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Biomedical subjects

R C Wesley

Publications and source records attributed to R C Wesley.

36 records · Page 2Linked to original sources

Patient response to variations in denture technique. Part VII: Twenty-year patient status.

Sixty-four patients were originally treated with complete dentures. Two different techniques, complex and standard, were used with 32 patients assigned to each group. Patients were recalled for their 20th year recall and 34 of the original 64 patients returned. Of those 34 patients, 26 patients were still wearing their original dentures. All 26 patients were judged by three project clinicians to have clinically acceptable dentures. In addition, all but two stated that their dentures were clinically acceptable. Neither of these patients were unhappy with fit, but with the esthetics. One patient had worn his denture teeth by pipe smoking and the other had bleached the pink out of her denture bases. The remaining eight patients who still participate in the project have had modifications in their original dentures or have had new dentures constructed.

Adult↗

Role of endogenous adenosine in postdefibrillation bradyarrhythmia and hemodynamic depression.

In halothane-nitrous oxide-anesthetized pigs, the effect of the competitive adenosine antagonist, BW-A1433U (a derivative of 1,3-dipropyl-8-phenylxanthine), on postdefibrillation bradyarrhythmia and hemodynamic depression was investigated. In protocol 1, repetitive episodes of ventricular fibrillation lasting 15 seconds before transthoracic DC shock were performed in five animals, before (control) and after the administration of BW-A1433U (5 mg/kg i.v.). An unsuccessful initial shock was immediately followed by a rescue shock of 40 A. In ventricular fibrillation episodes requiring rescue shocks, nine of 19 episodes (47%) exhibited second- or third-degree atrioventricular block at 15 seconds postdefibrillation compared with only one of 16 BW-A1433U episodes (6%). In protocol 2, the effect of BW-A1433U was determined in the presence of dipyridamole, a nucleoside uptake blocker known to potentiate the cardiac actions of adenosine. To counter the hypotensive effect of dipyridamole, methoxamine was continuously infused at 0.015 mg/kg/min i.v. Sequential episodes of ventricular fibrillation lasting 45 seconds were terminated by shocks of 40 A in the presence of methoxamine alone, after dipyridamole (1.5-7.5 mg i.v.), and after BW-A1433U (5 mg/kg i.v.). Over the first 15 seconds postdefibrillation, BW-A1433U significantly (p less than 0.05) increased the number of spontaneous beats (31 +/- 2) and systolic/diastolic blood pressure (111 +/- 4/67 +/- 5 mm Hg; mean +/- SEM; n = 9) compared with both methoxamine (16 +/- 2 beats; 98 +/- 14/52 +/- 12 mm Hg; n = 5) and dipyridamole (8 +/- 3 beats; 58 +/- 11/27 +/- 6 mm Hg; n = 9), respectively. Rapid infusion of BW-A1433U during dipyridamole postdefibrillation periods raised heart rate and blood pressure to preventricular fibrillation levels within 30 seconds. Thus, BW-A1433U can reverse and prevent postdefibrillation bradyarrhythmia and hemodynamic depression. Endogenous adenosine may be an important mediator of postdefibrillation cardiovascular collapse.

Adenosine↗

Electrophysiologic effects of dipyridamole on atrioventricular nodal conduction and supraventricular tachycardia. Role of endogenous adenosine.

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)

Adenosine↗

Antiadrenergic effects of adenosine on His-Purkinje automaticity. Evidence for accentuated antagonism.

The effects of adenosine on the human His-Purkinje system (HPS) were studied in nine patients with complete atrioventricular (AV) block. Adenosine had minimal effect on the control HPS cycle length, but in the presence of isoproterenol increased it from 906 +/- 183 to 1,449 +/- 350 ms, P less than 0.001. Aminophylline, a competitive adenosine antagonist, completely abolished this antiadrenergic effect of adenosine. In isolated guinea pig hearts with surgically induced AV block, isoproterenol decreased the HPS rate by 36%, whereas in the presence of 1,3-dipropyl-8-phenyl-xanthine, a potent adenosine antagonist, the HPS rate decreased by 48% and was associated with an increased release of adenosine. Therefore, by blocking the effects of adenosine at the receptor level, the physiologic negative feedback mechanism by which adenosine antagonizes the effects of catecholamines was uncoupled. The results of this study indicate that adenosine's effects on the human HPS are primarily antiadrenergic and are thus consistent with the concept of accentuated antagonism. These effects of adenosine may serve as a counterregulatory metabolic response that improves the O2 supply-demand ratio perturbed by enhanced sympathetic tone. Some catecholamine-mediated ventricular arrhythmias that occur during ischemia or enhanced adrenergic stress may be due to an imbalance in this negative feedback system.

Adenosine↗

Mechanism of atropine-resistant atrioventricular block during inferior myocardial infarction: possible role of adenosine.

Mechanisms responsible for atrioventricular (AV) block during acute inferior myocardial infarction are only partially understood. Increased parasympathetic tone is the factor usually postulated; however, persistence of AV block after atropine administration is frequently observed. Adenosine, an endogenous ischemic metabolite, has well established depressant effects on AV node conduction. In this report, an episode of atropine-resistant AV block was reversed by aminophylline, a competitive adenosine antagonist, in a patient with an acute inferior myocardial infarction. This observation suggests a role for adenosine in the mediation of ischemia-induced AV node block.

Adenosine↗

Role of adenosine as mediator of bradyarrhythmias during hypoxia in isolated guinea pig hearts.

