinus blood flow and coronary dye dilution curves with special computer analysis, oxygen and lactate determinations, thallium scannings, atrial pacing and dipyridamole tests. The following observations and conclusions were made: Patients with cardiac hypertrophy have a reduced circulating coronary blood volume in relation to the left ventricular mass; this may play a role in patients' vulnerability to ischaemia. During pacing-induced angina a significant imbalance between oxygen supply and demand can be demonstrated in patients with "syndrome X". Dipyridamole-induced chest pain as a result of myocardial ischaemia seems to occur in patients with normal coronary arteries. Marked ischaemia evidenced by a regional intensity reduction of 25% or more in thallium scans results in a significant increase in coronary volume. This is obviously due to mobilization of reserve vasculature as a response to ischaemia. A reduction in the ratio of myocardial oxygen supply to demand was demonstrated even in connection with milder defects, the regional intensity reduction being as low as 12.5%.

Pressure-induced changes in coronary flow and volume during reperfusion in canine hearts.

1. The effects of coronary artery occlusion and reperfusion on pressure-induced changes in coronary blood flow and blood volume were investigated. 2. The left anterior descending coronary artery (LAD) of canine hearts was cannulated and perfused independently with arterial blood by a controlled pressure system. LAD flow was measured continuously with an electromagnetic flowmeter and LAD volume was measured in the steady-state by indicator dilution. Measurements were made with perfusion pressure at 100 mmHg (control), 50 mmHg, and 150 mmHg before and after 2 h of LAD occlusion followed by 2 h of reperfusion. 3. With perfusion pressure at control, occlusion-reperfusion reduced LAD flow 19%, but had no significant effect on LAD volume. 4. Steady-state LAD flow and volume always varied directly with changes in perfusion pressure; after occlusion-reperfusion these variations were accentuated. 5. Analysis of transient and steady-state flow responses indicated diminished capability of arteriolar resistance vessels for active, autoregulatory adjustments in lumenal calibre following changes in perfusion pressure. 6. The results of this study demonstrate that occlusion-reperfusion causes derangement to pressure-volume and pressure-flow control mechanisms in the coronary circulation.

Small vessel and total coronary blood volume during intracoronary adenosine.

The effect of a maximally dilating dose of intracoronary adenosine on total (CBV) and small-vessel blood volume (MSVBV, an index of open-capillary density), hematocrit (MSVHct), and related parameters of O2 supply-demand ratio was examined in left ventricular myocardium of anesthetized open-chest dogs. CBV was measured from washout of 51Cr-labeled red blood cells (RBC) and MSVBV and MSVHct from contents of 51Cr-RBC and plasma label, either 131I-serum albumin or 59Fe-siderophilin, in samples of myocardium and blood. Coronary blood flow (CBF) was measured by electromagnetic flowmeter. Myocardial oxygen consumption (MVO2) was computed with the Fick equation. Myocardial oxygen tension (MPO2) was measured with bare-tipped platinum electrodes. Adenosine raised CBV 75%, CBF, 574%, and MPO2 122%, but did not affect significantly MSVBV, MSVHct, or MVO2. These results indicate that infusion of adenosine into a coronary artery perfused at constant pressure causes relaxation of smooth muscle of arteriolar resistance vessels and of other vessels larger than 100 micrometers diam, but not that of the precapillary sphincters. This may be explained by the opposing action of increased MPO2 on the sphincters when flow increases. MSVHct was consistently much less than large-vessel Hct. This warrants combined use of red blood cell and plasma labels for accurate measurements of MSVBV.

Hemodynamic responses initiated by coronary stretch receptors with special reference to coronary arteriography

Hyperosmotic solutions, of substances including polyvinylpyrrolidone, sodium or methylglucamine diatrizoate, sodium chloride, glucose, sucrose and mannitol, produced transient sinus bradycardia and a fall in arterial blood pressure when injected directly into the coronary arteries of the intact anesthetized dog. The same changes occurred with acute coronary venous hypertension induced by coronary sinus obstruction with a balloon catheter but not with injections of isosmotic saline solutions into the coronary artery or of the various substances into the aortic root, left ventricle or pulmonary artery. The bradycardia was prevented by atropine. Concomitant with the fall in blood pressure, femoral arterial blood flow increased and maximal rate of rise of left ventricular pressure ( dp dt ) decreased even when the bradycardia was prevented by pacing. In most experiments this reduction in maximal dp dt could be abolished by beta adrenergic blockade. All responses were abolished by bilateral vagotomy with the exception of the fall in pressure and maximal dp dt produced by the radiopaque media or 5 percent sodium chloride. These agents exert a direct myocardial depressant action. Simultaneously determined indicator-dilution curves using 125I-albumin and 131I-diatrizoate verified that the diatrizoate molecule leaves the circulation during its passage through the coronary vascular bed. Calculations derived from these curves demonstrated that injection of nonlabeled diatrizoate produces a large increase in coronary blood volume and flow. In 2 patients the bradycardia occurring with coronary injections of radiopaque media could be prevented by atropine. Sodium diatrizoate (50 percent Hypaque ®) usually produced more intense bradycardia than did methylglucamine diatrizoate (60 percent Renografin ®). The depressor effects of coronary injections of hyperosmotic solutions or coronary sinus obstruction result from activation of a reflex arc originating from stretch receptors in the coronary capillaries or small veins. The afferent limb of the reflex is bilaterally represented in the cervical vagosympathetic trunks of the dog. The efferent effects characterized in these experiments were increased vagal firing to the sinus node, decreased activity of adrenergic fibers to peripheral vascular alpha receptors and probably diminished adrenergic firing to beta receptors in the ventricular myocardium.

