Collateral conductance changes during a brief coronary occlusion in awake dogs.

Brazzamano, S; Fedor, John M.; Rembert, Judith C.; Greenfield, Joseph C.

doi:10.1161/01.cir.72.1.225

Cited by 9 publications

(6 citation statements)

References 18 publications

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“…Anatomic risk zone size was assessed using autoradiography (Bowney et al 1982) of radiolabeled microspheres injected intraatridly 30 min after coronary occlusion. Since coronary collateral flow is %owest (Brazzamano et al 1985) early after the onset of myocardial ischemia, the hypoperhsed myocardium defined by this technique corresponds closely to the anatomic risk zone. In these experiments, the LAD was severed immediately after cannulation and therefore residual blood flow within the hypoperfused zone was attributed to coronary collateral flow.…”

Section: Methodo Logic Consider~tionsmentioning

confidence: 99%

Influence of low-flow infusion and magnesium on tissue necrosis during regional ischemia in the canine myocardium

Kingma

Qiu²,

Dj³

1992

Can. J. Physiol. Pharmacol.

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Passive intracoronary perfusion of therapeutic agents has been used in the clinical setting to attenuate the effects of brief episodes of myocardial ischemia. The objective of this study was to assess the effects of low-flow coronary infusion with or without Mg2+ on tissue necrosis and cardiac hemodynamics after prolonged regional ischemia. In 33 anesthetized dogs (5 excluded during study), the left anterior descending coronary artery was occluded for 6 h. Dogs were assigned to three groups: the first group (n = 8) was subjected to 6 h coronary occlusion without low-flow perfusion (controls), the second group (n = 10) received a low-flow coronary infusion of Ringer's lactate (Mg(2+)-free), and the third group (n = 10) received a low-flow coronary infusion of Ringer's lactate plus Mg2+ sulfate (15 mM). Tissue necrosis was evaluated using tetrazolium staining and was normalized to the principal baseline predictors of infarct size including anatomic risk zone (microsphere autoradiography) and coronary collateral flow. In control hearts, infarct size comprised 51.1 +/- 4.1% of the risk zone (40.8 +/- 5.1% left ventricular cross-sectional area (LV)). In the Mg(2+)-free and Mg2+ groups, risk zone size was 17.3 +/- 2.2 and 16.8 +/- 1.8% LV (p < 0.05 vs. controls), while infarct size was 23.1 +/- 3.1 and 24.9 +/- 8.1% (p < 0.05 vs. controls), respectively. Coronary collateral flow in the endocardium was similar for all of the experimental groups; however, hearts subjected to ischemia with low-flow perfusion of Ringer's lactate demonstrated significantly higher epicardial coronary collateral flow levels compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Methodo Logic Consider~tionsmentioning

confidence: 99%

Influence of low-flow infusion and magnesium on tissue necrosis during regional ischemia in the canine myocardium

Kingma

Qiu²,

Dj³

1992

Can. J. Physiol. Pharmacol.

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“…The determinants of the magnitude and duration of reactive hyperemia in response to transient myocardial ischemia are multifactorial. 23,6 This vascular effect is due in part to (1) filling of the vascular tree and coronary driving pressure 36,21 myogenic relaxation 37,38 adenosine 30,23,31,19 other unrecognized factors causing vasodilation in response to myocardial metabolic demand (related to the duration of ischemia). 15,[39][40][41]23 The adenosine hypothesis of metabolic coronary flow regulation proposes that blood flow is adjusted to myocardial oxygen requirements by the augmented formation of adenosine.…”

Section: Discussionmentioning

confidence: 99%

“…Regional myocardial blood flow was measured using 11.4Ϯ0.01 m radiolabeled microspheres as described. 19,7,8 After the experiments, the locations of the optodes on the epicardium were marked with pins, and the hearts were removed and fixed in 10% buffered formalin. Two contiguous 1 cm 2 full-thickness sections of myocardium were excised from the tissue region spanning the sites of photon entry and photon reception.…”