Tissue concentrations of adenosine, an endogenous metabolite with negative chronotropic and dromotropic actions, are known to increase when myocardial oxygen supply is reduced. In this study the concentrations of endogenous adenosine released during a period of hypoxic perfusion were measured to determine whether they are sufficient to account for the effect of hypoxia on atrioventricular conduction in isolated perfused guinea pig hearts. In addition, the efficacy of competitive adenosine antagonism in reversing the effect of hypoxia on atrioventricular conduction and atrial automaticity were compared. Effluent samples for adenosine were collected at the onset of spontaneous and atrial pacing induced second degree atrioventricular block during hypoxic perfusion (PO2 3.07 kPa) and during the combined infusion of adenosine plus the nucleoside transport blocker, dipyridamole (PO2 71.1 kPa). The mean (SEM) atrial cycle lengths associated with the onset of atrioventricular block were 333(10) and 297(2) ms respectively. Effluent concentrations of adenosine associated with atrioventricular block during hypoxia (2342(160) pmol X min-1 X g-1 heart weight) were approximately equal to those obtained during the infusion of adenosine plus dipyridamole (2538(256) pmol X min-1 X g-1 heart weight) (no statistically significant difference). During hypoxic perfusion, among hearts showing spontaneous atrioventricular block and those in which atrial slowing prevented the onset of spontaneous block, the competitive adenosine antagonist aminophylline (60 mumol X litre-1) reversed either spontaneous or atrial pacing induced block without any effect on spontaneous atrial cycle length.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗

Role of adenosine on ventricular overdrive suppression in isolated guinea pig hearts and Purkinje fibers.

The present study was undertaken to demonstrate and characterize potentiation of ventricular overdrive suppression by adenosine. To substantiate that adenosine has an enhanced effect on overdrive suppression, it would be necessary to demonstrate that adenosine increases pause duration independent of slowing spontaneous pre-drive rate. In isolated perfused guinea pig hearts with surgically induced complete atrioventricular block, the effect of adenosine (2-20 microM) on pause duration was compared to two alternative means of slowing the pre-drive rate, i.e., hypothermia (28.0 degrees C to 34.0 degrees C) and cesium chloride (0.3-1.0 mM). The slope value of the linear regression line describing the relationship between pre-drive cycle length and pause duration for adenosine (15.8) was significantly greater than control (1.7), hypothermia (1.7), and cesium chloride (5.4). The competitive adenosine antagonist, aminophylline (60 microM), when infused at the initiation of overdrive during adenosine administration, significantly reduced the effect of adenosine on pause duration by 72.9 +/- 4.2% (mean +/- SEM). The reduction in pause duration by aminophylline was specific for adenosine and did not occur under control conditions or during cesium chloride administration. During hypoxia, aminophylline and adenosine deaminase, when infused at the initiation of overdrive, caused 72.3 +/- 5.6 and 63.3 +/- 6.1% reductions in pause duration, respectively. Endogenous adenosine levels rose significantly with hypoxia (1,687 +/- 202 vs. 36 +/- 4 pmol/min per g during normoxia) and increased significantly further during hypoxic overdrive (3,004 +/- 323 pmol/min per g). In isolated guinea pig Purkinje fibers (n = 4), adenosine (20 microM) increased pause duration by 73.6 +/- 9.9% while only minimally affecting the pre-drive cycle length (7.6 +/- 3.8%). These fibers, when stimulated at 1.5 Hz, also displayed an adenosine-induced reduction in action potential duration at 90% repolarization (16 +/- 2 msec). In addition, we demonstrated that adenosine had an enhanced effect on pause duration in the presence of ouabain (1 microM)-induced attenuation of overdrive suppression. Thus, in isolated Purkinje fibers, it is unlikely that the potentiating effect of adenosine on pause duration, which is independent of its chronotropic effect, is mediated via an enhancement of sodium potassium adenosine triphosphatase pump activity. The effect of adenosine is likely to be secondary to a direct action on outward potassium conductance.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine↗

Patient response to variations in denture techniques. Part VI: Mastication of peanuts and carrots.

This 5-year study was designed to determine if differences in masticatory ability existed among patients for whom dentures had been prepared with two different techniques. Patients were instructed to chew a given amount of a reliable test food for a certain number of strokes on each side of the mouth. After each trial the food was collected into a No. 8 mesh screen, washed, dried, and weighed. The percentage weight of food masticated per side per patient was recorded for each year. Results were combined for each group results and analyzed statistically. Statistical analysis of the two groups revealed changes in masticatory ability over the 5-year period. However, no significant statistical differences in masticatory ability existed between the two groups.

Arachis↗

Patient response to variations in denture technique. Part III: Five-year subjective evaluation.

Dentures were constructed for 64 patients by two different techniques. One technique, designated as "complex," involved more complicated procedures such as a true hinge axis location, balanced occlusion, dentures remounted on an articulator after processing with new interocclusal records, and occlusal corrections made on the articulator. The "standard" technique involved an arbitrary mounting of the maxillary cast on the articulator, arranging the occlusion with centric relation coincident with centric occlusion but without a balanced occlusion, and making occlusal corrections in the mouth. Subjective evaluations were made for each of the 64 patients at initial placement of the dentures and for all active patients at five yearly recall visits following placement. The evaluation method was designed to determine clinical differences between the dentures made by the two techniques. At the end of 5 years, the data obtained at five yearly recall visits were subjected to statistical testing. These tests were performed to determine if the technique by which the dentures were made had any effect on the performance of the dentures that could be detected clinically. The results of the test showed that there was no significant difference between dentures made using two denture techniques that could be detected by subjective means.

Alveolar Process↗