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Relaxation of potassium-depolarized canine, bovine and porcine large coronary arteries by nitroglycerin, chromonar and two dihydropyridine calcium antagonists.
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Determination of the chromonar hydrochloride metabolite in urine using derivative spectroscopy.
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Treatment of angina pectoris with chromonar hydrochloride.
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Antianginal effects of chromonar. A combined investigation.
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Metabolism and excretion of chromonar and its metabolite in dog and man.
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Differential effects of chromonar and nitroglycerin on intramyocardial oxygen tension.
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Nitroglycerin and chromonar on small-vessel blood content of the ventricular walls.
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[Clinical study of carbocromen (chromonar), new coronary vasodilator].
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Contrasting effects of pharmacologic vasodilation on true collateral and overlap perfusion in ischemic myocardium.
The effects of chromonar (3.5 and 7.0 mg/kg i.v.), a selective coronary vasodilator, on true collateral blood flow and overlap flow (noncollateral perfusion due to overlapping end arteries of adjacent coronary vessels) were measured independently in anesthetized dogs following acute coronary occlusion. Collateral flow in the ischemic zone was significantly (P less than 0.05) reduced by chromonar in a dose-related manner while transmural overlap flow was increased. True collateral flow was distributed primarily to the subepicardium and chromonar produced a significant reduction in both subepicardial and subendocardial perfusion. Overlap perfusion was distributed equally across the left ventricular wall and chromonar increased perfusion to both subepicardium and subendocardium. The results indicate that there are two independent sources of perfusion of ischemic myocardium and that pharmacologic vasodilation with chromonar produces opposite effects on each: a steal of true collateral blood flow and an increase in overlap perfusion.
Effects of acute atrial fibrillation on the vasodilator reserve of the canine atrium.
Acute atrial fibrillation appreciably alters atrial physiology by increasing atrial blood flow and atrial oxygen consumption. To determine the effects of atrial fibrillation on atrial vasodilator reserve atrial fibrillation was produced in dogs by electrical atrial stimulation. Reactive hyperaemic responses were measured using Doppler crystals fixed to the sinus node artery and to an adjacent right ventricular branch artery during sinus rhythm, after 20 minutes of atrial fibrillation, and after systemic administration of chromonar (a potent coronary dilator) during atrial fibrillation. During sinus rhythm the peak to resting blood flow velocity ratio after a 20 s occlusion of the sinus node artery was 3.2(1) (mean(SEM)). A 20 s occlusion of a right ventricular branch artery during sinus rhythm resulted in a significantly larger response (5.9(0.7). The repayment to debt area ratio in response to a 20 s occlusion was 1.1(0.2) for the sinus node artery but 3.9(1.0) for a right ventricular branch. During atrial fibrillation the peak to resting velocity ratio was substantially decreased in the sinus node artery (2.3(0.6)) but was not significantly changed in the right ventricular branch (4.4(0.6)). Atrial fibrillation plus chromonar abolished reactive hyperaemia in both the sinus node artery and the right ventricular branch vessel. Right atrial blood flow (microspheres) increased from 45(4) in sinus rhythm to 106(19) ml X min-1 X 100 g-1 in atrial fibrillation and to 208(22) ml X min-1 X 100 g-1 after chromonar administration during atrial fibrillation. Thus the quantitative characteristics of coronary reactive hyperaemia in the right atrium were substantially different from those in the right ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)
Separation of overlap and collateral perfusion of ischemic canine myocardium: important considerations in the analysis of vasodilator-induced coronary steal.
