Relationship between blood flow to ischemic regions and extent of myocardial infarction. Serial measurement of blood flow to ischemic regions in dogs.

Rivas, F.; Cobb, Frederick R.; Bache, Robert J.; Greenfield, Joseph C.

doi:10.1161/01.res.38.5.439

Cited by 219 publications

(66 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the other hand, Schaper et al '7 and Bishop et al'0 found that epicardial flows increased only mildly, while flow to the endocardial core remained unchanged. As in our study, all these investigators9' 10,16 found that collateral flow measured a few minutes before the dogs were sacrificed was much higher than early postocclusion flow. Recently, an average 20% loss of radioactive microspheres has been found to occur differentially from necrotic myocardium beyond 24 hours after occlusion.…”

Section: Discussionsupporting

confidence: 80%

Myocardial infarction in the conscious dog: three-dimensional mapping of infarct, collateral flow and region at risk.

Jugdutt¹,

Hutchins²,

Bulkley³

et al. 1979

Circulation

201

View full text Add to dashboard Cite

SUMMARY Myocardial infarcts were examined in dogs to determine the spatial distribution of infarction in the region at risk and the relation between infarction and collateral blood flow. Permanent occlusion of the left circumflex (LC) coronary artery at a constant site was made in 27 conscious dogs that were sacrificed 2 days later. The anatomic region at risk was defined by postmortem coronary arteriography as the volume of the occluded LC coronary bed. The masses of the left ventricle (LV), infarct (I) and risk region (R) were calculated from planimetered areas of weighed "bread-loaf" sections of LV. Infarct size was directly related to the mass of the risk region (I = 0.53 R -9.87; r = 0.97;p < 0.001). There was no infarction when R was less than about 20 g or 20% of the LV. The infarcts were mainly subendocardial and tapered from base to apex of the LV; 34% of the risk region became infarcted at the base compared with 22% at the apex. In all dogs, a significant rim of noninfarcted myocardium was identified at lateral aspects of the risk region, even at the endocardial surface. Using 9-u radioactive microspheres, initial postocclusion flow at the margin of the infarct, but well within the risk region, was higher than at the center, and outer flows were higher than inner flows. Postocclusion flow was even higher in the noninfarcted rim within the risk region, but was still significantly less than flow to normal, nonrisk areas. Collateral flows throughout the risk region increased during the first hour after occlusion, and were even higher at 2 days. Epicardially and laterally within the anatomic risk region there is a substantial amount of tissue that does not infarct despite initially reduced blood flow.THE CONCEPT of infarct size limitation implies the existence of a functional "border zone" in the ischemic region. Although myocardium located in the "border zone" is at risk because of reduced blood flow, it has sufficient flow for immediate survival. Subsequent increases in collateral flow occurring either naturally or after drug treatment provide for ultimate survival of this tissue. In contrast, other areas of the ischemic region have such low flow that necrosis occurs despite therapeutic efforts.Our goal was to characterize the spatial geometry of myocardial necrosis relative to the anatomic region at jeopardy and the distribution of collateral blood flow after permanent left circumflex (LC) coronary occlusion in untreated conscious dogs. We measured the amount and spatial distribution of myocardium that was located in the bed of the occluded coronary artery but survived infarction over a 2-day period. The amount of noninfarcted myocardium in the occluded bed in untreated dogs served as a baseline for measuring the effectiveness of infarct-limiting therapies. MethodsThirty-two mongrel dogs that weighed an average of 20 kg (range 18-23 kg) were instrumented under general anesthesia through a left lateral thoracotomy. A plastic snare was placed around the LC coronary artery just distal to the first margina...

show abstract

Section: Discussionsupporting

confidence: 80%

Myocardial infarction in the conscious dog: three-dimensional mapping of infarct, collateral flow and region at risk.

Jugdutt¹,

Hutchins²,

Bulkley³

et al. 1979

Circulation

201

View full text Add to dashboard Cite

show abstract

“…This degree of decreased collateral flow is quantitatively related to further decreases in regional left ventricular contraction24 25 and to further increases in myocardial infarction size. '19 [25][26][27][28][29] The mechanism of coronary steal when there are no stenoses proximal to the origin of the collaterals can be inferred to be the presence of some resistance in the large coronary arteries between the left main and the point of origin of the collaterals. Figure 4 intercepts the x-axis at -0.12 mm Hg ml-l*min, indicating that 12.5% of the total resting coronary vascular resistance value would have to be subtracted from the native coronary circulation between the left main and the origin of the collaterals to abolish the coronary steal.…”

Section: Discussionmentioning

confidence: 99%

Coronary steal mechanisms in dogs with one-vessel occlusion and other arteries normal.

