ContributorsGIW wrote and revised the manuscript in response to co-author comments. He finalized all the figures and tables, performed the literature search, and assisted with data interpretation. HJK critically reviewed the manuscript and made important suggestions to improve it. He assisted with data interpretation. IBA performed the data analysis, constructed the figures and tables, and made important suggestions to improve the manuscript. H-CK assisted with the data analysis and also reviewed the manuscript. GRC critically reviewed the manuscript and made important suggestions to improve it. He assisted with data interpretation. All other authors were given the opportunity to review the manuscript and make suggestions which GIW received, either revising the paper or providing explanations. All who are not deceased were involved with approval of the manuscript.
This novel protocol treatment induces a fast and long-term remission in severe pemphigus and seems to offer an improved side-effect profile compared with daily use of corticosteroids.
A B S T R A C T We have recently demonstrated enhanced a-adrenergic responsiveness assessed electrophysiologically in ischemic and reperfused myocardium. This study was performed to determine whether ischemia alters a,-adrenergic receptor number (Bmax) or affinity (KD) based on [3H]prazosin binding. Within 30 min after occlusion, Bmax increased in ischemic regions to 207% of control to 27+4 fmol/mg protein, with the increase persisting (+ 141% of control) during early reperfusion (2 min), before returning to control base-line values (13±1.6) after 15 min of reperfusion. KD was not altered at any interval studied. Beta receptor number ([3H]dihydroalprenolol) and Na+-K+ ATPase activity were comparable in control compared to ischemic myocardium although (3-receptor Bmax and KD in both regions decreased during early reperfusion. Thus, the enhanced a-adrenergic responsivity previously recognized with ischemia and reperfusion is correlated with an increase in aladrenergic receptors.
INTRODUCTIONRecently we have found that a-adrenergic blockade with either phentolamine or prazosin (but not ,3-adrenergic blockade) abolishes ventricular fibrillation induced by either coronary occlusion or subsequent reperfusion and that the enhanced idioventricular rate associated with reperfusion is abolished by phentolamine but not propranolol (1). In addition, efferent left stellate nerve stimulation during early reperfusion increases the idioventricular rate, a response abolished by phentolamine but not by propranolol (1). Thus, a-adrenergic stimulation contributes to the dysrhythmia.
We evaluated the contribution of intramural electrical events in initiation and maintenance of ventricular tachycardia in 15 dogs 3-8 days after either permanent (n = 2) or transient (n = 13) coronary artery occlusion. Seven of the dogs (47%) demonstrated eight distinct monomorphic ventricular tachycardia patterns which were mapped by means of a recently designed computerized system capable of simultaneously detecting, storing, and assessing information from 232 individual cardiac sites. Using both epicardial and intramural electrodes, we found definitive evidence for intramural reentry in seven of the eight monomorphic tachycardias analyzed. Furthermore, five of these animals (71%) demonstrated microreentry, in which small epicardial conduction loops exited intermittently into nonrefractory subendocardium to initiate succeeding beats, while, in the remaining two dogs, ventricular tachycardia was due to macroreentry, during which the broad subendocardial wavefronts depolarizing the ventricle constituted the proximal (fast) reentry limbs. Detailed anatomical analysis of the resultant infarcts demonstrated the thin surviving epicardial tissue rim to be the site of conduction delay necessary for reentry, whereas "preferred pathways" of exit into the subendocardial plane occurred at the infarct borders and were of variable configuration. Successful interruption of these rhythms should accompany interference with the process of exit into nonrefractory subendocardial tissue.
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