Search

The primary purpose of this study was to define regional blood flow in dogs with chronic tricuspid regurgitation (TR) in order to determine if the marked hypertrophy of the right atria resulted in compromised myocardial perfusion. Myocardial blood flow (ml/min/gm) was measured with radiolabeled microspheres in eight dogs with TR during rest, moderate exercise (5 dogs), and infusion of adenosine (1 mg/kg/min), an index of minimal vascular resistance. Similar measurements were obtained in eight normal dogs. In TR, the ratio of right atrium (RA) and right ventricle (RV) to body weight was greater than in normal dogs, 77% and 30%, respectively. During rest, flow in the RA appendage was less than in nonappendage region in the normal dogs; no differences were noted in TR dogs, indicating an augmented hemodynamic role of the appendage in TR. Both RA and RV blood flow was greater in TR during rest but no other differences in flow were found between the two groups. Minimum vascular resistance in RV but not RA was slightly increased in TR versus normal. During marked myocyte hypertrophy, the vasculature of RA develops sufficiently to provide the same flow capacity as in the normal heart.

This study was undertaken to determine whether adenosine release from myocardial cells plays a role in coronary reactive and functional vasomotion. Reactive hyperaemic blood flow responses to 10 s complete occlusions and 400 ms diastolic occlusions of the left circumflex coronary artery and to the vasomotor responses to the increased cardiac demand following ventricular extra-activation were examined in a chronic, heart-blocked dog preparation during a control period and following intravenous bolus administration of aminophylline (5 mg X kg-1). Aminophylline administration resulted in a 19% decrease in the blood flow debt repayment ratio of 10 s reactive hyperaemic responses compared with the control period. However, administration of aminophylline had no effect on the coronary vascular response to 400 ms diastolic occlusions or to ventricular extra-activations. These observations indicate that adenosine may play a role in the coronary vascular response to prolonged interventions but that other factors, as yet unidentified, may be implicated in the beat-to-beat regulation of coronary vascular resistance.

A cannulation technique for creating a nonobstructive port in a proximal coronary artery is described. The use of this technique in awake animals allows the blood pressure to be measured in a coronary artery distal to an experimentally produced stenosis. This port can also be used to inject drugs directly into the coronary bed.

Conductance of the coronary collateral circulation during the course of two abrupt circumflex coronary occlusions (pre- and posttreatment with nitroglycerin) was measured in awake dogs approximately 2 wk after collateral vessels were stimulated to develop. The pressure gradient from the central aorta to the distal circumflex coronary artery was measured, and myocardial blood flow was determined by 9-microns radioactive microspheres at 30 s and 4 min after coronary occlusions. Collateral conductance was calculated as mean collateral blood flow divided by the mean aorta-coronary pressure gradient. Before nitroglycerin, collateral conductance increased in all eight dogs from 30 s to 4 min by a mean value of 0.006 +/- 0.003 ml.min-1.g-1.mmHg-1. After nitroglycerin administration, the conductance at 30 s increased from the prenitroglycerin control value of 0.009 +/- 0.008 to 0.014 +/- 0.012 ml.min-1.g-1.mmHg-1, P less than 0.03. The mean change in conductance from 30 s to 4 min postnitroglycerin 0.003 +/- 0.003 ml.min-1.g-1.mmHg-1 was significantly less than during prenitroglycerin (P = 0.01). These data indicate that an increase in conductance during coronary occlusion occurs even in the immature collateral circulation. This effect presumably takes place in the arterial smooth muscle at the origin of the collateral vasculature.

This study was designed to examine local effects of acute cellular injury on regional myocardial blood flow. Studies were carried out in awake dogs chronically prepared with indwelling catheters in the aorta and left atrium and an occluder on the left circumflex coronary artery. Regional myocardial blood flow was measured by using 7-10-mum radioisotope-labeled microspheres after reestablishing inflow to a region subjected to a 2-h complete coronary occlusion. Microspheres were injected 15 s, 15 min, 4 h, and 3 days after reperfusion to assess effects of cell injury at varying intervals after reperfusion. Effects of acute cellular injury on blood flow were assessed by determining the relationship between regional blood flow and the extent of subsequent cellular necrosis measured in multiple tissue samples, weight 1-2 g, from the entire ischemic zone. The extent of cellular necrosis was determined from histological sections of each tissue sample. Prolonged ischemia effected local tissue responses which altered perfusion as a function of the interval after reperfusion and the subsequent extent of myocardial necrosis. Although the net response in each region immediately after reperfusion was vasodilation, the hyperemia in regions which subsequently suffered cellular necrosis was attenuated in direct proportion to the extent of subsequent infarction. Blood flow to acutely injured regions remained equal to, or in excess of, flow to nonischemic regions 15 min after reperfusion, but at 4 h and 3 days after reperfusion, flow was significantly decreased in regions with greater than 50% infarction. Thus, these data indicate that prolonged ischemia initiates tissue responses which progressively reduce myocardial perfusion after reperfusion. These effects on tissue perfusion may result from normal responses to irreversible injury and (or) abnormal responses to reversible and thus, potentially alterable, ischemic injury.

