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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exogenous adenosine has been shown to have potent electrophysiologic effects and antiarrhythmic properties within the atrioventricular (AV) node. Endogenous adenosine, a nucleoside with an increased release signaled by ischemia and hypoxia, is not believed to exert significant effects during homeostatic conditions. Recent experimental evidence suggests, however, that under normoxic conditions, the amount of adenosine released may be sufficient to mediate some of its physiologic effects. This study was designed to test the hypothesis that in humans the electrophysiologic effects of endogenously released adenosine on AV nodal conduction can be demonstrated under normoxic conditions by inhibiting uptake and degradation of the nucleoside. In the first protocol, the effects of intravenous dipyridamole (0.56 mg/kg bolus i.v., 5 micrograms/kg/minute infusion), a nucleoside-transport blocker that elevates endogenous plasma levels of adenosine, on AV nodal conduction were evaluated in seven patients. At a constant atrial paced cycle length, dipyridamole increased the AH interval from 110 +/- 19 to 164 +/- 26 msec, p = 0.002 (+/- SEM). Aminophylline (5.6 mg/kg i.v.), a competitive antagonist of adenosine, completely reversed the effects of dipyridamole on AV nodal conduction. Similarly, dipyridamole increased the cycle length at which pacing-induced AV nodal Wenckebach occurred, from 348 +/- 31 (control) to 388 +/- 33 msec (dipyridamole) (p = 0.002). In a second protocol, the effects of intravenous dipyridamole were evaluated in another group of six patients who had supraventricular tachycardia (SVT) in which the AV node was part of the reentrant circuit.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrophysiologic effects of dipyridamole on atrioventricular nodal conduction and supraventricular tachycardia. Role of endogenous adenosine. 259 20

The effects of intravenously (IV) administered magnesium chloride (MgCl) on electrophysiologic and electrocardiographic variables were studied in 13 patients undergoing a routine electrophysiologic assessment for clinical indications. An infusion of 12 mmol of MgCl was given during a 10-min period and relevant electrophysiologic variables were determined before and after the infusion. Serum Mg levels increased from 0.78 +/- 0.03 (mean +/- SEM) before to 1.52 +/- 0.08 ms after the infusion (p less than 0.0001). Magnesium treatment caused a significant prolongation in PR interval (from 151 +/- 8 to 174 +/- 8 ms, p less than 0.001) as well as in QRS duration (from 90 +/- 4 to 101 +/- 6 ms, p less than 0.05). Likewise, intra-atrial (PA) as well as atrioventricular (AV) nodal (AH) conduction times were significantly prolonged (from 33 +/- 3 to 46 +/- 3 ms, p less than 0.01, and from 85 +/- 6 to 94 +/- 6 ms, p less than 0.05, respectively). Mean effective and functional atrial refractory periods increased (from 228 +/- 8 to 256 +/- 10 ms, p less than 0.01 and from 292 +/- 9 to 320 +/- 11 ms, p less than 0.01, respectively), as did mean AV node functional refractory period (from 399 +/- 29 to 422 +/- 27 ms, p less than 0.02). No significant change occurred with regard to sinus node function (as estimated from heart rate, sinus node recovery time, and calculated sinoatrial conduction time) or ventricular refractoriness. It is concluded that IV Mg has several electrophysiologic effects that may be beneficial in the treatment/prevention of supraventricular tachyarrhythmias.
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PMID:The electrophysiological effects of intravenous magnesium on human sinus node, atrioventricular node, atrium, and ventricle. 265 79

