The relationship between myocardial blood flow and contraction by myocardial layer in the canine left ventricle during ischemia.

Weintraub, William S.; Hattori, Shigehiko; Agarwal, Jai B.; Bodenheimer, Monty M.; Banka, Vidya S.; Helfant, Richard H.

doi:10.1161/01.res.48.3.430

Cited by 134 publications

(39 citation statements)

References 24 publications

(22 reference statements)

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“…Thus, four separate lines of evidence, including a dose-related decrease in coronary flow, a decrease in intramyocardial pH, ECG ST-T wave changes, and a decrease in LVEF combine to provide very strong evidence that NPY causes coronary vasoconstriction severe enough to produce myocardial ischemia. The finding that the dose-related reduction in CBF at constant heart rate and AP would impair left ventricular function is consistent with the finding of sev- eral studies that a 10-20% decrease in CBF impaired cardiac contraction (32)(33)(34).…”

Section: Resultssupporting

confidence: 88%

Neuropeptide-Y. A peptide found in human coronary arteries constricts primarily small coronary arteries to produce myocardial ischemia in dogs.

Maturi

Greene²,

Speir³

et al. 1989

J. Clin. Invest.

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(LVEF), measured by radionuclide angiography, decreased from 0.52±0.08 to 0.42±0.12 U (n = 5, P < 0.01) during NPY. NPY-induced vasoconstriction was also associated with ST-T wave changes on the electrocardiogram (ECG) in eight of nine other animals (group V). In another group of six dogs (group IV), the change in small vessel resistance accounted for 94% of the increase in total resistance, so that the primary vasoconstrictor effect of NPY was exerted on small coronary arteries. Thus, NPY, a peptide found in human coronary arteries, caused constriction of primarily small coronary arteries that was severe enough to produce myocardial ischemia as determined by ECG ST-T wave changes, and decreases in intramyocardial pH and LVEF in dogs.

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Section: Resultssupporting

confidence: 88%

Neuropeptide-Y. A peptide found in human coronary arteries constricts primarily small coronary arteries to produce myocardial ischemia in dogs.

Maturi

Greene²,

Speir³

et al. 1989

J. Clin. Invest.

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“…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

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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...

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“…1,2 If MBF is Ͼ25% of normal, myocytes can remain alive despite prolonged coronary occlusion 1-3 and lack of function that occurs at this level of MBF. 16,17 Thus, if regions with low MBF that is adequate to sustain myocardial viability can be defined within the RA at the time of coronary occlusion, then the ultimate "worst-case scenario" IS can be predicted early after onset of AMI.…”

Section: Determinants Of Ismentioning

confidence: 99%

Noninvasive Prediction of Ultimate Infarct Size at the Time of Acute Coronary Occlusion Based on the Extent and Magnitude of Collateral-Derived Myocardial Blood Flow

et al. 2001

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Background We hypothesized that by detecting regions with adequate collateral-derived myocardial blood flow (MBF) within the risk area (RA), we could predict ultimate infarct size (IS) at the time of coronary occlusion. Methods and Results Group 1 dogs (n=15) underwent coronary occlusion without reperfusion, whereas group 2 dogs (n=6) underwent both occlusion and reperfusion. RA was measured with aortic root injections of microbubbles. Myocardial contrast echocardiography (MCE) was performed with high mechanical index intermittent harmonic imaging at pulsing intervals (PIs) of <1 to 30 cardiac cycles during an intravenous infusion of microbubbles (Sonozoid). MBF was measured with radiolabeled microspheres, and postmortem tissue staining was used to determine IS. Perfusion defect size (PDS) on MCE varied with the PI and was largest at a PI of 2.6±0.4 seconds, where it correlated well with RA ( r =0.82). PDS was smallest at a PI of ≥10.6±1.5 seconds, where it correlated closely with IS ( r ≥0.92). Areas that underwent necrosis could be identified early after coronary occlusion as having the lowest microvascular flow velocity (β) and MCE-derived MBF (A×β). The results were similar with or without reperfusion. Because of variability in collateral-derived MBF, there was no correlation between RA and ultimate IS ( P =0.37). The extent of regional dysfunction also correlated poorly with IS ( r =0.31). Conclusions MCE can be used immediately after coronary occlusion to define ultimate IS by measuring the magnitude and spatial extent of collateral-derived residual MBF within the RA. Thus, it could help individualize risk and management in acute myocardial infarction.

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The relationship between myocardial blood flow and contraction by myocardial layer in the canine left ventricle during ischemia.

Cited by 134 publications

References 24 publications

Neuropeptide-Y. A peptide found in human coronary arteries constricts primarily small coronary arteries to produce myocardial ischemia in dogs.

Neuropeptide-Y. A peptide found in human coronary arteries constricts primarily small coronary arteries to produce myocardial ischemia in dogs.

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

Noninvasive Prediction of Ultimate Infarct Size at the Time of Acute Coronary Occlusion Based on the Extent and Magnitude of Collateral-Derived Myocardial Blood Flow

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