Patterson¹,

Kirk²

1983

Circulation

View full text Add to dashboard Cite

SUMMARY The objectives of the present study were to determine whether coronary steal can occur in one-vessel coronary occlusion when other arteries are normally patent, and to determine the quantitative effect on the magnitude of coronary steal of a graded partial stenosis in the coronary circulation proximal to the origin of the collaterals. In 10 dogs, occlusion of the left anterior descending coronary artery (LAD) was induced and perfusion of the left main coronary artery was maintained with a special servo pump at constant pressure (measured distal to the cannula tip) during intracoronary adenosine infusion. Adenosine increased left main coronary blood flow from 85 + 15 to 229 42 ml/min, while mean pressure in the left main coronary artery was held constant at 83 + 3 mm Hg (mean + SD). Systemic hemodynamics did not change, but three indexes of collateral function decreased: peripheral LAD coronary pressure, from 14.0 2.7 to 12.5 2.9 mm Hg (p < 0.005); retrograde LAD flow, from 3.2 + 2.5 to 2.4 + 2.6 ml/min (p < 0.001);and microsphere blood flow to ischemic myocardium, from 0.055 + 0.029 to 0.040 ± 0.031 ml min-l g-1 (p < 0.03). Next, we added the resistance of the Gregg cannula to the perfusion system, i.e., in the same dogs we regulated constant pressure in the tubing proximal to the cannula tip. This added resistance created a 4.5-mm Hg pressure gradient (multivessel occlusion) and a larger drop in retrograde LAD flow (23% vs 36%, p < 0.05). Because a screwclamp caused graded increments in resistance of the left main coronary perfusion system and the resting pressure gradient, there was a linear increase in the magnitude of coronary steal (r = 0.71). Thus, arteriolar vasodilators increased flow velocity, which led to decreased pressure at the origin of the collaterals because there was some resistance in the native coronary circulation between the left main coronary artery and the origin of the collaterals (12% of total resting resistance). Further increments in vascular resistance proximal to the origin of the collaterals caused a linear increase in the magnitude of coronary steal. plied by a single partially occluded coronary artery.8-0 These studies and another study" showed associated decreases in aortic pressures, however, so they could not demonstrate coronary steal in the absence of partial occlusions on other coronary arteries. If the coronary vasodilator agent decreases aortic pressure, this fall in coronary perfusion pressure, per se, could explain the decreased collateral blood flow without invoking the specific mechanism described by Fam and McGregor. 2A previous study from this laboratory found that i.v. adenosine decreased collateral myocardial blood flow more than aortic pressure, yielding a decreased calculated value of conductance. The decreased value of conductance in that study did not prove the occurrence of coronary steal because the relationship between aortic pressure and collateral blood flow may not always be linear over the entire '4 range of aortic pressures. VASODILATOR-INDUC...

show abstract

“…The hearts were removed, the flowmeter probe and sonar crystals dissected free, and each heart fixed in 10% buffered formalin for at least 24 h. The atria, right ventricle, aorta, and large epicardial blood vessels were dissected from the left ventricle and discarded. The left ventricle was sectioned into four transverse rings as described (20). The rings were divided radially into six anatomic sections corresponding to the anterior papillary muscle, anterior free wall, septum, posterior free wall, posterior papillary muscle, and lateral free wall.…”

Section: Introductionmentioning

confidence: 99%

Effects of Nitroglycerin and Propranolol on the Distribution of Transmural Myocardial Blood Flow during Ischemia in the Absence of Hemodynamic Changes in the Unanesthetized Dog

Swain¹,

Parker²,

McHale³

et al. 1979

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T Chronically instrumented awake dogs were used to study the effects of nitroglycerin and propranolol on the transmural distribution ofmyocardial blood flow during transient ischemia. Studies were carried out 7-14 d after implantation of an electromagnetic flowmeter probe and balloon occluder on the left circumflex coronary artery, placement of epicardial minor axis sonar crystals, and implantation of left atrial, left ventricular, and aortic catheters. The occluder was inflated to completely interrupt flow for 10 s followed by partial release to reestablish flow at 60% of the preocclusion level. During this partial release, which served as the control for the study, regional myocardial blood flow was measured with 7-to 10-,um radioactive microspheres. After control measurements, seven dogs were given nitroglycerin (0.4 mg i.v.) and eight dogs propranolol (0.2 mg/kg i.v.). 5 min later the occlusion and partial release sequence was repeated, and regional myocardial blood flow was measured when heart rate, aortic and left ventricular end-diastolic pressure, and minor axis diameter were unchanged from control values.The data values were selected so that total flow to the ischemic region during partial release after nitroglycerin or propranolol administration was not significantly different from flow during the control partial release. After nitroglycerin administration, endocardial flow (endo) in the ischemic region increased from 0.46+0.07 to 0.59+0.06 ml/min per g (P < 0.006); epicardial flow

show abstract

Relationship between blood flow to ischemic regions and extent of myocardial infarction. Serial measurement of blood flow to ischemic regions in dogs.

Cited by 219 publications

References 30 publications

Myocardial infarction in the conscious dog: three-dimensional mapping of infarct, collateral flow and region at risk.

Myocardial infarction in the conscious dog: three-dimensional mapping of infarct, collateral flow and region at risk.

Coronary steal mechanisms in dogs with one-vessel occlusion and other arteries normal.

Effects of Nitroglycerin and Propranolol on the Distribution of Transmural Myocardial Blood Flow during Ischemia in the Absence of Hemodynamic Changes in the Unanesthetized Dog

Contact Info

Product

Resources

About