Total Coronary Blood Flow Research Articles

Myocardial protection during prolonged aortic cross-clamping: Comparison of blood and crystalloid cardioplegia

We compared the ability of blood and crystalloid cardioplegia to protect the myocardium during prolonged arrest. Twelve dogs underwent 180 minutes of continuous arrest. Group I (six dogs) received 750 ml of blood cardioplegic solution (potassium chloride 30 mEq/L) initially and every 30 minutes. Group II (six dogs) received an identical amount of crystalloid cardioplegic solution (potassium chloride 30 mEq, methylprednisolone 1 gm, and 50% dextrose in water 16 ml/L of electrolyte solution). Temperature was 10 degrees C and pH 8.0 in both groups. Studies of myocardial biochemistry, physiology, and ultrastructure were completed before arrest and 30 minutes after normothermic reperfusion. Biopsy specimens for determination of adenosine triphosphate were obtained before, during, and after the arrest interval. Regional myocardial blood flow, total coronary blood flow, and myocardial oxygen consumption were statistically unchanged in Group I (p greater than 0.05). Total coronary blood flow rose 196% +/- 49% in Group II (p less than 0.005), and left ventricular endocardial/epicardial flow ratio fell significantly in this group from 1.51 +/- 0.18 to 0.8 +/- 0.09, p less than 0.01 (mean +/- standard error of the mean. The rise in myocardial oxygen consumption was not significant in this group (34% +/- 36%, p greater than 0.05). Ventricular function and compliance were statistically unchanged in both groups. In Group II, adenosine triphosphate fell 18% +/- 3.4% (p less than 0.005) after 30 minutes of reperfusion; it was unchanged in Group I. Ultrastructural appearance in both groups correlated with these changes. We conclude that blood cardioplegia offers several distinct advantages over crystalloid cardioplegia during prolonged arrest.

Changes in total and transmural coronary blood flow induced by ethanol.

We studied the effects of ethanol on total coronary resistance and on the resistance across the left ventricular wall in the isolated empty beating heart of the dog. The coronaries were perfused with homologous fresh blood, thermoregulated at 37 degrees C and equilibrated with a gas mixture of O2 (95%) and CO2 (5%). Coronary flow distribution was measured with radioactive microspheres. In 22 experiments in which coronary flow was kept constant, ethanol (calculated concentration in the perfusing blood, 2.9 +/- 0.2 g . litre-1) produced a significant decrease in perfusion pressure (from 14.2 +/- 0.5 to 11.9 +/- 0.5 kPa, P less than 0.005). This decrease in perfusion pressure was not caused by metabolic autoregulation since ethanol produced a decrease in the oxygen consumption of the heart (2.19 +/- 0.43 to 1.62 +/- 0.31 cm3 . min-1 . 100 g-1, P less than 0.05). It was not caused, either, by a decrease in extravascular compression since ethanol did not produce any further decrease in perfusion pressure after maximal dilatation of the coronaries with dipyridamole. In experiments performed either at constant coronary flow or at constant perfusion pressure, flow across the left ventricular wall was redistributed towards the subendocardium during the vasodilatory effect of ethanol. Since in our experimental conditions, changes in the neurohumoral, metabolic and cardiac mechanical factors that influence coronary flow were discarded, this study demonstrates a direct vasodilatory effect of ethanol on the coronary vessels with a redistribution of flow towards the subendocardium.

Myocardial Metabolism and Hemodynamic Responses to Halothane or Morphine Anesthesia for Coronary Artery Surgery

Eighteen patients having coronary artery bypass grafts were randomly anesthetized with morphine (1 mg/kg) or halothane and oxygen. Central and peripheral pressures were measured serially, plus cardiac output and total coronary sinus blood flow, both by thermodilution catheters, starting before induction of anesthesia and continuing until completion of sternotomy. No significant differences in hemodynamic responses were seen between the two anesthetic techniques during induction: blood pressure and peripheral vascular resistance decreased significantly, but not cardiac output or coronary flow. Myocardial oxygen consumption decreased significantly with induction as oxygen content of coronary sinus blood increased, indicating preservation of oxygen balance. Heart rate and blood pressure increased after sternotomy in the patients given morphine, with the myocardium producing lactate in two of six patients and with nitroprusside being required in four patients to decrease arterial pressure. Halothane-oxygen anesthesia effectively controlled autonomic responses to sternotomy, although one of 12 patients had myocardial lactate production at that time. Neither rate-pressure product or ST segment changes were useful predictors of the ratio between myocardial oxygen consumption and supply. Myocardial oxygen balance can be maintained in coronary patients before cardiopulmonary bypass if pulse rate and blood pressure are kept at less than awake levels.