Medical grade silicone rubber has long been considered a suitable meniscal replacement, but there has been increasing concern about migration of this material into adjacent tissues. The objectives of this study were to determine the definitive composition of tissue-incorporated material which is presumed by light microscopy to be silicone and to identify long term histopathologic sequelae of meniscal replacements. Adult female patients underwent meniscectomy and replacement with silicone rubber (Silastic) implants. After 12 to 18 months, recurrence of symptoms in 8% of these cases led to implant removal with excision of peri-implant fibrous pseudocapsules. Excised tissues, including one preauricular lymph node and implants were submitted for light microscopy, SEM, and energy dispersive x-ray microanalysis (EDX) for the identification of elemental composition, critical surface tension measurement, and internal reflection infrared spectroscopy. EDX revealed prominent peaks for silicon in both pseudocapsular and nodal tissues. Morphologic findings surrounding the long-term implants included foreign body reaction, synovitis, dystrophic calcification, fibrocartilaginous metaplasia, hyalinization, and scarring. Particulate silicone debris induced a pathologic response in the tissues and migrated to nodes. These findings suggest that periodic evaluation be performed over the life of such implants to rule out breakdown under function. These findings should intensify the search for improvements or replacements for silicone rubber as an interpositional material in the temporomandibular joint.
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PMID:Silicone rubber temporomandibular joint (TMJ) meniscal replacements: postimplant histopathologic and material evaluation. 341 Aug 67

Electrophysiologic studies were performed in 11 patients with atrioventricular (AV) nodal reentrant tachycardia (SVT) before and after intravenous administration of 1.5 to 2 mg/kg ethmozin. Initially, 9 of 11 patients had induction of sustained SVT, and two remaining patients had nonsustained SVT and atrial echoes, respectively. Ethmozin terminated induced SVT in six of nine patients. In six of nine patients ethmozin prevented the development of sustained SVT, indicating that ethmozin depressed retrograde fast pathway AV nodal conduction. In four of these patients atrial echoes were abolished. In the two remaining cases ethmozin prevented the induction of nonsustained SVT. In only three of these nine patients was sustained SVT induced. Anterograde fast and slow pathway properties did not significantly change with ethmozin administration. Effective refractory period (ERP) of the ventriculoatrial (VA) conduction system and ventricular paced cycle length producing VA block was 305 +/- 40 (mean +/- SEM) and 347 +/- 38 msec before and 424 +/- 105 and 475 +/- 71 msec after ethmozin administration, respectively (p less than 0.01, n = 8), suggesting depression of retrograde pathway with ethmozin administration. Ethmozin significantly (p less than 0.05) lengthened PA, AH, HV, and PR intervals (36 +/- 11 to 45 +/- 14 msec, 84 +/- 21 to 93 +/- 17 msec, 42 +/- 8 to 50 +/- 7 msec, and 163 +/- 23 to 190 +/- 31 msec, respectively). No significant change was observed in sinus rate, QRS and QT intervals, or ERP of atrium and ventricle. Thus, a single intravenous dose of ethmozin terminated induced SVT and prevented induction of sustained SVT in most patients, reflecting depression of retrograde fast pathway conduction.
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PMID:Ethmozin. II. Effects of intravenous drug administration on atrioventricular nodal reentrant tachycardia. 638 89

Although isolated popliteal node perfusion studies have shown intranodal exchange of water between blood and lymph, questions remain about the significance of such studies. Do some nodes exchange protein with blood, and are there shunt pathways around nodes which tend to buffer intranodal exchange of water? Finally, what is the magnitude of difference in using postnodal lymph to compute tissue capillary membrane parameters of reflection coefficient, sigma, and permeability-surface area product, PS? Seventeen conditioned dogs were randomly divided into matched experimental (N = 8) and sham (N = 9) groups in which lumbar trunk lymph was measured for flow (JV) and lymph/plasma protein concentration ratios (R) before and after ligation or sham ligation of the medial iliac lymph node (MILN). Ligation reduced (JV) from 25.89 +/- 4.21 SEM microliter . min-1 . kg-1 to 20.45 +/- 1.84 (P less than .008), decreased R from .66 +/- .04 to .55 +/- .02 (P less than .0000), increased sigma from .42 +/- .04 to .55 +/- .04 (P less than .004), and did not change PS which was 11.45 +/- 2.13 before and 14.43 +/- 4.19 after ligation. No similar changes occurred in the sham group. Of four hypotheses tested, the data were compatible only with post ligation flow equal to the sum of tissue lymph production and efferent flow from upstream nodes. Protein moved from blood into the nodal lymph nearly with the ease of water. Reflection coefficient was 23% higher at the afferent level than in the post nodal lymph, but PS was unaffected by the MILN. Differences in using post nodal sigma and PS to compute tissue fluid levels of protein are about 10% at these flow, and shunt flow is as high as 79% of lumbar trunk flow. Conclusions based upon sigma and PS differences across the node must be tempered because of the possibility of the trend toward lymph-blood equilibration of afferent lymph if it passed through several upstream nodes.
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PMID:Dynamics of water and protein transport through and around the canine medial iliac lymph nodes. 654 62

