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)

This report described initiation of A-V nodal reentrant tachyycardia in a patient with acute inferior myocardial infarction. The onset of tachycardia was preceded by an abortive A-V nodal Wenckebach periodicity. A-V nodal ischemia with or without vagotonia was implicated as the cause of induction of critical functional dissociation between the two A-V nodal conduction pathways. Since the tachycardia manifested its rate between 95-110 beats/min during the evolutionary phase of acute inferior myocardial infarction, it simulated, electrocardiographically, an accelerated A-V junctional rhythm. Analysis of the onset of tachcardia was of diagnostic importance.
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PMID:A-V nodal reentrant tachycardia vs accelerated A-V junctional rhythm in acute inferior myocardial infarction. 73 96

Accurate electrocardiographic diagnosis of myocardial ischemia or infarction is difficult in patients with the Wolff-Parkinson-White syndrome; however, myocardial ischemia may also have profound effects on the electrophysiologic characteristics of the bypass tract in these patients. Comparison of studies performed during and two months following an episode of significant myocardial ischemia demonstrated substantial prolongation of the refractoriness of the bypass tract during the period of ischemia. Bypass refractoriness was prolonged by 196 msec, yet atrioventricular nodal refractoriness was not significantly different from normal. These studies, therefore, suggest that, on occasion, the presence of acute myocardial ischemia may, in fact, obscure the electrocardiographic diagnosis of the Wolff-Parkinson-White syndrome.
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PMID:Wolff-Parkinson-White syndrome. Alterations in electrophysiologic characteristics of the bypass tract secondary to ischemia. 88 79

The effect of reduction in anterior septal arterial flow on the conduction system was studied in seven anesthetized dogs. After 2 hours of occlusion P-Q, A-H, and H-V intervals as well as atrioventricular nodal effective and functional refractory periods were significantly prolonged, sinoatrial conduction time was prolonged and the heart rate was decreased. The duration of the His bundle electrogram was significantly prolonged and the configuration altered. However, QRS duration did not prolong significantly. Fifteen minutes after reperfusion, A-H interval, duration of the His bundle electrogram, effective refractory period and functional refractory period returned toward control values. However, the H-V and QRS intervals as well as sinoatrial conduction time were unchanged after reperfusion. Thus, reduction of anterior septal arterial flow influences not only the distal but also the proximal portion of the conduction system; the most vulnerable part is probably the His bundle. The distal portion of the conduction system is directly influenced by ischemia itself, whereas the proximal portion is influenced through other mechanisms induced by reduction of anterior septal arterial flow.
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PMID:Electrophysiologic effects of anterior septal arterial occlusion. 92 Jun 9

Ajmaline, a rauwolfia derivative, has been found to possess potent antiarrhythmic effects. The present study has been designed to define the cardiovascular effects of this drug. Hemodynamic studies performed in anesthetized and conscious dogs demonstrated no significant changes in measured hemodynamic parameters at doses equal to or less than 2 mg. per kilogram. Studies in isolated papillary muscle demonstrated no negative inotropic effects until concentrations of 1 X 10(-4). Disparate results were obtained with regard to heart rate reflecting the state of autonomic tone. Electrophysiologic studies in both anesthetized and conscious dogs demonstrated a significant depression of intraventricular conduction with no significant effect on AV nodal conduction; ventricular automaticity was not affected. Ajmaline did not alter digitalis-induced AV nodal conduction prolongation. However, ajmaline dramatically altered or abolished ventricular arrhythmias secondary to acute ischemia. In conclusion, these studies demonstrate that ajmaline specifically depresses intraventricular conduction, suggesting that this drug would be particularly effective in the treatment of re-entrant ventricular arrhythmias.
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PMID:Cardiovascular effects of ajmaline. 96 88

Several large series have supported the success of retroperitoneal lymphadenectomy as a primary therapeutic modality in the management of non-seminomatous germ cell testicular neoplasms. In 1963 Tavel and associates reported on the inadequacy of this procedure in the complete extirpation of all the retroperitoneal lymph nodes. Our investigation was undertaken to test their conclusions, the sole difference in technique being that the infrarenal lumbar vessels were ligated and divided during the lymph node dissection. Results in 12 cadavers revealed that all retroperitoneal nodal tissue could be excised with the modified technique. These findings were further verified by the absence of any residual retroperitoneal lymph nodes in 3 patients who died of metastatic embryonal cell carcinoma. The extirpative efficacy of this procedure having been established, any major deleterious effects of lumbar ligation, primarily spinal cord ischemia, must be considered. Based on our experience and that of others it may be concluded that this complication represents a minimal risk that should not discourage use of this effective therapeutic procedure.
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PMID:Radical retroperitoneal lymph node dissection: how effective in removal of all retroperitoneal nodes? 124 16

Preliminary experiments in a canine model of Mobitz type II atrioventricular (AV) block showed improvement of conduction after premature ventricular beats. In this investigation, the authors studied the mechanism(s) responsible for this response. In vivo studies were performed in 16 anesthetized dogs. Block was induced by ischemia after septal artery occlusion or by mechanical trauma. Two pairs of plunge electrodes were inserted in the proximal and distal His bundle. An electrode catheter was positioned at the level of the aortic root to provide an overall view of His bundle activation. Bipolar pacing was performed from the high right atrium, right ventricular outflow tract, and proximal and distal His bundle. Infra-nodal 2:1 AV block was consistently induced at an atrial rate of 238 +/- 21 beats/min. In 15 dogs a narrow time window (10-60 ms; mean, 32 +/- 6 ms) was found during which premature beats resulted in transient (2-11 beats; n = 9) or persistent (n = 8) restoration of 1:1 AV conduction. Retrograde penetration of the site of block, that is, Hb, was found even when the anterograde impulse was blocked, demonstrating the asymmetric nature of anterograde versus retrograde conduction. In vitro studies were performed in the same hearts. Intracellular recordings were obtained in the damaged His bundle and proximal right bundle. The site of block showed frequent displacements along the bundle. The introduction of a retrograde stimulus during 2:1 block restored 1:1 anterograde conduction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Conversion of Mobitz type II AV block to 1:1 AV conduction by premature ventricular beats. 128 1