Effects of enflurane-nitrous oxide anaesthesia and surgical stimulation on regional coronary haemodynamics in a patient with LAD bypass graft.

Central and regional coronary haemodynamics were studied in a patient with a left anterior descending artery (LAD) graft and angiographically visible collaterals from a normal right coronary artery. A three-thermistor thermodilution catheter was used for measuring total coronary sinus blood flow and great cardiac venous blood flow, the latter being a good representative of blood flow through the LAD. Enflurane-nitrous oxide anaesthesia induced marked coronary vasodilatation and redistribution of blood flow from the LAD to other areas draining into the coronary sinus. The most likely mechanism for the redistribution of blood flow in this patient was steal via the collaterals between the LAD and the right coronary artery. During surgical stimulation, the flow through the LAD was further compromised due to pronounced coronary vasoconstriction, probably mediated by catecholamine release.

Myocardial Metabolism and Hemodynamic Responses to Halothane or Morphine Anesthesia for Coronary Artery Surgery

Eighteen patients having coronary artery bypass grafts were randomly anesthetized with morphine (1 mg/kg) or halothane and oxygen. Central and peripheral pressures were measured serially, plus cardiac output and total coronary sinus blood flow, both by thermodilution catheters, starting before induction of anesthesia and continuing until completion of sternotomy. No significant differences in hemodynamic responses were seen between the two anesthetic techniques during induction: blood pressure and peripheral vascular resistance decreased significantly, but not cardiac output or coronary flow. Myocardial oxygen consumption decreased significantly with induction as oxygen content of coronary sinus blood increased, indicating preservation of oxygen balance. Heart rate and blood pressure increased after sternotomy in the patients given morphine, with the myocardium producing lactate in two of six patients and with nitroprusside being required in four patients to decrease arterial pressure. Halothane-oxygen anesthesia effectively controlled autonomic responses to sternotomy, although one of 12 patients had myocardial lactate production at that time. Neither rate-pressure product or ST segment changes were useful predictors of the ratio between myocardial oxygen consumption and supply. Myocardial oxygen balance can be maintained in coronary patients before cardiopulmonary bypass if pulse rate and blood pressure are kept at less than awake levels.

Effects of calcium on the coronary and systemic circulation in patients after coronary surgery.

Nine patients were studied three hours after aorto-coronary bypass. Before anaesthesia a radial arterial cannula was inserted and a thermodilution catheter placed into the pulmonary artery by fluoroscopy. A special thermodilution catheter was manipulated into the coronary sinus. Haemodynamic measurements were made plus cardiac output and coronary sinus blood flow. Content of oxygen and lactate in arterial and coronary sinus blood was determined. Series of measurements were done before and after 1 gm of CaCl2 given intravenously over 15 minutes. Calcium increased cardiac index and arterial pressure but not systemic vascular resistance. Total coronary sinus blood flow did not change, nor did myocardial oxygen consumption or coronary sinus oxygen content. Content of lactate in arterial and coronary sinus blood was unaltered and lactate extraction by the heart continued, in eight of nine patients. The improved haemodynamics were accomplished without inordinate risk to global ventricular energy metabolism.

Phasic coronary blood flow velocity in intramural and epicardial coronary arteries.

