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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

While calcium entry blockers have a beneficial influence on the postischemic recovery of the nonhypertrophied heart, their influence on the hypertrophied heart has not been determined. The aim of this study was to assess postischemic recovery of myocardial performance and energy metabolites in rat hearts with left ventricular hypertrophy pretreated either chronically or acutely with verapamil. Left ventricular hypertrophy was induced by suprarenal constriction of the abdominal aorta. Hemodynamics and phosphorus 31 magnetic resonance spectra were monitored simultaneously in the isolated hearts during control perfusion, after 30 minutes of global ischemia, and after 30 minutes of reperfusion. All hypertrophied hearts had significantly higher rate-pressure products than normal hearts. Compared with normal hearts, oxygen consumption was significantly lower in all hypertrophied hearts, especially untreated hypertrophied hearts. Also, before ischemia all normal or hypertrophied hearts (treated or untreated) began with comparable phosphorylation potentials (i.e., the supply of energy was not significantly different). Postischemic recovery was not related to energy supply-oxygen demand before onset of ischemia. Furthermore, it was not related to energy levels or intracellular pH during ischemia. For postischemic recovery, the rate-pressure product was 40 +/- 5% in the hypertrophied heart, 83 +/- 5% in the normal, 100 +/- 3% in the hypertrophied heart chronically treated with verapamil, and 82 +/- 5% in the hypertrophied heart acutely treated with verapamil. The degree of recovery was related to coronary flow both before and after ischemia. The latter is important for flushing deleterious metabolites and ions from the interstitial space as well as for delivery of oxygen and substrate to the myocardium.
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PMID:Verapamil preserves myocardial performance and energy metabolism in left ventricular hypertrophy following ischemia and reperfusion. Phosphorus 31 magnetic resonance spectroscopy study. 253 75

The Langendorff perfused rat heart was used to investigate whether myocardial damage during ischemia and reperfusion could be protected by free radical scavengers, calcium antagonist and adenosine. Myocardial high energy phosphates were measured by phosphorus-31 NMR spectroscopy during normal perfusion, 20 min of ischemia and 20 min of reperfusion. In hearts, which were treated both with free radical scavengers (FRS) (Superoxide dismutase): 24 IU/ml and catalase 22 IU/ml) and verapamil (10(-7) M), beta-ATP was significantly higher than that of FRS at the end of ischemia. However, beta-ATP recovered only to 83% of baseline value at the end of reperfusion. In view of myocardial metabolism, verapamil treated hearts were good for recovery of creatine phosphate (PCr) but not ATP at the end of reperfusion. Hearts which were treated with only adenosine did not differ from control hearts. However, when hearts were treated with both verapamil and adenosine (10(-4) M), recovery of both ATP and PCr content was significantly greater than that of control hearts. These results suggested that pretreatment with both verapamil and adenosine before and after global ischemia could protect ischemic myocardium, but, further studies are necessary to clarify the precise mechanism of protection.
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PMID:Effects of calcium antagonists and free radical scavengers on myocardial ischemia and reperfusion injury: evaluation by 31P-NMR spectroscopy. 260 Oct 5

1. Isovolumic left ventricular pressure was measured at various coronary arterial pressures in Langendorff-perfused ferret hearts. The concentrations of phosphorus-containing metabolites were measured using 31P nuclear magnetic resonance (NMR). Intracellular free calcium concentration ([Ca2+]i), was measured with 19F NMR in a group of hearts that were loaded with the calcium indicator 5F-BAPTA. 2. Developed pressure increased when coronary arterial pressure was raised from the control value of 80 to 100-160 mmHg and decreased when coronary pressure was lowered to 40-70 mmHg. The changes were reversible. 3. Coronary flow varied directly with coronary pressure over the entire range from 40 to 160 mmHg. 4. The concentrations of phosphorus-containing metabolites and the efflux of lactate from the heart remained unchanged at coronary pressures of 60 mmHg or higher. Below 60 mmHg, intracellular pH decreased, while inorganic phosphate concentration and lactate efflux increased. 5. In contrast to the developed pressure during twitch contractions, maximal Ca2+-activated pressure remained constant at coronary pressures of 60-160 mmHg. Only below a coronary pressure of 60 mmHg did maximal Ca2+-activated pressure decline. 6. An increase in coronary pressure produced an increase in developed pressure even in hearts stretched to the peak of the Frank-Starling relation. 7. When coronary pressure was lowered from 80 to 60 mmHg, [Ca2+]i decreased during systole; the opposite effect was apparent when coronary pressure was raised from 80 to 120 mmHg. 8. We conclude that coronary perfusion (pressure or flow) modulates intracellular calcium and, consequently, contractile force. Ischaemia cannot fully explain this phenomenon, nor can changes in sarcomere length.
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PMID:Cellular mechanism of the modulation of contractile function by coronary perfusion pressure in ferret hearts. 260 38