Conduction block is electrophysiologically defined and is shown to be an important pathologic condition encountered in both central and peripheral nervous system disorders. The conduction block is encountered most frequently in peripheral nerve injuries, which are the results of compression and ischemia. It is impossible to study morphologically the particular myelinated fibers showing the conduction block in human cases, but the alterations of myelinated fibers in the experimental models have been studied. The disturbance and/or destruction of the axoglial junction, with or without subsequent paranodal and segmental demyelination, is the major cause of the conduction block and is relatively easily identified morphologically in teased fiber and electron microscopic preparations of myelinated fibers. Following paranodal and segmental demyelination, the compensatory increase of large intramembranous particles, probably corresponding to the sodium channel, may enable the continuous conduction to be successful across the demyelinated axon. The abnormality of the nodal axolemma, dysfunction and/or loss of sodium channels, is another major cause and is not easily proven by light and electron microscopic techniques. Both causes may be concomitant under certain clinical and experimental conditions. Clinical and experimental conditions characterized by the conduction block are also listed.
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PMID:[Morphologic basis of conduction block]. 181 4

A new method has been developed for analyzing transmural distributions of finite deformation in canine ventricular myocardium without the need to assume that the strain in a finite volume of the wall is homogeneous. The three-dimensional nodal geometric parameters of bilinear-cubic or bilinear-quadratic finite elements are fitted by least squares to the measured coordinates of 12-18 radiopaque markers implanted in the left ventricular free wall. For six dog hearts, root-mean-squared errors in the fitted in-plane coordinates ranged from 0.079-0.556 mm in the end-diastolic reference state and 0.142-0.622 mm at end-systole. The corresponding error ranges in the radial coordinate were 0.042-0.264 mm at end-diastole and 0.106-0.279 mm at end-systole. Smoothly continuous transmural profiles of wall strain computed as the element deformed during the cardiac cycle from end-diastole to end-systole showed good agreement with the discrete results of conventional homogeneous analysis. Using the kinematics of a thick-walled incompressible cylinder, overall absolute errors due to the non-homogeneity of myocardial deformation were found to be reduced in the new analysis by 30-35% for typical experimental parameters. Overall relative errors were also reduced (from 23 to 20%). Since measurement errors in the reconstructed marker coordinates were spatially smoothed by the fitting procedure, noise in the computed deformations was also substantially attenuated, and transmural gradients of three-dimensional strain components could be obtained with improved accuracy. Hence physiological factors affected by transmural stress and strain distributions, such as myocardial blood flow, ischemia and hypertrophy, may be better understood.
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PMID:Non-homogeneous analysis of three-dimensional transmural finite deformation in canine ventricular myocardium. 188 Jan 38

The fine structural alteration and histochemical changes of the cardiac conduction system were studied in dogs and rats using various models of ischemic and reperfusion injury. The role of Ca2+ overload and reactive oxygen species (ROS) per se were also investigated. In all models of injury the activity of glycogen phosphorylase (histochemical indicator of the early ischemic changes) was present in nodal and conducting cells, although it was markedly diminished or absent in surrounding contractile muscle. Fine structural ischemic alterations progressed more slowly in conducting cells in comparison with working myocardial cells. Changes induced by Ca2+ paradox or ROS were reversible in conducting tissue in contrast to working myocardial tissue. The observations support the concept that conducting cells are more resistant to ischemia and also to reperfusion related injury than contractile myocardial cells.
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PMID:Vulnerability of specialized conductive tissue to ischemia and reperfusion related injury. 202 50

Whether compression nerve injury is due to ischemia, direct mechanical injury, or both remains unsettled. To assess structural changes of nerve during compression, peroneal nerves of rats were compressed at various pressures for different times, and the structural alterations were stopped by simultaneous in situ and perfusion fixation. The structural changes observed during a few minutes of compression cannot be explained by ischemic injury because the pathologic alterations characteristic of ischemia take many hours to develop and in any case are different from the ones found here. The pressure- and time-related structural changes observed in the present study under the cuff were (i) decrease in fascicular area and increase in fiber density due to expression of endoneurial fluid; (ii) compression and expression of axoplasm, sometimes to the point of fiber transection; (iii) lengthening of internodes; and (iv) obscuration of nodes of Ranvier due to cleavage and displacement of myelin and overlapping of nodes by displaced loops of myelin. At the edges of the cuff the changes were (i) increase of fascicular area probably from expressed endoneurial fluid; (ii) widening of nodal gaps, perhaps mainly from translocated axonal fluid; and (iii) disordered structure of axoplasm. We suggest that the process of paranodal demyelination and axonal transection are linked, occur during the act of compression, and are due to shear forces. The initial event is expression of endoneurial fluid, followed by compression and expression of axoplasm and cleavage and displacement of layers of myelin. Conceivably, with prolonged cuff compression ischemic injury might be found to be superimposed on mechanical injury.
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PMID:Structural alterations of nerve during cuff compression. 226 33


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