Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study determined whether the rapidity of myocardial metabolic and contractile recovery after brief coronary occlusion depends upon the intensity of reactive hyperemia. We also tested the hypothesis that coronary flow rate modulates contractility after brief myocardial ischemia, independent of changes in phosphorus metabolites. Eight open-chest pigs were studied with phosphorus-31 nuclear magnetic resonance (NMR) spectroscopy with 14 s time resolution. After a 29-s anterior descending coronary occlusion, peak Doppler coronary flow velocity was alternately unrestricted (normal hyperemia, 443 +/- 40% of control) or limited to 159 +/- 9% of control. During 29 s coronary occlusion, phosphocreatine-to-inorganic phosphate ratio (PCr/Pi) and systolic segment shortening in the ischemic region fell to 28 +/- 4 and 7 +/- 7% of control, respectively. With normal hyperemia, PCr/Pi and segment shortening recovered within 29 s. With blunted hyperemia, recovery of both parameters was delayed an additional 29-43 s, associated with reduced subendocardial blood flow (measured with radioactive microspheres) and persistent intracellular acidosis. However, the relationship between segment shortening and PCr/Pi was unaffected by the intensity of reactive hyperemia. Thus blunted reactive hyperemia significantly delays metabolic and contractile recovery from brief ischemia, probably via transient maldistribution of transmural perfusion. However, coronary blood flow rate does not independently modulate contractility after brief reversible ischemia.
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PMID:Metabolic and functional consequences of blunted myocardial reactive hyperemia. 188 33

Phosphorus-31 nuclear magnetic resonance (P-31 NMR) spectroscopy is able to identify alterations in myocardial high energy phosphate metabolism associated with acute infarction. It was hypothesized that the extent of acute myocardial infarction could be quantitated from changes in the tissue content of inorganic phosphate (Pi), phosphocreatine (PCr) and adenosine triphosphate (ATP) derived from P-31 NMR spectra. Nine isolated, perfused rat hearts were studied at 121.5 MHz. After baseline spectra were obtained, varying locations of either the right or the left coronary artery were occluded without removing the heart from the spectrometer. Spectra were then collected during regional ischemia at 15 and 45 min after occlusion. Phosphate metabolites were quantitated from the baseline and 45-min regional ischemia spectra, times at which the metabolites are at steady state for the normal and ischemic conditions. The heart was removed from the spectrometer, perfused for a total duration of 2 h and sectioned into 2-mm thick slices for triphenyltetrazolium chloride staining. Percent infarct was determined by manual tracing of magnified, digitized images of the stained sections. Coronary blood flow, heart rate and blood pressure were monitored throughout the experiment. Significant linear relations were found between percent infarct (by triphenyltetrazolium chloride staining) and the percent change of beta-ATP (r = -0.74), Pi (r = 0.83) and the PCr/Pi ratio (r = -0.71) at 45 min after coronary occlusion. Coronary flow was also found to correlate significantly with percent infarct (r = -0.70). These results are applicable to in vivo P-31 NMR studies of acute infarction where the volume of interest may include both normal and acutely infarcted myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitation of the extent of acute myocardial infarction by phosphorus-31 nuclear magnetic resonance spectroscopy. 191 16

The current study determined the effectiveness of nicardipine, a 1,4-dihydropyridine calcium antagonist, in preserving reperfused myocardium in a cat model of temporary coronary occlusion and ascertained if replenishment of myocardial phosphate stores during reperfusion as defined by phosphorus-31 nuclear magnetic resonance (NMR) spectroscopy was indicative of salvage. Twenty open chest, anesthetized cats were studied with use of a snare ligature around the proximal left anterior descending coronary artery, with a coil sutured to the epicardial surface overlying the distribution of the artery. Peak areas of phosphocreatine, inorganic phosphate and adenosine triphosphate (ATP) NMR signals were measured during 1 h of occlusion followed by 1.5 h of reperfusion. Infarct size and jeopardy area were determined in vitro by simultaneous infusion of phthalocyanine blue dye and triphenyltetrazolium chloride into the aorta and the left anterior descending coronary artery, respectively, after 5 h of myocardial reperfusion. Nicardipine-treated and control groups had similar jeopardy area values (41.2 +/- 1.6% versus 47.4 +/- 3.1% of the left ventricle), but infarct area was significantly reduced in the nicardipine-treated group (3.2 +/- 1.1% versus 24.9 +/- 7.5% of jeopardy area, p less than 0.01). High energy phosphate compounds remained markedly altered during reperfusion in both groups. No significant improvement in phosphocreatine or inorganic phosphate recovery was observed in animals pretreated with nicardipine despite an 87% reduction in infarct size. Myocardial ATP was greater during reperfusion in the nicardipine-treated compared with the control group (average over initial 90 min of reperfusion 58 +/- 6% versus 46 +/- 3% of baseline values, p less than 0.05), suggesting improved recovery of ATP. However, the measured levels of high energy phosphate compounds during reperfusion and their ratios did not correlate with infarct size and thus were not predictive of myocardial salvage.
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PMID:Effects of nicardipine, a calcium antagonist, on myocardial salvage and high energy phosphate stores in reperfused myocardial injury. 225 60

