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During Angina Induced by Rapid Atrial Pacing

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During Angina Induced by Rapid Atrial Pacing Release of Adenosine from Human Hearts during Angina Induced by Rapid Atrial Pacing ARnURm C. Fox, GEORGE E. REED, EPmum GLAsSMAN, ALUmm J. KALAN, and BmWiARA B. SnK From the Departments of Medicine and Surgery, New York University School of Medicine, 550 First Avenue, New York 10016 A B S T R A C T This study was designed to determine INTRODUCTION whether human hearts release adenosine, a possible reg- In human hearts with restricted coronary circulation, ulator of coronary flow, during temporary myocardial temporary increases in oxygen needs can produce angina ischemia and, if so, to examine the mechanisms involved. pectoris, changes in electrical repolarization, and the Release of adenosine from canine hearts had been re- release of lactate and potassium into coronary venous ported during reactive hyperemia following brief coro- blood (1). In animals, temporary myocardial ischemia nary occlusion, and we initially confirmed this observa- has also been shown to cause release of inorganic phos- tion in six dogs hearts. Angina was then produced in 15 phate (2) as well as adenosine, inosine, and hypo- patients with anginal syndrome and severe coronary xanthine (3). The release of adenosine is of particular atherosclerosis by rapid atrial pacing during diagnostic interest, both as an index of the effects of ischemia on studies. In 13 of these patients, adenosine appeared in myocardial purines and as a possible regulator of coro- coronary sinus blood, at a mean level of 40 nmol/100 ml nary blood flow. Adenosine is a potent coronary vaso- blood (SE = ±9). In 11 of these 13, adenosine was not dilator, has a rich pool of precursors within myocardial detectable in control or recovery samples; when mea- cells, readily crosses cell membranes, is quickly de- sured, there was concomitant production of lactate and graded, is present in the well oxygenated myocardium at minimal leakage of K+, but no significant release of cre- low basal levels, and increases during ischemia (3, 4, atine phosphokinase, lactic acid dehydrogenase, creatine, 5). The nucleotide precursors of adenosine are more or Na+. potent vasodilators (6), but do not diffuse 'freely from There was no detectable release of adenosine by hearts normal cells; the degradation products of adenosine, during pacing or exercise in three control groups of pa- inosine and hypoxanthine, are diffusible but do not in- tients: nine with anginal syndrome and severe coronary crease coronary flow (3). atherosclerosis who did not develop angina or produce Adenosine appeared in coronary sinus (CS) 1 blood lactate during rapid pacing, five with normal coronaries when reactive hyperemia was induced in canine hearts and no myocardial disease, and three with normal coro- by transient coronary occlusion (3). Although there is naries but with left ventricular failure. no direct evidence that adenosine increases coronary The results indicate that human hearts release sig- flow in man, dipyridamole, which inhibits the uptake nificant amounts of adenosine during severe regional and degradation of adenosine by cells, is a potent coro- myocardial ischemia and anaerobic metabolism. Adeno- nary vasodilator (7). sine release might provide a useful supplementary index In these studies, we initially confirmed the observation of the early effects of ischemia on myocardial metabo- that, in dogs, adenosine appears in CS blood after tran- lism, and might influence regional coronary flow during sient ischemia, and then we examined an analogous situ- or after angina pectoris. ation in man. In patients with severe coronary athero- A preliminary abstract of this work appeared in: 1971. 1Abbreviations used in this paper: c-AMP, cyclic 3'5'- Circulation. 44(Suppl. II): 65. AMP; CPK, creatine phosphokinase; Cr, creatine; CS, coro- Received for publication 3 August 1973 and in revised nary sinus; LDH, lactic acid dehydrogenase; Pi, inorganic form 29 November 1973. phosphate. The Journal of Clinical Investigation Volume 53 May 1974* 1447-1457 1447 sclerosis, we found that adenosine was released in sig- pacing during hemodynamic studies and caused similar in- nificant amounts when angina and concomitant lactate creases in heart rate. For measurement of lactate before, during, and after production were induced by rapid atrial pacing. angina, samples of blood from the CS and the femoral artery were simultaneously collected into cold 6% perchloric METHODS acid. Small samples of CS blood were also collected for measurement of CPK, LDH, Cr, cyclic 3',5'-AMP (c- Studies in dogs AMP), inorganic phosphate (Pi), Nat, and K+. Studies were preliminary and were designed to perfect techniques and to confirm earlier work (3). CS blood (75- Analytic techniques 140 ml) was collected from open-chest animals during con- Rapid processing of blood samples was essential to trol periods and during evident reactive hyperemia induced minimize uptake of adenosine by red cells. The procedure by transient tightening of coronary arterial ligatures. CS was modified from that described by Rubio, Berne, and