The application of in vivo MR spectroscopy to the study of the liver is currently an expanding field of research. Owing to technical difficulties, the results obtained thus far were mainly those of animal observations. Several nuclei have been considered: hydrogen, phosphorus, carbon or fluorine. This non-traumatic method allows following and quantifying the various metabolic pathways, especially during hepatic diseases. The major metabolic pathways, i.e. neoglycogenesis, glycogenolysis, Krebs' cycle, etc., are studied, as well as their alterations during diseases such as ischemia, diabetes or alcoholism. The development of this promising technique requires the cooperation of various clinical and fundamental disciplines.
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PMID:[In vivo NMR spectroscopy of the liver]. 267 30

Magnetic resonance spectroscopy (MRS) has been used effectively in the evaluation of cardiac physiology. Studies have been done at various levels of complexity extending from isolated hearts to man. Correlation of high-energy phosphate compounds with contractile function is achieved by simultaneous or immediate sequential measurement of ventricular contractile function and the phosphorus-31 MR spectra. Studies in isolated hearts have monitored the response to ischemia of normal and hypertrophic hearts and the preservation of myocardial function and high- energy phosphate stores by drugs administered prior to the ischemic event. Regional myocardial ischemia has been evaluated by simultaneous monitoring of myocardial regional segment length by sonomicrometry and regional myocardial 31P MRS in the intact heart of larger animal models. Function and metabolism have been assessed in man by the combined application of cine MRI and 31P MRS acquired with a surface coil.
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PMID:Magnetic resonance spectroscopy of the heart. Overview of studies in animals and man. 269 42

Magnetic resonance spectroscopy (MRS) is a valuable tool for the study of myocardial ischemia. Phosphorus (31P) MRS can detect changes in high-energy phosphates resulting from ischemia and has been used to determine the sensitivity of metabolic changes to ischemia as well as to investigate the metabolic factors important for myocardial dysfunction. The mechanisms mediating postischemic dysfunction have been investigated using 31P MRS, as have interventions to limit metabolic and functional damage from ischemia. These investigations have laid the groundwork for human cardiac studies. While abnormalities following myocardial infarction have been shown in man, further work must be performed to reliably acquire localized spectra under conditions of ischemia.
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PMID:Magnetic resonance spectroscopy. Evaluation of ischemic heart disease. 269 43

Phosphorus-31 (31P) magnetic resonance spectroscopy of the kidneys promises to provide metabolic information leading to better assessment of renal physiology. However, the problems of studying the metabolism of the heterogeneous renal architecture by precisely localizing the origin of the signal obtained from small voxels and eliminating motion artifacts have not been solved as yet. The normal 31P MRS spectra show a characteristic fingerprint of six peaks including phosphomonoesters, phosphodiesters, inorganic phosphorus, and gamma, alpha, beta adenosine triphosphate (ATP). Renal failure, regardless of its etiology and mechanism of inducement (hypoxia, ischemia, acidosis, or obstruction) produces a loss of ATP with a progressive increase of inorganic phosphorus and a decline in intracellular pH. The severity of renal failure correlates with the severity of the metabolic disturbance. The potential use of 31P MRS in the assessment of renal viability has been applied to the study of renal preservation methods and prediction of renal function following transplantation.
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PMID:Phosphorus-31 MRS of the kidney. 269 45