Recovery of myocardial high-energy phosphate (HEP) metabolism after coronary occlusion and reperfusion may vary with ischemic duration and may provide information about the extent of tissue viability. To evaluate the differences between varying durations of ischemia and to attempt to identify metabolic indexes of salvaged viable tissue, intact New Zealand white rabbits underwent either 30 (group 1; n = 8) or 60 (group 2; n = 8) minutes of coronary occlusion followed by reperfusion. HEP metabolism was evaluated with cardiac gated phosphorus 31 (31P) nuclear magnetic resonance (NMR) spectroscopy with a 2.0 T spectrometer. While similar HEP changes were observed during ischemia in both groups, differences in HEP recovery between groups were seen following reperfusion. Group 1 animals demonstrated a gradual decrease in inorganic phosphates (Pi) (p less than 0.05 versus group 2), an immediate recovery of phosphocreatine (PCr) (p = ns versus baseline), and a gradual increase of adenosine triphosphate (ATP) to pre-ischemic levels. Group 2 animals had elevated levels of Pi (p less than 0.05 versus baseline; p less than 0.05 versus group 1), slow recovery of PCr, and continued reduction of ATP (p less than 0.05 versus baseline; p less than 0.05 versus group 1). Group 1 rabbits had a greater extent of viable myocardium than group 2 (77.1 +/- 9.7% of risk area versus 39.4 +/- 9.4%; p less than 0.001). Significant correlations were found between PCr and Pi reperfusion values and myocardial viability (r = 0.59, p less than 0.05; r = 0.73, p less than 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of myocardial viability following ischemic and reperfusion injury using phosphorus 31 nuclear magnetic resonance spectroscopy in vivo. 236 May 15

Changes in high-energy phosphate metabolism may be important in the regulation of myocardial contractile function during ischemia. This study sought to determine the dynamic relation between myocardial contractile function and high-energy phosphate metabolism during and following brief (24-second) coronary occlusion, when large and rapid changes in both parameters occur. Eight anesthetized, open-chest pigs were instrumented with a Doppler flow probe and occluder on the anterior descending coronary artery, segment length crystals in the anterior left ventricular wall, and a surface coil for phosphorus-31 nuclear magnetic resonance spectroscopy. Phosphorus-31 spectra were reconstructed with a 4.8-second time resolution by summing corresponding short blocks of data from multiple occlusions. Metabolic and functional parameters were unchanged during the first 4.8 seconds of occlusion. During the remainder of occlusion, phosphocreatine progressively declined to 66 +/- 3% of control, inorganic phosphate rose to 170 +/- 8% of control, and segment shortening fell to 25 +/- 9% of control. A strong linear correlation was found between dynamic changes in segment shortening and phosphocreatine (r2 = 0.97), inorganic phosphate (r2 = 0.96), and the ratio of phosphocreatine to inorganic phosphate (r2 = 0.98) during occlusion. At any level of the ratio between phosphocreatine and inorganic phosphate, segment shortening was greater during reflow than during occlusion. The close, dynamic relation between segment shortening and phosphorus metabolites supports the regulation of contractility by changes in energy metabolism or its by-products during ischemia. During reactive hyperemia, the high coronary flow rate may be an independent factor modulating contractility.
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PMID:Dynamic relation between myocardial contractility and energy metabolism during and following brief coronary occlusion in the pig. 237 83

The ability of in vivo phosphorus-31 magnetic resonance (MR) spectroscopy to permit accurate distinction between reperfused-viable and reperfused-infarcted myocardium was examined in a canine model of acute coronary occlusion. In vivo myocardial pH and phosphocreatine, adenosine triphosphate, and inorganic phosphate levels were measured at baseline and for the first 90 minutes after reperfusion of a total coronary artery occlusion producing either predominantly viable (nine animals) or infarcted (nine animals) myocardium in the region of metabolic study. Myocardial viability was assessed in each animal by means of postmortem triphenyltetrazolium chloride staining. Tissue was characterized from the in vivo P-31 MR data by means of logistic regression analysis. The accuracy of using the P-31 MR data for distinguishing reperfused-viable from reperfused-infarcted myocardium was 100% (69 of 69 data points, 18 of 18 animals). Results of the logistic regression procedure indicated that phosphocreatine was the metabolic variable enabling most effective separation of reperfused-viable and reperfused-infarcted myocardium. Thus, metabolic data obtained with P-31 MR spectroscopy permit effective separation of reperfused-viable from reperfused-infarcted myocardium.
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PMID:Reperfused-viable and reperfused-infarcted myocardium: differentiation with in vivo P-31 MR spectroscopy. 274 May 21