Knowledge concerning phasic coronary blood flow is based primarily on measurements obtained from epicardial coronary arteries, which, in part, function as capacitors. If present, epicardial capacitance effects could obscure the dynamic nature of phasic intramyocardial perfusion. To analyze this effect of epicardial capacitance, we simultaneously measured coronary blood flow velocity in an epicardial artery (left anterior descending) and an intramural artery (septal) in open-chest, anesthetized dogs. During control conditions, the percentage of total coronary blood flow velocity occurring during diastole per cardiac cycle was significantly greater (P less than 0.05) in the septal artery (92%) than in the left anterior descending artery (75%). Furthermore, blood flow velocity during mid-systole in the septal artery was retrograde (-7.2%), whereas blood flow velocity at this time was antegrade in the left anterior descending artery (+3.5%). Blood flow velocity measurements from small epicardial arteries just before they penetrated into the myocardium revealed a phasic pattern similar to that of the septal artery. This suggests that the phasic blood velocity pattern in penetrating coronary arteries, in general, is different than that in large epicardial arteries. During vasodilation following nitroglycerin, dipyridamole, or a 20-second occlusion of the left main coronary artery, the retrograde component of mid-systolic blood velocity persisted in the septal artery, despite large increases (300-400%) in the mid-systolic antegrade component of blood flow velocity in the left anterior descending artery. These qualitative and quantitative differences in phasic blood flow velocity between intramural and large epicardial arteries are best reconciled by postulating the existence of a significant coronary capacitor.

Effects of new calcium channel blocker of niludipine on the coronary hemodynamics, diastolic properties, and metabolic responses to tachycardia stress in patients with coronary disease.

A new calcium channel blocker, niludipine, was administered intravenously to nine patients with coronary artery disease in order to investigate its effects on left ventricular systolic and diastolic function, coronary sinus blood flow, and myocardial lactate metabolism. Coronary sinus pacing was performed in all patients and produced angina in six patients. Niludipine increased the resting heart rate from 75+/-3 beats/min (mean+/-SEM) to 82+/-3 (NS) and decreased the left ventricular systolic pressure from 155+/-4.7 mm Hg to 134+/-2.8 (p less than 0.05). Coronary sinus blood flow increased by 9%(NS). During pacing after niludipine, clinical improvement occurred in the six patients who had initially experienced angina. The extent of ischemic ST segment depression was decreased (-1.56+/-0.27 mm to -0.78+/-0.38, p less than 0.02) and myocardial lactate metabolism was improved. When pacing was terminated, niludipine suppressed the elevation of left ventricular end-diastolic pressure compared to pretreatment values (16.2+/-2.5 mm Hg vs 8.5+/-0.9, p less than 0.05) and decreased the left ventricular time constant T(26.4+/-3.6 msec to 20.2+/-2.4 p less than 0.05). The results suggest that niludipine appears to be beneficial in reducing systolic and diastolic work of the left ventricle during pacing induced angina without a significant change in total coronary sinus blood flow. Niludipine appears to have less of a hypotensive and reflex tachycardic effect than nifedipine.

Myocardial protection by coronary washout during global ischemic cardiac arrest

The effect of intermittent coronary washout (WO) during global ischemic cardiac arrest (ICA) was evaluated in isolated blood perfused dog hearts undergoing 90 min normothermic ICA and 90 min reperfusion. WO consisted of infusion of 100 ml normothermic dog plasma at 100 mm Hg every 10 min during ICA. Systolic and diastolic pressures were measured at constant volume with a left ventricular balloon. Coronary blood flow (CBF) was measured, and transmyocardial oxygen, lactate, and glucose differences were calculated. Adenosine triphosphate (ATP), creatine phosphate (CP), calcium (Ca 2+), glycogen, and water content were measured from left ventricular biopsies. During 90 min of WO, hearts extracted glucose (15 ± 4 mg/g dry wt LV) and lost lactate (90 ± 5 μmole/g dry wt LV). ATP and CP were significantly depressed at arrest in both groups although WO resulted in significantly higher levels of ATP and CP. CP returned to control levels at 90 min reperfusion in the WO group but remained depressed in the ICA group. Calcium accumulation was greater in hearts with ICA. With reperfusion, both ICA and WO groups demonstrated early hyperemia and rapid lactate washout. There were no differences in total CBF, AVO 2, MOV 2, and myocardial glycogen or water content. Systolic performance was equally depressed in both groups at 90 min of reperfusion. Diastolic compliance, while still impaired, was better preserved in WO when measured in the arrested heart at 90 min ICA ( P < 0.01) and in the contracting heart after 90 min reperfusion ( P < 0.02). Normothermic coronary washout during 90 min of normothermic ischemic arrest without cardioplegic agents produces improved ventricular compliance and energy metabolism, and reduces myocardial calcium accumulation.