Coronary steal was studied in dogs with a left anterior descending (LAD) coronary artery occlusion by use of a special technique to exclude contamination from overlapping circulations with true collateral blood flow. Different degrees of vasodilation in nonischemic myocardium were produced by the selective coronary dilator, chromonar, at a constant heart rate and aortic blood pressure. A map of the ischemic area was made, and criteria used to identify ischemic tissue samples included: (1) all samples within the LAD perfusion area, as defined by a dye technique; (2) tissue samples with blood flows less than 25% normal area flow; (3) samples from within the central ischemic zone; and (4) tissue samples with overlap blood flow less than 2% normal area flow. When criteria 1 and 2 were used to identify ischemic myocardium, chromonar (5 and 7.5 mg/kg, i.v.) produced no change in ischemic blood flow. On the other hand, when tissue samples from the central ischemic zone or those which had less than 2% overlap flow (criteria 3 and 4) were used to identify ischemic myocardium, chromonar produced a dose-related decrease (p less than 0.01) in transmural collateral perfusion (25 +/- 4 and 33 +/- +/- 5;33 +/- 3 and 41 +/- 6%, respectively). Other indices of collateral function, peripheral coronary pressure (23 +/- 4 and 25 +/- 3%), retrograde flow (20 +/- 3 and 26 +/- 4%), and retrograde conductance (21 +/- 4 and 30 +/- 4%), also decreased significantly. These results indicate that moderate to maximal coronary vasodilation produces a true coronary steal in the absence of changes in aortic pressure and heart rate. In addition, these data demonstrate that significant amounts of overlap flow are contained in superior, inferior, and lateral borders of the ischemic zone, and that strict criteria to identify ischemic myocardium are needed when studying the effect of drugs on true coronary collateral blood flow.
Microregional blood flow and high energy phosphates under conditions of high O2 supply in left ventricular subendocardium.
Blood flow and high energy phosphate (HEP) content were determined simultaneously in multiple microregions of the left ventricular subendocardium in 49 anaesthetized open-chest rabbits, to determine the relationship between the parameters during high O2 supply with hypercapnia and chromonar treatment. ATP and CP content were quantitated in quick-frozen hearts by fluorometry in 1-2 mg sites where perfusion was measured by H2 clearance employing bare-tipped platinum electrodes. Both hypercapnia and chromonar elevated subendocardial tissue perfusion approximately 30% and O2 supply 45% above control. Blood flow was normally distributed with either treatment, but was more homogeneous with hypercapnia. Neither treatment altered absolute levels of either HEP, but the variance of ATP was less than control. CP distribution was normal in both treatments. There was no significant linear correlation between blood flow and HEP under hypercapnia or chromonar treatment. We conclude that tissue HEP content is a variable not only dependent on O2 supply and blood flow, but also on the size of the ATP and CP pool and the energy demand of the local microregion. The variability of ATP in microregions of the rabbit subendocardium is reduced under conditions of high O2 supply.
Transmural gradient of coronary blood flow following dihydropyridine calcium antagonists and other vasodilator drugs.
The effects of the dihydropyridine calcium antagonists, nifedipine, nitrendipine and FR 7534 on the transmural distribution of coronary blood flow (endo/epi) were compared to the structurally unrelated calcium antagonists, verapamil and diltiazem and to the non-calcium antagonist vasodilator drugs, chromonar and dipyridamole in anesthetized dogs. The increase in transmural blood flow produced by diltiazem, verapamil, chromonar and dipyridamole was equally distributed between subendocardium and subepicardium (no change in endo/epi). On the other hand, the increase in myocardial blood flow produced by the dihydropyridine calcium antagonists nifedipine, nitrendipine and FR 7534 was relatively selective for subepicardial regions resulting in a significant and dose-related decrease in endo/epi. This unusual effect of the dihydropyridine calcium antagonists to produce a redistribution of flow within normal myocardium was not shared by the non-dihydropyridine calcium antagonists or non-calcium antagonist vasodilators studied. The redistribution of flow was not related to changes in heart rate, aortic blood pressure or to the level of total coronary blood flow. Such an effect may be related to the distribution of dihydropyridine receptors across the left ventricular wall, antagonism of the action of adenosine, or changes in regional intramyocardial tissue pressure and extravascular resistance.
Coronary steal-induced increase in myocardial infarct size after pharmacologic coronary vasodilation.