Electrophysiologic studies before and after administration of 50 mg of intravenous (IV) acebutolol were performed in 20 patients. Four of the 20 had persistent preexcitation, two had intermittent preexcitation, and 14 had a concealed retrogradely conducting accessory pathway (AP). Acebutolol depressed anterograde AP conduction with loss of preexcitation in one patient and increased the effective refractory period of AP in the remaining three; in most, it depressed anterograde normal pathway conduction. The longest atrial paced cycle length producing atrioventricular (AV) nodal block increased from 290 +/- 7 to 39 +/- 6 msec (mean +/- SEM) after acebutolol (p less than 0.01). Acebutolol had no significant effect on retrograde AP conduction. Sustained AV reentrant tachycardia was inducible in all 20 patients before acebutolol and in 19 after acebutolol. The cycle length of tachycardia increased from 323 +/- 8 to 352 +/- 8 msec after acebutolol (p less than 0.01), reflecting an increment of A-H interval from 148 +/- 8 to 174 +/- 9 msec (p less than 0.01). Electrophysiologic studies were reported after 800 mg of oral acebutolol given in four divided doses at six-hour intervals in eight patients. The results were comparable to those of IV acebutolol. Thus, acebutolol depresses AV nodal conduction and slows the rate of AV reentrant tachycardia, but is generally ineffective in inhibiting the induction of sustained tachycardia. It occasionally depresses anterograde AP conduction.
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PMID:Effects of acebutolol on paroxysmal atrioventricular reentrant tachycardia in patients with manifest or concealed accessory pathways. 684 37

Flecainide acetate (R818) is a new antiarrhythmic agent for oral and intravenous use; it has predominantly class I properties and a long plasma half-life. Electrophysiologic effects were evaluated in 11 patients with sinus nodal dysfunction before administration of flecainide acetate and 15 to 60 minutes after intravenous administration of 1.5 mg/kg body weight of flecainide acetate given over 15 minutes. In 8 of 11 patients with maximal sinus nodal recovery time increased after flecainide acetate. However, the mean maximal sinus nodal recovery time was not statistically significantly increased from 1,929 +/- 184 (mean +/- standard error of the mean [SEM]) to 2,770 +/- 500 ms (p less than 0.10). The corrected sinus nodal recovery time increased from 875 +/- 181 before to 1,727 +/- 507 ms after administration of flecainide acetate (p less than 0.05). The sinus cycle length and sinoatrial conduction time were not significantly changed. Flecainide acetate induced a marked prolongation of the H-V interval (from 41 +/- 3 to 52 +/- 4 mg [p less than 0.01]) as well as a significant increase in the A-H interval, QRS duration, and QT100 interval. The effective and functional refractory periods of the atria increased by 12% (p less than 0.01) and 11% (p less than 0.01), respectively. The atrioventricular (AV) nodal functional refractory period increased significantly by 7% (p less than 0.01), whereas the 9% prolongation of the effective refractory period was not statistically significant. No side effects were observed. It is concluded that flecainide acetate prolongs atrial and ventricular conduction and refractoriness, and thus appears to be a potent antiarrhythmic agent. However, the sinus nodal function is depressed, and thus caution is advised in the use of flecainide acetate in patients with sinus nodal dysfunction.
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PMID:Electrophysiologic effects of flecainide acetate in patients with sinus nodal dysfunction. 713 36