Effects of continuous nitroglycerin infusion on acute myocardial ischemia in dogs

The effects of a continuous infusion of nitroglycerin (NTG) were evaluated by hemodynamic measurements and measurements of regional myocardial blood flow (RMBF) in dogs on right heart bypass with left anterior descending coronary artery ligation. NTG infusion which decreased afterload, mean aortic pressure (MAP) decreased from 100 to 85 mm Hg, thus also decreasing coronary perfusion pressure) resulted in an 11.8% increase in total coronary blood flow (CBF), a 19.1% decrease in coronary vascular resistance index (CVRI), and a 21.7% decrease in myocardial oxygen consumption (MV̇O 2). When MAP was returned to the control level (100 mm Hg) with continuing infusion of NTG, CBF increased 49.1%, and CVRI decreased by 23.4% compared to the pre-NTG ischemic state. Regional myocardial blood flow (microsphere technique) to ischemic tissue at the border of the infarct remained stable with NTG infusion despite decreased MAP, in contrast to the significant fall in RMBF in this region with decreased MAP in the control group without NTG. When MAP was elevated back to pre-NTG levels, an 18.6% increase in RMBF to the border of the infarct was seen compared to an insignificant change in RMBF in untreated (control) animals. These data are consistent with the concept that under conditions of regional myocardial ischemia, coronary blood flow to the “border zone” (ischemic myocardium) is maintained or enhanced by NTG, even when coronary perfusion pressure is modestly reduced.

Myocardial flow distribution. II : Empty beating heart, ventricular fibrillation and cardiac arrest.

Myocardial oxygen consumption (MVO2) and coronary blood flow (CBF) distribution were studied in 21 isolated, metabolically supported dog hearts. Measurements of MVO2 and CBF distribution were carried out in three different experimental conditions : empty beating heart (EBH), ventricular fibrillation (VF) and high potassium-induced cardiac arrest (CA). MVO2 was approximately the same in EBH and VF (4.09 +/- 0.77 and 4.28 +/- 0.68 ml O2 min-1 100 g-1 respectively), and significantly lower in the group with CA (2.40 +/- 0.18 ml O2 min-1 100 g-1, P less than 0.05). Total CBF showed no significant differences among the three groups (84 +/- 7 ml/min in EBH; 78 +/- 7 ml/min in VF and 83 +/- 7 ml/min in CA). Subendocardial CBF per unit of tissue mass was significantly lower in hearts with VF (0.43 +/- 0.01 ml/min-1 g-1, P less than 0.05) when tested against the other two groups of experiments (0.69 +/- 0.03 ml min-1 g-1 in EBH and 0.65 +/- +/- 0.04 ml min-1 g-1 in CA). This was also reflected in the endo/epi ratio, that was significantly lower in VF (1.41 +/- 0.07, P less than 0.05) with respect to the other two groups (2 +/- 0.09 in EBH and 2.21 +/- 0.07 in CA). From data presented here we can conclude that cardioplegia, even in absence of hypothermia, is a method that will assure myocardial protection providing : (1) a lower subendocardial MVO2; (2) a higher subendocardial CBF, which helps for a prompt recovery during reperfusion.

Coronary blood flow in conscious miniature swine during +GZ acceleration stress.

One of the factors determining tolerance to +GZ acceleration may be the ability to maintain adequate coronary blood flow. Consequently, the purpose of these studies was to determine the effect of acute exposure (60 s) to several levels of positive acceleration (+GZ) on total and regional coronary blood flow in conscious adult miniature swine. Blood flow was measured with the radiolabeled microsphere technique in chronically instrumented miniature swine during 60-s exposures to accelerations of +3 GZ, +5 GZ, or +7 GZ with anti-G suit support. All levels of acceleration stress caused two- to threefold increases in coronary blood flow. The regional distribution of coronary blood flow during +GZ was similar to that under resting control conditions as long as aortic diastolic pressure was maintained. All left ventricular endocardial/epicardial flow ratios were significantly greater than one, except in two animals, during exposure to +7 GZ. These were the only animals to have aortic diastolic pressures less than 100 Torr during +GZ stress. These studies indicate that, if an animal is able to compensate and maintain a cardiovascular steady State, coronary blood flow will remain adequate for myocardial needs. However, if decompensation occurs and aortic diastolic pressure falls below a critical value, subendocardial blood flow may become inadequate.

