Phosphorus (31P) NMR spectra showing the relative concentrations of phosphocreatine, ATP, and Pi were recorded noninvasively from localized regions in the left ventricles of dog hearts in situ by using depth-resolved surfacecoil spectroscopy at 1.5 T. Proton (1H) NMR surface-coil imaging was used to position 31P NMR coils and to determine the location of depth-resolved volumes immediately prior to 31P examination. Occlusion of the left anterior descending coronary artery produced regional ischemia detected as changes in the ratios of phosphocreatine, ATP, and Pi and by changes in the pH measured from the spectra. Spectral changes were not typically observed in regions adjacent to ischemic myocardium. Reperfusion produced some recovery, and ventricular fibrillation resulted in deterioration in high-energy metabolites. The location and size of ischemic tissue was measured by singlephoton-emission computed tomography (SPECT) and gammaray counting or by staining excised hearts. The technique should permit the long-term noninvasive monitoring of the metabolic response of the heart to pathologic processes and allow assessment of interventions. NMR spectrum is a profile of the relative concentrations of the high-energy phosphate metabolites phosphocreatine (PCr) and ATP as well as inorganic phosphate, Pi (1-6). Such spectra are responsive to changes in myocardial metabolism as early as 90 s after the onset of ischemia (3). To date, applications of 31P NMR spectroscopy to heart metabolism have proved invasive because of (i) the difficulty of achieving adequate spatial localization of the 31p signal to the heart, and (ii) the small magnet apertures of available

To determine the characteristic appearance of phosphorus (31P) nuclear magnetic resonance spectra in acute and chronic myocardial infarction in situ, cardiac-gated depth-resolved surface coil spectroscopy (DRESS) at 1.5 T was used to monitor 31P NMR spectra from localized volumes in the left anterior canine myocardium for up to 5 days following permanent occlusion of the left anterior descending coronary artery. Coronary occlusion initially produced regional ischemia manifested as significant reductions in the phosphocreatine (PCr) to inorganic phosphate (Pi) ratios and intracellular pH (P less than 0.05, Student's t test) in endocardially displaced spectra acquired in periods as short as 50 to 150 s postocclusion. Spectra acquired subsequently revealed either (i) restoration of near-normal phosphate metabolism sometime between 10 and about 50 min postocclusion or (ii) advancing ischemic phosphate metabolism at about an hour postocclusion, and/or (iii) maintenance of depressed PCr/Pi ratios for up to 5 days postocclusion with a return of the apparent pH to near normal values between 6 and 15 h postocclusion. Postmortem examination of animals exhibiting the first type of behavior revealed the existence of coronary collateral vessels. The last type of behavior indicates that Pi remains substantially localized in damaged myocardium for days following infarction. The location and size of infarctions were determined postmortem by staining excised hearts. The smallest infarctions detected by 31P DRESS weighed 4.9 and 7.5 g. The most acidic pH measured in vivo was 5.9 +/- 0.2. Infarctions aged 1/2 day to 5 days were characterized by elevated but broad Pi resonances at 5.1 +/- 0.2 ppm relative to PCr and significantly depressed PCr/Pi ratios (P less than 0.002, Student's t test) relative to preocclusion values. Contamination of Pi resonances by phosphomonoester (PM) components is a significant problem for preocclusion Pi and pH measurements. These results should be applicable to the detection and identification of human myocardial infarction using 31P NMR and DRESS.

Function of the coronary collateral circulation during the course of a single abrupt coronary occlusion was evaluated in awake dogs instrumented over the long term. Studies were performed approximately 2 weeks after collateral development had been stimulated in the dogs by partial stenosis of the proximal left circumflex coronary artery.

SUMMARY. The effects of occlusion, reperfusion, reocclusion (n = 13), and nitroglycerin (n = 10) on regional transmural myocardial collateral blood flow was tested in conscious dogs in which collateral development was stimulated by partial stenosis of the left circumflex coronary artery. Hemodynamics and collateral blood flow were measured during the awake state using 9-/im radioactive microspheres. Regional transmural flow was measured during transient occlusion of the circumflex artery at 7 and at 14 days postoperatively. On the 14th postoperative day, two sets of circumflex occlusions and blood flow measurements were carried out. The first set consisted of two occlusions separated by 15 minutes. The second set performed 2 hours later included two occlusions, separated by 15 minutes, and nitroglycerin administration. Mean collateral blood flow increased significantly (P = 0.002) from 0.10 ± 0.07 ml/min per g on day 7 to 0.25 ± 0.18 ml/ min per g on day 14. A significant increase in mean collateral blood flow from occlusion one to two was observed (0.28 ± 0.17 to 0.37 ± 0.22 ml/min per g, P = 0.005). Mean collateral flow increased significantly (P = 0.01) between pre-to post-nitroglycerin occlusions, 0.28 ± 0.20 to 0.46 ± 0.32 ml/min per g. Although this increase appeared to be greater than during the first set of occlusions, it did not reach statistical significance (P = 0.08). These data indicate that when immature collaterals are present, occlusions, reperfusion, and reocclusions of a major coronary artery produce augmentation in collateral flow. This must be considered in evaluating interventions which may alter collateral flow. (CircRes 54: 204-207, 1984) IN the event of coronary artery occlusion, collateral vessels can provide an alternate source of blood flow. Little is known, however, about the functional physiology of immature collateral vessels. If a partially stenosed major coronary artery is suddenly totally obstructed, the integrity of the myocardium will become entirely dependent upon the functional adequacy of the collateral vessels. It is important, therefore, to determine whether immature collateral vessels function to deliver a fixed maximal amount of flow immediately after total occlusion of the stenosed coronary, or if blood flow to the collateraldependent area can be augmented by prior brief episodes of total occlusion, or by drug administration.In order to carry out these studies, a model was developed in our laboratory in which collateral vessel growth was stimulated by partial stenosis of the left circumflex coronary artery. In our model, the blood flow to a region of myocardium was supplied by both the partially stenosed circumflex artery, and by immature but developing collateral vessels. During complete temporary occlusion of the circumflex artery, the immature collaterals were the primary source of flow to this area of myocardium.The primary aim of the study was to determine whether (after a brief occlusion of a major coronary artery and reperfusion), a second occlusion would elic...