Effects of intravenous atropine on postpacing impulse recovery time of the subsidiary pacemakers were studied by incremental atrial pacing in 9 patients with sinus nodal (SN) dysfunction. Patients having either or both of the following anomalies are used: 1) persistent sinus bradycardia (sinus cycle length greater than 1000 msec), or documented episodes of sinoatrial block or arrest and/or 2) maximum corrected SN recovery time of longer than 525 msec before and after atropine. Seven patients had a history of cerebral ischemic symptoms. The mean +/- SEM of the maximum A-V junctional recovery times (MJRTs) before and after atropine, measured in 5 patients, were 2,485 +/- 825 msec and 1,164 +/- 281 msec, respectively (p less than 0.01). The average percent reduction of the junctional escape times in these 5 patients was 53.2%. In all 9 patients MJRT shortened to less than 1,610 msec after atropine. Moreover, a low atrial pacemaker also was the escape mechanism following pacing in 2 patients after atropine; the maximum atrial recovery times were 2,500 msec and 1,220 msec, respectively. We conclude that atropine can markedly enhance escape mechanism of the subsidiary pacemakers in patients with SN dysfunction.
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PMID:Effect of atropine on escape mechanism of the subsidiary pacemakers in patients with dysfunction of the sinus node. 714

The effects of oral disopyramide phosphate on laboratory induction of paroxysmal supraventricular tachycardia (PSVT) were studied in 16 patients with clinical PSVT. After control electrophysiologic study to determine the inducibility and mechanism of PSVT, patients were given 200-300 mg (275 +/- 45 mg, mean +/- SD) of disopyramide for three to five doses over 24 hours and were then restudied. All patients had inducible, sustained PSVT during the control study. After disopyramide, PSVT was noninducible in eight patients (50%), including six of nine with atrioventricular nodal reentrance and two of seven with atrioventricular reentrance; inducible but nonsustained in two (12.5%) (both with atrioventricular reentrance); and inducible and sustained in six (37.5%). The benefit of disopyramide seemed predominantly to reflect depression of conduction in the retrograde limb of the circus movements, although effects upon the antegrade limb were also observed. In the eight patients with inducible PSVT before and after disopyramide, tachycardia cycle length increased from 348 +/- 33 to 404 +/- 29 msec (mean +/- SEM) (p less than 0.001). These results suggest that disopyramide would be effective in preventing recurrence of clinical PSVT in selected patients.
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PMID:Effects of oral disopyramide phosphate on induction of paroxysmal supraventricular tachycardia. 723 16

Electrophysiologic studies were performed in 14 patients with atrioventricular nodal reentrant paroxysmal tachycardia (PSVT) before and after oral administration of 1.2-1.6 g quinidine sulfate over a 24-hour period (0.3-0.4 g every 6 hours). Studies were performed after 0.5-1 mg i.v. atropine before and after quinidine. All 14 patients had induction of sustained PSVT before quinidine, with or without atropine. After quinidine, 11 patients lost the ability to induce echoes or sustain PSVT, reflecting depression of the retrograde pathway with either absence of atrial echoes (six patients) or induction of nonsustained PSVT, with termination of echoes or PSVT occurring after QRS (block in retrograde pathway) (five patients). In only one of these 11 patients was sustained PSVT inducible after addition of atropine. All 11 were discharged on the same dose of quinidine. In three patients, quinidine was discontinued because of side effects. Follow-up in the remaining eight patients for 8 +/- 2 months showed no recurrence of sustained PSVT. Three of the 14 patients had induction of sustained PSVT after quinidine. Ventricular paced cycle length producing ventriculoatrial block was 314 +/- 7 msec (mean +/- SEM) before and 392 +/- 13 msec after quinidine (p less than 0.01) in the 14 patients, suggesting depression of the retrograde pathway with quinidine. In summary, quinidine inhibited induction of sustained atrioventricular nodal reentrant tachycardia with depression of the retrograde pathway. It is very effective in preventing recurrence of PSVT in most patients.
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PMID:Effects of quinidine on atrioventricular nodal reentrant paroxysmal tachycardia. 727 82


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