blood was also collected after production of myocardial in- Katori (3). The diluted samples of chilled heparinized farction, to demonstrate that rises in serum creatine phos- blood were centrifuged at 40C for 5 min at 1,800g. The phokinase (CPK), lactic acid dehydrogenase (LDH), and supernates were heated at 1000 C for 10 min to denature creatine (Cr) could be detected by our methods. proteins, which were separated at 24,500g. Samples had to be concentrated considerably because of the low concen- Studies in man trations of adenosine in human blood. The supernate and Studies were made during routine diagnostic cardiac washings of the precipitates were ultrafiltered through a catheterizations, performed with the informed consent of Diaflo UM-2 membrane (Amicon Corp., Lexington, Mass.) the patients. These studies did not interfere with, nor un- to remove material over mol wt 1,000. This improved ad- duly delay, requisite procedures. Four groups were studied, sorption of the nucleosides contained in 90 ml of blood onto group A: patients with histories of angina pectoris and 2 g of highly purified Norite A charcoal. The charcoal with significant (at least 75%) obstruction of one or more was collected on a no. 40 Whatman filter and washed with major coronary arteries, as demonstrated by selective an- water until free of salts; nucleosides were eluted by shak- giography, who developed definite angina pectoris on pac- ing in 3% NH40H-60% ethanol for 10 h at 370C. The ing; group B: patients with similar histories and similar charcoal was washed with ethanol to remove all material degrees of coronary artery disease who developed no an- absorbing at 260 nm, and fine particles were removed by gina or only questionable chest discomfort on pacing; filtration through a Millipore membrane. Filtrates were group C: patients with no significant coronary artery dis- flash-evaporated to dryness and redissolved in 1 or 2 ml ease or hemodynamic abnormalities who were catheterized of 50% ethanol at pH 10. Either all or one half of this because of questionable angina or heart disease; group D: was streaked on thin layer (0/5 mm) plates of the ion ex- patients with no coronary artery disease who were in change resin, Selectacel-P (Schleicher and Schuell, Inc., severe heart failure. Keene, N. H.), and developed at 4°C with 15% ethanol at Coronary venous blood was obtained through a no. 7 pH 7.0. Separated nucleosides were identified under UV pacing catheter positioned in the CS at 2 cm beyond the light by their migrations relative to known standards and orifice. Six samples of 15 ml were rapidly drawn into were eluted. Eluates were lyophilized in test tubes and syringes containing 25 ml of chilled heparinized saline. An- redissolved in H20 or in 0.05 N NaOH for hypoxanthine. giographic procedures followed sampling of blood, since The identity and purity of each eluted streak was confirmed even small amounts of the contrast medium, meglumine on a second plate by development with 25% ethanol at pH 10. diatrizoate, interfered with separation of nucleosides by When eluates showed background absorbance which inter- chromatography. Femoral arterial blood was sampled fered with the spectrophotometric assay, unidentified blood through cannulas inserted by the Seldinger technique. chromagens were further removed by a second development. The ventricular rate was accelerated by increments of 10 Adenosine. Adenosine was measured with a micro- beats/min until definite anginal pain or atrioventricular modification of the adenosine deaminase technique described block appeared. The intensity of the anginal pain relative by Kalckar (8). Assays were made with a Beckman D-U to the patient's previous pain pattern was evaluated through spectrophotometer (Beckman Instruments, Inc., Fullerton, close questioning by two observers and was roughly Calif.), using a reaction mixture of 400 pl and sample scored on a scale of 1+ to 4+. Pacing was continued in volumes of 50 or 100 /Al, representing 1/4 to 1/16 of the most experiments for 1-2 min during the rapid collection original sample. Accurate measurement required changes of CS blood. In a few instances, when angina was very in absorbance at 260 nm greater than 0/01. The enzymatic severe, the rate was lowered and collection of CS blood technique could precisely measure 1.0 nmol of adenosine. was rapidly completed as pain subsided. When anginal pain Standards containing 10 nmol of adenosine were measured did not appear or was questionable and unaccompanied by enzymatically during each experimental assay and were electrocardiographic changes, pacing was continued at rates regularly recovered at 90% or more. Duplicate enzymatic between 140 and 180/min for 10 min and collections were assays of all experimental samples agreed to within 10%o. made during continued tachycardia. The assay was linear with respect to concentration and was Control samples of 90 ml of CS blood were collected in not affected by addition of ATP, ADP, or AMP, which an identical fashion for measurement of adenosine, either were well separated from adenosine during thin layer chro- before pacing or at 10 min after complete recovery from matography.
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