Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ultrastructure of myocytes was studied in the left ventricular myocardium of the cat heart after 3 h of LAD ligation. The ischemic, borderline, and normally perfused myocardium was defined by in vivo injection of fluorescein and by regional myocardial blood flow measurements with 15.5 microns radio-labeled microspheres. A semiquantitation of the number of irreversible injured cells in per cent of total counted in the three different zones showed that 53%-63% were irreversibly injured in the ischemic zone, 7%-26% in the borderline area, while none were irreversibly injured in the normally perfused myocardium. The interior excitation-contraction couplings in the normally perfused myocardium comprise interior dyads, triads, reversed triads, and encircling couplings. While the couplings in general were structurally resistant to ischemia, injured interior couplings were apparent in severely damaged cells of the hypoperfused tissue. Such injuries comprise a widening of the junctional gap and a disintegration of the junctional processes.
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PMID:The ultrastructure of the myocyte in different regions of experimental infarcts in the cat heart. 376 92

In dog myocardium, the changes in the levels of creatine phosphate, inorganic phosphate, ATP, ADP, AMP, adenosine and inosine with 8 min of ischemia and subsequent reperfusion for 2, 4, 8, 16 and 32 min have been followed. Creatine phosphate and inorganic phosphate recovered completely within a few minutes as did the energy charge. However, total nucleotides remained depressed, the decrease being compensated for by the increase in inosine levels during ischemia. There was a rapid removal of the latter with reperfusion. Low oral doses of mioflazine (2.5 mg X kg-1), given 2.5 h before LAD occlusion, did not affect the pattern of changes seen in control animals, except for the nucleosides. The drug induced a complete reversal of the adenosine to inosine ratio during ischemia and a remarkable prolongation of the accumulation within the tissue of mainly adenosine during early reperfusion and inosine afterwards. Assuming that the main action of mioflazine is through inhibition of nucleoside transport, the present results provide interesting information about the mechanism of release, metabolism and final washout of adenosine.
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PMID:Oral pretreatment with mioflazine completely changes the pattern and remarkably prolongs the accumulation of nucleosides in ischemic and reperfused myocardium. 377 20

Regional myocardial dysfunction is a very sensitive and early parameter of myocardial ischemia. One minute occlusion of the left anterior descending (LAD (n = 8) and circumflex coronary artery (CCA) (n = 8) by means of hydraulic occluders was performed in 10 chronically instrumented conscious dogs. In a left ventricular cross-section diastolic and systolic area (DA, SA) and area shortening (AS) as well as regional function of 6 radial sectors were evaluated with 2D echocardiography. After occlusion of the LAD, SA increased by 33% (p less than 0.05), AS decreased by 22% (p less than 0.05) while the DA remained unchanged. In 2 of 6 radial sectors (anteroseptal) shortening decreased by 41% (p less than 0.01) and 54% (p less than 0.001) respectively. Occlusion of the circumflex coronary artery CCA caused an increase in DA (18%) and SA (33%) and a reduction of AS by 24% (p less than 0.01). Contraction of the anterior wall (sectors 2 and 3) was reduced by 61% and 57% (p less than 0.001). In the same animal 10 one minute occlusions of the LAD with 5 min intervals of reperfusion caused a reproducible depression of sector 6 (septal) from 63.2 +/- 5.4% to 16.3 +/- 3.4%. In another animal 11 one minute CCA occlusions with 5 min intervals of reperfusion reproducibly decreased the contraction of sector 3 (anterior) from 85.2 +/- 6.7% to 21.4 +/- 17.0%. 2D-E allows a reproducible estimation of regional left ventricular dysfunction during ischemia. Our model has the advantage that numerous studies can be performed in the same animal, so that the results can be compared intraindividually.
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PMID:[Regional myocardial ischemia in the conscious dog under echocardiography control]. 378 63

We studied the mechanisms of ST segment displacement in the ECG recorded from the epi- and subendocardium of ischemic ventricles in the isolated and perfused canine heart. ST segment changes were observed in association with a relatively large area of ischemia produced by occlusion of the left anterior descending and septal arteries (LAD + Sept.) or of the left circumflex artery (LCx). Contrary to previous reports, we found that the amount of subendocardial ST elevation was not always greater than that in the epicardial ECG recorded at the center of ischemia. Also, in the non-ischemic area, the degree of the ST depression in the subendocardial record was nearly the same as the epicardial record. On the other hand, the degree of the epicardial ST elevation on the border zone was always smaller than that at the ischemic center, which seemed to be due to the broadness of the border zone. The amplitude of the ST depression in the non-ischemic area was greater when the recording electrode was near the ischemic border, which supports the solid angle theory. The degrees of both ischemic ST elevation and reciprocal ST depression in the LCx perfused area were always greater than in the LAD + Sept. perfused area. These results strongly suggest that ST segment displacement depends on the relative position of the recording electrode to the electric double layer which exists at the border between the ischemic and non-ischemic area.
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PMID:ST segment changes under occlusion of the proximal portion of major coronary arteries in the isolated canine heart. 383 15