The purpose of this study was to correlate dimensions and transmural blood flow in a segment of myocardium supplied by a coronary artery undergoing gradual closure. Nine adult dogs were instrumented with an electromagnetic flow probe, pneumatic occluder, and an ameroid constrictor on the circumflex coronary artery. Ultrasonic crystals were implanted 10 mm from the external surface of the left ventricle in a segment perfused by the circumflex artery. Regional blood flow was determined with 7- to 10-microns radiolabeled microspheres. Data were collected in the awake state at rest before closure began (control), during partial closure, and immediately after total closure. Seven of the nine animals were studied after occlusion during treadmill exercise. During both partial and total closure at rest the rate and extent of systolic shortening as well as the transmural blood flow were unchanged from control. During treadmill exercise mean flow increased. However, flow was redistributed away from the inner two layers causing deterioration in both the rate and extent of shortening of this segment. These data suggest that, although regional myocardial function and flow can be maintained at rest by the immature canine collateral circulation, these parameters are impaired markedly during augmented flow with exercise.

This study was designed to determine whether coronary vasodilation distal to a flow-limiting coronary artery stenosis could result in redistribution of myocardial blood flow to produce subendocardial underperfusion. Studies were performed in 10 awake dogs chronically prepared with electromagnetic flow-meters and hydraulic occluders on the left circumflex coronary artery. Regional myocardial blood flow was measured using radionuclide-labeled microspheres, 7-10 mum in diameter, injected into the left atrium. A 5(-s) coronary artery occlusion was followed by reactive hyperemia with excess inflow of arterial blood effecting 375+/-20% repayment of the blood flow debt incurred during occlusion. When, after a 5(-s) occlusion, the occluder was only partially released to hold arterial inflow to the preocclusion level for 20 s before complete release, the delayed reactive hyperemia was augmented (mean blood flow repayment = 610+/-45%, P < 0.01). This augmentation of the reactive hyperemia suggested that ischemia was continuing during the interval of coronary vasodilation when coronary inflow was at the preocclusion level. Measurements of regional myocardial blood flow demonstrated that endocardial flow slightly exceeded epicardial flow during control conditions. When arterial inflow was limited to the preocclusion rate during vasodilation after a 5(-s) total coronary artery occlusion, however, flow to the subepicardial myocardium was increased at the expense of underperfusion of the subendocardial myocardium. Thus, in the presence of a flow-limiting proximal coronary artery stenosis, ischemia-induced coronary vasodilation resulted in redistribution of myocardial blood flow with production of subendocardial ischemia in the presence of a net volume of arterial inflow which, if properly distributed, would have been adequate to prevent myocardial ischemia.

Proximal epicardial coronary artery luminal diameters were measured from silicone casts formed in situ in freshly excised hearts under a constant pressure of 100 mm Hg. Twenty-five coronary arteries from 15 normal dogs and 22 coronary arteries in 13 dogs with either chronic pressure or volume overload hypertrophy were studied. Mean left ventricular (LV) body weight ratios were 4.75 +/- 1.01 g/kg in the normal dogs, 8.4 +/- 1.7 g/kg in the pressure-overload dogs, and 6.2 +/- 0.6 g/kg in the volume-overload dogs. The cross-sectional area of the left circumflex (LC) coronary artery was determined at 11 branch sites. The ratio of the area of the branches to the area of the parent vessel was 1.095 +/- 0.105, indicating that the cross-sectional area after a branch point increased. A poor correlation existed between LV mass and coronary artery diameter in both normal and hypertrophy groups for the LC (r = 0.44), the left anterior descending (LAD) (r = 0.63), and the combined LC and LAD (r = 0.52). The mean cross-sectional area of the combined LC and LAD was 0.12 cm2 in the normal group and 0.15 cm2 in the hypertrophy group; this increase was not statistically significant (p = 0.13). When the mean cross-sectional area of the combined vessels was adjusted for heart weight, there was a decrease in the cross-sectional area/100 g of myocardium in the hypertrophy group compared with the control group. These data demonstrate that coronary artery luminal diameter in the dog does not increase commensurately with the increase in mass associated with myocardial hypertrophy.

