Spatial distribution of [14C]-lidocaine and blood flow in transmural and lateral border zones of ischemic canine myocardium

Patterson, Randolph E.; Weintraub, William S.; Halgash, Doris A.; Miao, Joseph; Rogers, John R.; Kupersmith, Joel

doi:10.1016/0002-9149(82)90010-8

Cited by 16 publications

(2 citation statements)

References 39 publications

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“…'19'21 After the dogs were killed, Evans Blue dye was injected into the LAD cannula to stain the region of myocardium supplied by the LAD. Biopsy samples (0.80-1.20 g) were taken 5-10 mm inside the blue-stained ischemic region supplied by the LAD to minimize contamination by normal tissue.1, [19][20][21] The potentially ischemic region supplied by the LAD was identified more precisely by a modification of a microsphere labeling method previously developed'9 and used13 [19][20][21][22] in this laboratory. Briefly, the first set of microspheres was injected into a mixing chamber in the left main coronary perfusion tubing distal to the side arm that perfused the LAD so that the LAD branch did not receive these microspheres ( fig.…”

Section: Microsphere Estimates Of Myocardial Blood Flowmentioning

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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Section: Microsphere Estimates Of Myocardial Blood Flowmentioning

confidence: 99%

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

Patterson¹,

Kirk²

1983

Circulation

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“…This layer may play a role in the genesis of late ventricular tachy-arrhythmias (1,5,9). Collateral blood supply may be responsible for its survival (4,16,17). During acute ischemia diffusion of Oz from the cavity may contribute to survival by causing local continuation of oxidative metabolism and maintenance of local transsarcolemmal ion gradients (6,7).…”

Section: Introductionmentioning

confidence: 99%

Transmural inhomogeneity of extracellular [K+] and pH and myocardial energy metabolism in the isolated rat heart during acute global ischemia; dependence on gaseous environment

et al. 1990

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We investigated in the isolated rat heart the influence of the gas surrounding the globally ischemic heart on transmural inhomogeneity of energy metabolism, extracellular K+ accumulation, and change of extracellular pH. Hearts were made ischemic in 100% N2 (N2-ischemia), 100% O2 (O2-ischemia) or 100% CO2 (CO2-ischemia). We measured: 1) Midmural, subepicardial, and epicardial changes of extracellular [K+] and pH during successive 6-min periods of global ischemia, and 2) content of creatinephosphate (CrP) in consecutive tissue sections of 100 microns, from the subepicardium after 10 min of ischemia. A) During O2-ischemia both extracellular [K+] and change of pH in the subepicardium are significantly less than in the midmyocardium. During N2-ischemia only minor differences exist in [K+] and pH between the subepicardium and the midmyocardium. During CO2-ischemia midmural and subepicardial [K+] are similar to those during N2-ischemia. The midmural change of pH resembles that during N2-ischemia; subepicardial change of pH, however, was slightly larger. Midmural changes in [K+] and pH were not influenced by the nature of the surrounding gas. B) After 10 min of O2-ischemia a gradient of tissue content of CrP extends from the epicardium (CrP about 30 mumoles/g dry weight) to a distance of about 1000 microns (CrP 1 mumoles/g dry weight). In N2- and CO2-ischemia a CrP gradient is absent; CrP is appreciably less than 1 mumoles/g dry weight at any distances from the epicardium. C) We conclude that diffusion of O2 into the myocardium and of CO2 from the myocardium affects transmural gradients of [K+], pH, and energy metabolism during ischemia. Local availability of O2 increases the capacity of the ischemic tissue to generate high energy phosphates and mitigates ischemia-induced changes of transsarcolemmal ion gradients.

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Prolongation of refractoriness and activation time in normal canine ventricular myocardium following bolus administration of lidocaine

Mdrtins

Kelly

1985

American Heart Journal

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Spatial distribution of [14C]-lidocaine and blood flow in transmural and lateral border zones of ischemic canine myocardium

Cited by 16 publications

References 39 publications

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

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

Transmural inhomogeneity of extracellular [K+] and pH and myocardial energy metabolism in the isolated rat heart during acute global ischemia; dependence on gaseous environment

Prolongation of refractoriness and activation time in normal canine ventricular myocardium following bolus administration of lidocaine

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