The effects of verapamil on the [K+]o rise produced by myocardial ischaemia were assessed in 26 open chest mongrel dogs. Ischaemia was produced by intermittent occlusion of the LAD artery (15 dogs) or by reduction of flow of the cannulated LAD (11 dogs). Specially constructed valinomycin K+ sensitive electrodes were inserted into the mid myocardium in the central zone of ischaemia (CZ); in the margin (MZ) and in the nonischaemic zone (NZ). Occlusion of the coronary artery under controlled conditions produced significant [K+]o rise, greater in the CZ than in the MZ. During the infusion of verapamil the ischaemic [K+]o rise was substantially reduced in both zones. During controlled 75% reduction of coronary flow the [K+]o reached a plateau that remained stable until reperfusion was re-established. During verapamil infusion, the plateau showed a steady decline, both in the CZ and in the MZ. The changes in [K+]o produced by verapamil, during myocardial ischaemia are probably due to: coronary dilatation of the marginal arteries and+or to a reduction of the late cellular K+ conductance due to a decrease in the intracellular Ca2+, produced by verapamil.
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PMID:Effects of verapamil on the extracellular K+ rise during myocardial ischaemia in dogs. 401 14

We investigated whether the postischemic acceleration of adenosine triphosphate (ATP) synthesis by means of precursor infusion is beneficial for the contractile function of reperfused myocardium. A coronary artery was occluded for 45 min in 21 dogs to produce a marked but reversible ischemia. During the following 3 hours of reperfusion either adenosine (n = 6) or AICAR (5-amino-imidazole-4-carboxamide-riboside) (n = 6) was infused intracoronarily by a small transfemoral catheter positioned in the LAD. ATP repletion by adenosine was nearly 50% of the deficit caused by the previous ischemia, the effect of AICAR on steady-state tissue ATP concentration was insignificant. Regional systolic function of these both groups was compared to that of a control group (n = 9) receiving only a saline infusion. We measured the regional function by subendocardially implanted ultrasound transducers using the transit time method. All three groups showed a reduction to about 25% of the initial segment shortening at the end of ischemia, followed by a quick recovery to half of the preocclusion segment shortening after reopening of the vessel. No further changes were observed in the control series during the 3 hours of reperfusion (50 +/- 10% SE segment shortening at the end). With adenosine infusion - in spite of the resulting considerable ATP elevation - no significant change of segmental contractile function occurred (44 +/- 5% SE segment shortening). Only the AICAR treated group differed from control. It produced a continuous deterioration during reflow resulting in a holosystolic bulging of -20% +/- 10% SE at the end of 3 hours of reperfusion. Our results show that there is no correlation between different ATP tissue levels achieved by adenosine infusion and systolic function in reperfused myocardium after regional reversible ischemia. We hypothesize that reperfusion dyskinesia is caused by a failure of energy utilisation rather than of energy supply.
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PMID:Effect of adenosine and AICAR on ATP content and regional contractile function in reperfused canine myocardium. 405 46

Dog experiments were performed to describe the time course of lipid peroxidation after various ischemic influences of the heart measured by formation of malondialdehyde (MDA), and the scavenger action determined by reduced glutathione (GSH) content and superoxide dismutase (SOD) activity. Experimental groups consisted of control dogs having intact hearts and dogs with acute ramus descendens anterior ligature (LAD) having ischemic areas through 15, 30, 45 minutes and 1, 2, 3, 24 hours. Heart tissue for biochemical assays was excised from both the ischemic areas and from nonischemic left ventricle. The acute ischemia caused characteristic alterations in the biochemical parameters: MDA level gradually increased with its peak value being found at the end of 3 hours ligature. GSH levels decreased moderately, whereas SOD levels reduced sharply. As increased MDA formation indicates breakdown of the polyunsaturated fatty acids (PUFA) in the membranes and decreased GSH and SOD levels indicate impairment of the natural scavengering, the observed changes clearly outline the extent of disintegration of membrane structure and function.
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PMID:Lipid peroxidation and scavenger mechanism in experimentally induced heart infarcts. 407 87