The effect of 100% oxygen inhalation on regional transmural myocardial blood flow following 45 s of actue total left circumflex coronary artery occlusion was studied in six awake dogs chronically instrumented with a coronary occluder and catheters in the aorta and left atrium. After inhalation of either room air or 100% oxygen for at least 30 min and following the 45-s occlusion, transmural myocardial blood flow was determined with radioactive microspheres (7--10 micrometers). Each dog underwent two occlusions of the left circumflex coronary artery; one during inhalation of rrom air and the other during 100% oxygen. During room air inhalation, mean regional myocardial blood flow to nonischemic, intermediate, and ischemic regions was 0.92 +/- 0.05, 0.51 +/- 0.08, and 0.10 +/- 0.02 ml . min-1 . g-1, respectively. During 100% oxygen administration, flow was significantly diminished in each region to 0.75 +/- 0.04, 0.41 +/- 0.07, and 0.06 +/- 0.01 ml . min-1 . g-1, respectively. Transmural blood flow to each layer was uniformly reduced in all regions. These data indicate that 100% oxygen further reduces myocardial blood flow to ischemic regions.

Phasic coronary flow and transmural myocardial perfusion were studied during coronary artery constriction in 10 dogs with electromagnetic flowmeters and hydraulic occluders on the left circumflex coronary artery. Regional blood flow was estimated using left atrial injections of radionuclide-labeled microspheres 9 micron in diameter. During control conditions, 14+/-0.7% of coronary flow occurred in systole and subendocardial (endo) flow exceeded subepicardial (epi) flow in the region of the posterior papillary muscle (endo/epi=1.16). Immediately following partial inflation of the occluder to reduce coronary inflow 39+/-3%, systolic flow was unchanged while diastolic flow fell 42+/-3%, thereby increasing the portion of flow in systole to 22+/-1.4%. At this time blood flow was reduced nearly uniformly across the wall of the left ventricle. When coronary constriction was maintained for 30 s, an additional shift of flow from diastole to systole occurred (systolic flow=29+/-2.3% of total inflow), and transmural perfusion was redistributed from subendocardium to subepicardium (endo/epi=0.37). This redistribution of flow was accompanied by a fall in coronary pressure distal to the occluder, indicating vasodilation of the distal coronary vasculature.

The aim of this study was to determine whether or not coronary vasoconstriction occurs in response to a transient increase in coronary perfusion pressure. Eleven awake dogs with formalin-induced heart block, chronically instrumented with aortic and left ventricular catheters and left circumflex coronary and aortic electromagnetic flowprobes, were studied at a paced heart rate of 60 beats/min. A transient increase in aortic diastolic pressure of 17.3 +/- 1.5% for 330 +/- 20 ms and of 33.6 +/- 2.2% for 520 +/- 20 ms, via the inflation of an intra-aortic balloon, resulted in an increase in diastolic coronary vascular resistance index in the first response beat of 6 +/- 1% and 11 +/- 1%, respectively. An identical increase in diastolic coronary flow produced by the omission of a single paced beat resulted in no significant change in diastolic coronary vascular resistance index in the first response beat. Thus, the increase in diastolic coronary vascular resistance index following diastolic pressure augmentation is related to the increase in aortic diastolic pressure and not to the increase in diastolic coronary flow. These data are consistent with that of a brief myogenic response.

Pressure-flow measurements were obtained from the vein graft of 57 patients undergoing a single aorta-to-coronary bypass procedure. The flow contour was similar to phasic left coronary artery flow in dogs except for a transient increase during systole possibly related to elongation of the graft. Flow was highest during bypass and decreased to a stable value 30 min after bypass. In 42 patients, flow at this time was 35+/-2 cm(3)/min (mean+/-sem).NO CORRELATIONS WERE DEMONSTRATED BETWEEN FLOW AND THE FOLLOWING: left vs. right grafts, presence or absence of collaterals, total vs. partial block, or the presence or absence of ventricular dyskinesis. In 32 patients, no correlation between these anatomic findings and the presence of reactive hyperemia was demonstrated. In 17 patients, occlusion of the graft for 10 sec resulted in a mean 51.5% flow debt repayment. In nine patients, injection of 0.3 mug of isoproterenol into the graft increased flow from 45+/-6 to 69+/-9 cm(3)/min within 4-7 sec without changes in rate, pressure, time derivative of left ventricular pressure (LV dp/dt), or left ventricular end diastolic pressure (LVEDP). Maximum increases to 87+/-10 cm(3)/min occurred 12-20 sec after injection with concomitant changes in these parameters. Intravenous infusion of norepinephrine did not change vascular resistance, whereas phenylephrine did. In six patients, injection of 0.2 mug of norepinephrine into the graft decreased flow from 49+/-6 to 25+/-5 cm(3)/min within 5-8 sec. Intravenous infusion of 0.15 mg of nitroglycerin decreased coronary vascular resistance from 2.7+/-0.4 to 2.3+/-0.3 mm Hg/cm(3) per min. In five patients, 0.12 mg of nitroglycerin injected into the graft increased flow from 46+/-7 to 71+/-13 cm(3)/min and lasted 20-40 sec.