Section: Quantitation Of Myocardial Blood Flowmentioning

confidence: 99%

Myocardial Oxygenation in Dogs During Reactive Hyperemia

Parsons¹,

Rembert

Bauman

et al. 1998

J. Biomed. Opt.

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The mechanisms of myocardial oxygenation during reactive hyperemia were studied in the beating heart using continuous near infrared (NIR) spectroscopy. In open chest dogs, NIR spectroscopy was used to monitor brief occlusions of the left anterior descending artery. These occlusions produced a precipitous drop in tissue oxygen stores (tHbO2+MbO2), tissue blood volume, and the oxidation level of mitochondrial cytochrome a,a3. Reperfusion produced a rapid increase in the NIR signals to supranormal levels, followed by gradual return to baseline. When the duration of occlusion was increased from 20 to 120 s, an essentially linear increase was produced in the overshoot areas defined by the NIR signals. Near infrared spectroscopy (NIRS) separated reactive hyperemia into two phases according to the tissue level of deoxyhemoglobin and deoxymyoglobin (tHb+Mb): (1) an early phase during which the tHb+Mb level was supranormal, reflecting enhanced O2 extraction; and (2) a late phase during which the tHb+Mb level was below baseline, reflecting decreased O2 extraction and increased tissue O2 availability. During reactive hyperemia, when O2 availability was maximal by NIR spectroscopy, O2 consumption was elevated but submaximal, indicating that MVO2 was not limited by O2 availability. Cytochrome a,a3 oxidation state also was restored fully. Thus, myocardial oxygenation is highly regulated during reactive hyperemia. Cellular O2 supply and mitochondrial oxidation state are restored early during reactive hyperemia by increased O2 delivery, increases in tissue blood volume and enhanced O2 extraction. © 1998 Society of Photo-Optical Instrumentation Engineers.

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“…An important advantage of this technique compared with postmortem injection of barium gels [13,15] or dyes [24][25][26] is that radiolabeled microspheres can be injected in vivo under physiologic hemodynamic conditions [27]. Since residual coronary blood flow via collateral anastomoses is lowest immediately following coronary occlusion [28] the hypoperfused myocardium defined by this technique corresponds closely to the anatomic risk zone. Since residual coronary blood flow via collateral anastomoses is lowest immediately following coronary occlusion [28] the hypoperfused myocardium defined by this technique corresponds closely to the anatomic risk zone.…”

Section: Methodologic Considerationsmentioning

confidence: 99%

Limitation of myocardial necrosis with verapamil during sustained coronary occlusion in the closed-chest dog

Kingma

Yellon

1988

Cardiovasc Drug Ther

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Studies were undertaken to determine whether cardioprotection afforded by verapamil could be sustained in the dog heart during permanent coronary artery occlusion. In 48 dogs a coronary artery was occluded for 24 or 48 hours using a closed-chest embolization procedure. Dogs were assigned to either untreated control or to verapamil-treated (200 micrograms/kh, intravenous bolus within 5 minutes after coronary occlusion and then 5 micrograms/kg/min as a continuous intravenous infusion for 24 or 48 hours) groups. After 24 or 48 hours of permanent coronary occlusion, tissue necrosis was evaluated using tetrazolium staining and was related to the major baseline predictors of infarct size including anatomic risk zone (radiolabeled microsphere autoradiography) and coronary collateral flow. The correlation between infarct size and subepicardial coronary collateral flow was calculated in untreated control dogs (r = -0.91 and -0.80 for 24 and 48 hour controls, respectively); analysis of covariance indicated that verapamil treatment shifted this relation downward in both the 24- and 48-hour drug treatment groups. The equation of this regression was used to calculate the size of the infarct that would have occurred in treated dogs if drug treatment had not been initiated. The ratio of observed and calculated infarct size provides a "salvage index." In conclusion, verapamil was able to limit the extent of tissue necrosis and this cardioprotection appears to be sustained during 48 hours of permanent coronary occlusion.

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Collateral conductance changes during a brief coronary occlusion in awake dogs.

Cited by 9 publications

References 18 publications

Influence of low-flow infusion and magnesium on tissue necrosis during regional ischemia in the canine myocardium

Influence of low-flow infusion and magnesium on tissue necrosis during regional ischemia in the canine myocardium

Myocardial Oxygenation in Dogs During Reactive Hyperemia

Limitation of myocardial necrosis with verapamil during sustained coronary occlusion in the closed-chest dog

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