Relationship of ischemic contracture to high energy phosphate content and mitochondrial function in hypertrophied myocardium

Relationship of ischemic contracture to high energy phosphate content and mitochondrial function in hypertrophied myocardium

Effects of extracorporeal circulation on cardiac performance and coronary blood flow (total and regional). A study of differences arising from pre-existent left ventricular load and anoxic arrest.

It was researched how the ECC affects on cardiac performance and the total and regional coronary blood flow, using two groups of dogs with a hypertrophied heart and a non-hypertrophied heart, each group of which was further divided into two subgroups depending on whether the intermittent 40 mins. anoxic arrest was applied or not. Cardiac performance before and 60 mins. after cessation of ECC were compared each other. Coronary hemodynamics was studied before, during (immediately before and after anoxic arrest), and 60 mins. after cessation of ECC, using 15 +/- 5 diameter radioactive microspheres. 1) In the group of a non-hypertrophied heart, no obvious changes of cardiac performance were seen before and after ECC. The total coronary blood flow increased after ECC than before. Though the regional coronary blood flow pattern showed no differences in this group except only immediately after anoxic arrest, when the regional blood flow into the right ventricle, inner and middle layers of the left ventricle increased. 2) In the group of a hypertrophied heart, cardiac performance decreased after ECC, and further significant decrease was observed in the subgroup of anoxic arrest. No significant changes of the total coronary blood flow were observed before and after ECC in this group, even when compared with that in the group of a non-hypertrophied group. However, the increase of blood flow to the right ventricle, inner and middle layers of the left ventricle immediately after anoxic arrest was not observed, that was seen in the group of a nonhypertrophied heart. 3) It follows that the decrease of cardiac performance after ECC in the group of a hypertrophied heart is not due to the changes of the total and regional coronary blood flow. It is considered that the difference of the regional coronary blood flow pattern changes immediately after anoxic arrest between the non-hypertrophied heart group and hypertrophied group may cause the different changes of cardiac performance before and after ECC between the two groups. This consideration should be more justified by evaluating not only coronary hemodynamics but also the relationship between cardiac metabolic needs and the regional coronary blood flow.

Myocardial protection by intermittent perfusion with cardioplegic solution versus intermittent coronary perfusion with cold blood

The myocardial protection provided by cardioplegic solution using buffered, isosmotic potassium (30 mEq. per liter) was compared with intermittent cold coronary perfusion for 2 hours of aortic cross-clamping in dogs. The cardioplegic solution (Group CS) or cold blood (Group CB) was infused every 15 minutes through a cooling coil to reduce the perfusate temperature to 5 degrees C. Myocardial function after 30 minutes of reperfusion and rewarming was reduced in Group CB with a significant reduction in peak systolic pressure at a left ventricular (LV) balloon volume of 20 ml. and a significant reduction of dp/dt. In contrast, in Group CS, LV function was unchanged from the base-line period. LV compliance also was significantly reduced in Group CB while being unchanged in Group CS. Myocardial extravascular water content, obtained by dessication, was significantly higher in Group CB than in Group CS, which may explain the reduction in compliance. Electron microscopy showed normal ultrastructure in Group CS but extracellular edema in Group CB. Total coronary blood flow showed a sustained increase during reperfusion in both groups. Oxygen consumption rose with rewarming to base-line levels in both groups, whereas lactate and pyruvate consumption was reduced in both groups, particularly Group CB. Cardioplegic solution thus appears to be superior to the intermittent perfusion of cold blood for myocardial protection. The addition of potassium arrest, by markedly reducing myocardial metabolism, improves the protection afforded by cold blood perfusion alone.

Coronary blood flow in experimental canine left ventricular hypertrophy.