This study was performed to determine if maximal coronary arterial vasodilation of nonischemic areas would produce an increase in myocardial infarct size through a "steal" of collateral flow from an ischemic region. Myocardial infarction was produced by a 2 hour occlusion and reperfusion of the distal left anterior descending coronary artery in anesthetized dogs. Five minutes after occlusion, 7 dogs were given saline solution, and in 12 dogs the coronary vasodilator chromonar (8 mg/kg, intravenously) was administered. Chromonar produced a significant increase (p less than 0.05) in blood flow to nonischemic regions and a concomitant decrease in flow to ischemic areas. Associated with these changes in flow was an elevation in total release and peak plasma creatine kinase compared with values in saline-treated control dogs. Myocardial infarct size determined with nitroblue tetrazolium stanining was significantly increased (p less than 0.05). These demonstarte that maximal coronary vasodilation of nonischemic areas can result in an extension of myocardial infarction by a steal of collateral flow away from the ischemic region.
Thyroxine-induced hypertrophy of the rabbit heart. Effect on regional oxygen extraction, flow, and oxygen consumption.
The effects of the administration of 0.5 or 1 mg/kg of 1-thyroxine for 3 or 16 days were studied in 55 New Zealand white rabbits. Heart size was 29% above control after 16 days of 1-thyroxine, despite lower body weights. In an anesthetized open-chest animal, regional microspectro-photometric observations of small arteries and veins to determine oxygen extraction were combined with regional blood flow measurements using radioactive microspheres to determine regional oxygen consumption by the Fick principle. Vascular flow reserves were studied through measurement of blood flow after the administration of chromonar HCl, 10 mg/kg. Myocardial oxygen consumption was, respectively, 2.4 and 3.8 times control after 3 and 16 days of 1-thyroxine. This was accompanied by significant increases in both coronary blood flow and oxygen extraction. In control, oxygen extraction and consumption were higher in the subendocardial region compared to the subepicardial area. No significant regional differences were found in flow, oxygen extraction, or consumption after 1-thyroxine administration. Chromonar increased coronary blood flow 2.8 times in the control animals, but did not significantly increase flow or decrease vascular resistance in the rabbits given 1-thyroxine. Adenosine increased coronary blood flow 3.5 times in the control animals but only 2.2 times in animals given 1-thyroxine for 3 days. Animals given 1-thyroxine had hypertrophied hearts with increased oxygen consumption, markedly increased flow, and increased oxygen extraction but without regional left ventricular differences.
Transmural coronary flow reserve patterns in dogs.
To investigate transmural variations in coronary flow reserve, we studied 20 anesthetized dogs with a Gregg cannula in the left main coronary artery. In 11 dogs, radionuclide-labeled microspheres were injected over a range of perfusion pressures in the control state and during maximal coronary vasodilation produced with chromonar or adenosine. In another nine dogs, control, reactive hyperemic, and adenosine-vasodilated flows were compared at the same perfusion pressures. Adenosine dilated vessels more than did reactive hyperemia, which in turn vasodilated more than did hypoperfusion. Adenosine or chromonar vasodilated more than did hypoperfusion alone in all layers of the heart at perfusion pressures as low as 30 mmHg (P less than 0.05). This effect was greatest in the subepicardium and least in the subendocardium and varied with perfusion pressure (P less than 0.05). Subendocardial-to-subepicardial flow ratios declined with diminishing perfusion pressure despite the fact that flow reserve was present in all layers. We conclude that exhaustion of flow reserve is not the mechanism by which subendocardial ischemia occurs.
Measurement of regional myocardial blood flow in dogs by ultrafast CT.
We measured blood flow within each of eight segments of the left ventricular myocardium in dogs by an Ultrafast CT scanner. The results were compared with flow determined by radiolabeled microspheres. Computed tomography (CT) flow was measured by an intravenous injection of nonionic contrast agent done simultaneously with the left atrial injection of microspheres. We calculated flow from the CT data by obtaining CT number versus time curves for regions of interest in the myocardium and by using a formula that related flow to both the time and value of the peak enhancement. Measurements were obtained in five dogs at rest and during hyperperfusion induced by chromonar. Based on 169 regional measurements, the Ultrafast CT and microsphere-determined flows correlated moderately (r = 0.68) over a range of 0.4 to 8 mL/min/g. However, when the data were divided into resting and hyperperfusion (ie, 20 to 30 minutes after the injection of the chromonar) states, a significant (P less than .001) increase in regional flow was determined from the CT measurements. The conclusion was that Ultrafast CT can distinguish between low and high myocardial flow states in dogs and has considerable potential for evaluating coronary flow reserve.