This study was designed to define the effect of postischemic low Ca2+ perfusion on recovery of high-energy phosphates, intracellular pH, and contractile function in isolated rat hearts. Phosphorus-31 nuclear magnetic resonance spectroscopy was used to follow creatine phosphate, adenosine triphosphate, intracellular inorganic phosphate, and intracellular pH during control perfusion (15 minutes), total ischemia (30 minutes), and reperfusion (30 minutes). In Group I the perfusate [Ca2+] was 1.3 mmol/l throughout the experiment, whereas in Group II the perfusate [Ca2+] was reduced to 0.05 mmol/l during the first 10 minutes of reperfusion. Hearts from Group III were not made ischemic but were subjected to 10 minutes of low Ca2+ perfusion followed by 20 minutes of normal Ca2+ perfusion. During low Ca2+ reperfusion (Group II) recovery of high-energy phosphates and pH was significantly better than in controls (Group I). However, after reexposure to normal Ca2+, metabolic recovery was largely abolished, coronary flow was suddenly impaired, and contracture developed without any rhythmic contractions. These observations indicated the occurrence of a calcium paradox rather than postponed ischemia-reperfusion damage. On the other hand, normoxic hearts (Group III) tolerated temporary perfusion with 0.05 mmol/l Ca2+ very well with respect to left ventricular developed pressure, coronary flow, and metabolic parameters. In conclusion, postischemic low Ca2+ (0.05 mmol/l) perfusion may reduce reperfusion damage, but at the same time ischemia appears to enhance the susceptibility of the heart to the calcium paradox.
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PMID:Low Ca2+ reperfusion and enhanced susceptibility of the postischemic heart to the calcium paradox. 272 Sep 16

The ability of 1-carboxymethyl-2-iminoimidazolidine (cyclocreatine), a synthetic creatine analog, to protect myocardium during global ischemia was assessed in isovolumic rat hearts using phosphorus-31 nuclear magnetic resonance spectroscopy. Wistar rats were fed a 1% cyclocreatine diet. After 2 weeks, cyclocreatine-fed (n = 8) and control (n = 7) rats were anesthetized, the heart was excised and retrograde perfusion was begun at 10 ml/min per g with 37 degrees C, phosphate-free buffer containing glucose and oxygen. Hemodynamic and spectroscopic data were obtained during baseline, ischemia and recovery periods (each 24 min). During ischemia, the heart of control rats developed a rigor-like increase in tonic pressure (ischemic contracture) not seen in the heart of cyclocreatine-fed rats (22 versus 1 mm Hg, p less than 0.01). This change was associated with significantly more adenosine triphosphate (ATP) at end-ischemia in the cyclocreatine group (1.6 versus 0.6 mumol/g, p less than 0.01) and delayed development of acidosis (p less than 0.001). With reperfusion, the heart of cyclocreatine-fed rats spontaneously defibrillated sooner than did the heart in control rats (178 versus 346 s, p less than 0.03). Diastolic pressure remained significantly elevated throughout recovery in control hearts compared with treated hearts (p less than 0.001). Prior feeding with cyclocreatine preserves myocardial adenosine triphosphate during ischemia, delays the development of acidosis and ischemic contracture and improves recovery of mechanical function on reperfusion.
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PMID:Myocardial protection during ischemia by prior feeding with the creatine analog: cyclocreatine. 273 67

Phosphorus NMR spectroscopy is an important technique for the investigation of metabolism in tissues and intact organisms (including man). However, quantitation of the signals from an NMR experiment is difficult because it is not known from which regions of a cell metabolites are detected. It is generally believed that only metabolites free in the cytosol are observed. In this study a comparison of concentration measurements obtained by NMR and after freeze extraction was made in the normoxic and ischemic rat heart. The influence of ischemia was examined because of its potential effect on the level of phosphate metabolites in various compartments. The same fraction of ATP always appears visible to NMR, whereas inorganic phosphate is largely NMR invisible until after a period of ischemia and the phosphomonoesters are only partially observed early in ischemia.
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PMID:Effect of ischemia on NMR detection of phosphorylated metabolites in the intact rat heart. 277 10


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