To determine whether left ventricular hypertrophy [LVH] altered total and regional coronary blood flow, we inflated a balloon around the ascending aorta of nine dogs; six acute and six sham-operated dogs were controls. After 6 weeks, all dogs were studied with an open chest under anesthesia; the balloons were deflated. There was moderate LVH as shown by increased left ventricular weight and fiber diameter. At rest there were no major differences of coronary flow or resistance per gram of muscle. With maximal coronary vasodilation due to adenosine or carbochrome, mean coronary vascular resistance was 84% higher in LVH than in normal hearts; with isoproterenol, resistance was 54% higher in LVH. These changes were similar in right and left ventricles. Minimal coronary resistance at end diastole also was higher in LVH--64% and 94% for the two sets of vasodilators, respectively. There were no significant differences in capillary or large vessel proportional volumes in LVH and control dogs, but arterial capacity could not be estimated. The raised minimal coronary resistance suggests the possibility that, with stress, coronary flow, especially to subendocardial muscle, might be inappropriate and perhaps cause ischemic damage. However, the changes noted might have been due to coronary arterial responses to raised coronary pressures rather than to hypertrophy itself.

Coronary blood flow in physically trained rats.

Coronary blood flow was measured using labelled microspheres (15 micrometer diameter) in sedentary and endurance trained rats during hypoxaemic conditions designed to develop coronary dilatation (Pa,O2 6.0 to 6.7 kPa [45 to 60 mmHg]). Rats that were trained for 12 to 18 weeks (26.8 m per minute, 15% gradient, 1 hour per day) had a significantly greater coronary blood flow conductance (15.3 +/- 1.0 mm3.min-1.kPa-1 aortic diastolic pressure, n = 20) than sedentary animals (10.8 +/- 0.9, n = 19). Even though cardiac hypertrophy (17%) was found in the trained animals, this increase in perfused mass accounted for only one-third of the increase in total coronary blood flow. Thus, there was a greater coronary blood flow per unit mass of the myocardium in the trained rats.

Myocardial oxygen delivery after experimental hemorrhagic shock.

The two components of myocardial oxygen delivery, coronary blood flow to capillaries and diffusion from capillaries to mitochondria, were studied in six dogs, (1) prior to shock, (2) after three hours of hemorrhage shock at a mean systemic arterial pressure of 40 torr, (3) after reinfusion of shed blood, and (4) during the irreversible late posttransfusion stage. There was a maldistribution of left ventricular coronary flow during late shock consistent with subendocardial ischemia. Cardiac performance was significantly impaired after resuscitation and all dogs became irreversible. Total and regional left ventricular coronary blood flow and myocardial oxygen delivery to capillaries were significantly greater than preshock values in (3) but not different from preshock values in (4). However, the myocardial oxygen diffusion area to distance ratio was significantly lower than preshock values in (3), and slightly lower in (4). These data suggest that myocardial oxygen diffusion may be impaired in the early post transfusion period, (3). Accordingly, the probable etiology of left ventricular dysfunction and possibly irreversibility after resuscitation from hemorrhagic shock is subendocardial ischemia during shock with either post-resuscitation impairment of myocardial oxygen diffusion, or in cellular oxygen utilization, or both.

Effects of methoxamine on the coronary circulation during cardiopulmonary bypass

Effects of perfusion pressure augmentation with methoxamine on transmural distribution and adequacy of coronary blood flow during cardiopulmonary bypass were investigated. Flow in normal, nonworking canine hearts was measured with tracer microspheres and electromagnetic flow probes while heart rate, myocardial oxygen consumption, left ventricular contractility and epicardial ST-segment stability were monitored. Measurements during normotensive cardiopulmonary bypass were compared with values during intraoperative hypotension and subsequent normotension achieved following methoxamine infusion. Total and regional coronary blood flow returned to levels not different from normotensive controls after methoxamine infusion with a redistribution of flow to the subendocardium. We conclude that elevating perfusion pressure during cardiopulmonary bypass with methoxamine infusion increases total coronary and subendocardial blood flow by means of peripheral and selective subepicardial alpha adrenergic vasoconstriction.

Regional distribution of coronary blood flow during left ventriculography in anesthetized dogs.

Changes in total and regional left coronary blood flow in response to ventriculography were studied using electromagnetic and microsphere techniques. Correlation of coronary flows by these methods showed excellent agreement (r = 0.947). Ventriculography produced a characteristic triphasic response in total flow and in endocardial/epicardial perfusion ratios. Changes in coronary flow can be explained as a result of hypotension and vasodilatation.