We investigated if the loss of nicotinamide coenzymes in ischemic-infarcted myocardium may be responsible for the transition from reversibly ischemic to irreversibly infarcted cell damage. The LAD was occluded in 6 dogs for 4 h. Transmural needle biopsies were taken from he ischemic-infarcted region after 1/2, 1, 11/2, 2, and 4 h of ischemia and further divided into subepicardial and subendocardial halves. At each time interval the concentration of the nicotinamide coenzymes NAD, NADH, and NADPH were measured, and the degree of cellular injury was evaluated by electron microscopy. The glycohydrolase activity (EC 3.2.2.5), the enzyme which splits NAD, was determined in brain, myocardium, kidney, and skeletal muscle of 4 rats. Total NAD, the sum of NAD and NADH, started to decrease significantly in the ischemic subendocardium 1 h after onset of ischemia. Degradation of NADPH occurred later. Loss ot total NAD was about 60-70% when electron microscopy diagnosed irreversible cell injury. The glycohydrolase activity was the highest in brain followed by myocardium, kidney, and skeletal muscle, reflecting the different tolerances of these tissues towards ischemia. The key mechanism for ischemic injury seems to be the tissue acidosis which activates the glycohydrolase leading to a loss of the vital coenzymes.
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PMID:Loss of canine myocardial nicotinamide adenine dinucleotides determines the transition from reversible to irreversible ischemic damage of myocardial cells. 627 93

The purpose of this study was to evaluate the detectability of stress-induced ischemic lesion in patients with previous myocardial infarction using single photon emission computed tomography (SPECT) producing thallium-201 (T1-201) myocardial perfusion imagings (MPI). Seventy patients underwent stress SPECT by symptom-limited graded bicycle ergometer exercise using a dual-headed rotating gamma camera (Toshiba GCA70A) equipped with a computer system (GMS90). After intravenous administration of 2.5 mCi of T1-201, stress SPECT data at 10 minutes and delayed SPECT data at 3 hours after the injection were collected in the 64 X 64 matrix form covering 360 degrees directions by camera sweep of 180 degrees in 6 minutes, which were immediately followed by conventional planar imagings (PL). Transaxial tomographic image reconstruction was performed by convolution method using a Shepp-Logan's filter. Thereafter, sagittal and coronal tomographic images were reconstructed for about 2 minutes. Image interpretation was assessed visually. The results were as follows: Sensitivity and specificity in detecting the affected vessel with more than 75% stenosis by segmental analysis of myocardial images were higher by SPECT than by PL (LAD 89% and 65%, LCX 68% and 56%, RCA 89% and 76% in sensitivity and LAD 94% and LCX 75%, 92% and 94%, RCA 81% and 59% in specificity, respectively). Sensitivity in detecting both single (82%) and multivessel disease (76%) was fairly high. Detectability of stress-induced ischemia (i.e. occurrence of a new defect in patients with previous myocardial infarction and ST-segment depression in ECG) was significantly higher in SPECT (67%) than in PL (39%, p less than 0.005) and in ECG (39%, p less than 0.005). A perfusion defect in the extensive anterior wall, marked left ventricular dilatation and the widening of the angle toward the apex composed of septal and anterolateral walls in transaxial images were the findings characteristic of anterior myocardial infarction with severe dyskinesis. We conclude that stress SPECT is a useful noninvasive technique for the documentation of the number of vessels affected and severe wall motion abnormality of the LV and for the detection of stress-induced ischemia in previous myocardial infarction.
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PMID:[Detectability of stress-induced ischemic lesion in previous myocardial infarction using 201T1 myocardial single photon emission computed tomography]. 633 58

In 8 pentobarbital-anesthetized mongrel dogs the correlation between regional myocardial blood flow (RMBF) and regional cardiac uptake of 15-(p-123I-phenyl)-pentadecanoic acid (IPPA) was determined. Three animals were studied under control conditions, in three dogs an acute ischemia was produced by LAD ligation, and two dogs were paced at 195 beats/min. RMBF values were 20-50 ml/min X 100 g in acutely ischemic myocardium. 90-120 ml/min X 100 g under normal conditions and 200-250 ml/min X 100 g during pacing-induced stimulation. Total cardiac uptake of IPPA was 4.5-6% of the injected dose. In normal and acutely ischemic myocardium a good correlation between RMBF and IPPA uptake was obtained. Under stimulated conditions only a moderate increase of IPPA accumulation was found. At RMBF values above 150-170 ml/min X 100 g an upper limit of IPPA uptake was observed and can be explained by limited diffusion or an increased utilization of alternative substrates.
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PMID:Relation of myocardial blood flow and initial cardiac uptake of 15-(p-123I-phenyl)-pentadecanoic acid in the canine heart. 647 17


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