CIRCULATING CORONARY BLOOD VOLUME.

The circulating coronary blood volume was calculated in dogs from independent determinations of the rate of coronary blood flow and the mean circulation time from the root of the aorta to the mouth of the coronary sinus. The average value was 14.2±2.2 ml/100 g lean myocardium. Coronary blood volume was inversely related to the heart rate, which ranged from 126 to 212 beats/min, but was not correlated with other hemodynamic variables within the relatively narrow range of values present.

Messung der Durchblutung und der Blutfüllung des coronaren Gefäßbettes mit der Teststoffinjektionsmethode am narkotisierten Hund bei geschlossenem Thorax

The results show, that with the testsubstance dilution method the outflow of the coronary sinus can be estimated on anaesthetized closed chest dogs. In addition it is possible to measure the mean circulation time in the coronary vascular bed and the coronary blood volume. Coronary flow is not impeded mechanically by the method. Measurements can be done frequently (1 measurement/min) and in an unlimited number.

Influence of coronary perfusion and myocardial edema on pressure-volume diagram of left ventricle.

Pressure-volume diagrams of paced, isolated hearts were derived from isovolumic contractions and auxotonic contractions (simultaneous changes of pressure and volume). Coronary perfusion, fluid accumulation in heart muscle, and left ventricular volume and pressure were measured and controlled. Pressure-volume diagrams from isovolumic and auxotonic contractions were virtually identical in the same heart and were influenced by the same factors to a similar degree. At equal diastolic volumes the magnitude of systolic, as well as of diastolic pressures, and the occurrence of a systolic descending limb were directly related to coronary perfusion pressure. At equal diastolic volumes, other factors being constant, myocardial edema did not influence the contractile strength (i.e., maximum contractile tension development) of a ventricle, but did decrease its distensibility (i.e., increase diastolic pressure) in proportion to fluid accumulation. Myocardial water content and coronary factors (coronary arterial and venous pressures, coronary blood volume and flow) therefore constitute intrinsic mechanisms which can regulate the performance of a ventricle by changing its contractile strength, its distensibility, or both. The effects of coronary factors and of myocardial edema on the distensibility of a ventricle are sufficient in magnitude to explain hemodynamic abnormalities which characterize certain types of congestive heart failure.

Physiological factors influencing coronary blood volume in isolated dog hearts.

Measurements of the weight and of the residual blood in an isolated, perfused heart permitted investigation of factors which influence coronary blood volume. Coronary blood volume was a near linear function of coronary arterial pressure between 30 and 125 mm Hg and was also linearly related to coronary flow in fresh preparations. For each 1 mm Hg change of mean coronary perfusion pressure, a corresponding change of the coronary blood volume occurred, amounting to about 100 mg blood/100 gm perfused heart. Decreases of contractile strength or heart rate caused reversible increases of the coronary blood volume.

Influence of coronary artery pressure upon myocardial elasticity.

The marked intensification of experimental left ventricular failure by veno-arterial pumping which was seen in earlier experiments suggested changes of myocardial elasticity as a mechanism. Two experimental procedures were therefore applied here, in which the pressure in the coronary arteries and veins could be varied at will, where the left ventricle was distended by an air-filled balloon, and where the coronary tree did not communicate with the left ventricle. Changes of the coronary arterial or venous pressures were accompanied by homodirectional changes of the left ventricular diastolic pressure which were of large magnitude and which could not be explained by unobserved blood flow into the left ventricle or by other factors. The inverse relationship between coronary vascular pressures and myocardial distensibility was probably caused by the increasing volume of blood which was retained in the coronary arteries and veins when the coronary arterial or venous pressures were increased. This passive increase in coronary blood volume (turgor) must have changed the resiliency of the coronary tree. The changed elastic properties of the coronary tree then resulted in a change of the elastic properties of the heart.

On the theory of the indicator-dilution method for measurement of blood flow and volume.

On the theory of the indicator-dilution method for measurement of blood flow and volume.