The ability of phosphorus-31 magnetic resonance (MR) spectroscopy to accurately characterize myocardium as normal, ischemic, or reperfused but viable was examined in the canine model of acute coronary artery occlusion. P-31 MR measurements of in vivo myocardial pH, phosphocreatine, adenosine triphosphate, and inorganic phosphate levels were made at baseline and for 6 hours after sustained coronary occlusion (ten animals) or coronary occlusion reperfused after 60 minutes (12 animals). Ten control animals were studied in parallel fashion, without coronary occlusion. Myocardial tissue characterization derived from the P-31 MR spectroscopy data by logistic regression analysis had an overall accuracy of 89%. Overall accuracy was unaffected by duration between coronary occlusion and P-31 MR study. Thus, metabolic data obtained with P-31 MR spectroscopy effectively separate normal, acutely ischemic, and reperfused but viable myocardium.
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PMID:Effective separation of normal, acutely ischemic, and reperfused myocardium with P-31 MR spectroscopy. 338 Sep 86

Phosphorus-31 magnetic resonance spectroscopy was used to study the relationship between metabolic and functional alterations during acute regional ischemia in vivo. Phosphocreatine, adenosine triphosphate (ATP), inorganic phosphate, and intracellular pH (pHi) were monitored in 11 pigs at 2-minute intervals during 4 and 20 minutes of acute left anterior descending coronary artery occlusion followed by 20 minutes of reperfusion. In a parallel series of experiments, segment shortening was continuously monitored by sonomicrometry during the early ischemic period. Segment shortening decreased precipitously after coronary occlusion, and systolic expansion was noted within 30 seconds. Phosphocreatine levels decreased rapidly and reached a minimum value of 44 +/- 13% (mean +/- SE) of the control value by 20 minutes of ischemia. Ischemia-induced reduction of ATP was small and not statistically significant. Inorganic phosphate increased rapidly to a peak level of 158 +/- 9% of the control value by 4 minutes of ischemia. Intracellular pH decreased 0.76 +/- 0.04 units during the initial 10 minutes of ischemia and subsequently stabilized. After reperfusion, phosphocreatine, inorganic phosphate, and pHi recovery occurred within 4 minutes and was similar in the 4- and 20- minute ischemia groups. These results indicate that the changes in high-energy phosphates and pHi observed during both 4 and 20 minutes of coronary occlusion are rapidly reversible. The temporal course of metabolic and functional alterations during early ischemia suggests that if these are causally related the decline in contractility is mediated by an increase in inorganic phosphate, a decrease in pHi, or both rather than by loss of ATP.
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PMID:In vivo alterations of high-energy phosphates and intracellular pH during reversible ischemia in pigs: a 31P magnetic resonance spectroscopy study. 341 85

Postreperfusion regional myocardial dysfunction may be associated with depletion of high energy phosphate compounds during ischemia and with their relatively slow repletion during reperfusion. However, few studies have correlated relatively rapid changes in regional myocardial function (sonomicrometers) and blood flow (microspheres) with high energy phosphate concentrations measured using phosphorus-31 nuclear magnetic resonance spectroscopy in intact large animal models of regional myocardial ischemia. The left anterior descending coronary artery of mongrel dogs was abruptly occluded for 17.1 +/- 1.9 minutes and then completely released; measurements were made for an additional 22 minutes. Transmural blood flow decreased from 1.07 +/- 0.25 to 0.25 +/- 0.10 ml/(min X g) and holosystolic expansion was observed in all dogs (segmental systolic shortening decreased from 9.3 +/- 3.7 to -6.3 +/- 6.0%). Phosphocreatine (PCr) measured during 4.4 minute sampling intervals decreased to steady state within the first sampling period after occlusion and was 45.9 +/- 17.0% of control at the end of the occlusion, whereas beta-adenosine triphosphate (beta-ATP) reached its lowest level early after reperfusion (72.7 +/- 13.3% of control). The ratio of PCr to inorganic phosphate (Pi) decreased during the occlusion (3.34 +/- 0.75 versus 1.01 +/- 0.61) but returned to control level early during reperfusion. The ratio of PCr to beta-ATP also decreased during coronary occlusion (2.16 +/- 0.39 versus 1.29 +/- 0.39) but did not return to control level during reperfusion. Significant correlations were observed between the intensity of ischemia (reduced blood flow) and reductions in regional contractile function, PCr, beta-ATP, myocardial pH and the increase in Pi during the coronary occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional myocardial blood flow, function and metabolism using phosphorus-31 nuclear magnetic resonance spectroscopy during ischemia and reperfusion in dogs. 362 71

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.
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PMID:The fate of inorganic phosphate and pH in regional myocardial ischemia and infarction: a noninvasive 31P NMR study. 365 2


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