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Biomedical subjects

R J Anderson

Publications and source records attributed to R J Anderson.

At least 217 records · Page 12Linked to original sources
PubMed1988

Stability of normal joint findings in persistent classic rheumatoid arthritis.

We reviewed the records of 44 patients, retrospectively selected because they had had persistently active rheumatoid arthritis for more than 5 years (mean +/- SD followup 9.8 +/- 2.6 years) and because they met the American Rheumatism Association criteria for classic disease, to determine the change in extent of the anatomic distribution of joint involvement over time. The positive predictive value of a lack of inflammation in a joint during the first year for the lack of involvement over the ensuing 4 years was 87%. Thirty-eight of the 43 joints that required replacement were inflamed in the first year of disease.

Arthritis, Rheumatoid↗
PubMed1988

A comparison of epinephrine and methoxamine for resuscitation from electromechanical dissociation in human beings.

Electromechanical dissociation (EMD) is an organized electrical depolarization of the heart without synchronous myocardial fiber shortening and, therefore, without cardiac output. Patients in EMD have a poor prognosis for resuscitation and long-term survival. The beneficial effect in resuscitation of epinephrine, the adrenergic agent currently recommended, has been shown to depend on stimulation of alpha-adrenergic vasoconstriction. The beta-adrenergic inotropic and chronotropic effects of epinephrine are theoretically detrimental by increasing myocardial oxygen consumption and subendocardial ischemia. The purpose of our study was to determine whether the pure alpha agonist methoxamine was superior to epinephrine in human beings in EMD as determined by survival at one hour. These two agents were compared in a prospective, randomized, and double-blinded study involving 80 patients with EMD of various causes seen in the emergency department and internal medicine inpatient service. The advanced cardiac life support (ACLS) algorithm (current at the time of our study) for resuscitation from EMD was used, with the blinded study drug (epinephrine 1 mg or methoxamine 10 mg) administered where the algorithm calls for epinephrine. Calcium and isoproterenol also were used in the majority of cases according to ACLS standards but never prior to the use of methoxamine or epinephrine. Survival data are summarized as: survival less than one hour, 22 patients receiving methoxamine, 22 receiving epinephrine; one to six hours, 15 patients receiving methoxamine, 13 patients receiving epinephrine; six to 12 hours, one patient receiving epinephrine; more than 24 hours but not surviving to discharge, three patients receiving methoxamine, two patients receiving epinephrine; and survival to discharge, one patient receiving epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Sodium taurocholate increases hydraulic conductivity in rabbit collecting tubule.

Abnormalities in renal tubular function occur commonly in the setting of hyperbilirubinemia. In the present studies, the possibility that the bile salt sodium taurocholate exerts a direct effect on renal epithelial transport was investigated in vitro. We found that addition of sodium taurocholate to fluid bathing perfused rabbit cortical collecting tubules increases hydraulic conductivity (Lp) in a manner similar in time course and significantly less in magnitude to that observed with maximal concentrations of arginine vasopressin. Sodium taurocholate reversibly potentiates rabbit cortical collecting tubular Lp stimulated by maximal concentrations of arginine vasopressin and a nonhydrolyzable cyclic AMP analogue. We also found that sodium taurocholate induces a dose-dependent leak from tubular lumen to bathing fluid of a small molecular weight substance (125I-iothalamate). Our studies suggest that sodium taurocholate increases rabbit cortical collecting tubular Lp by a cyclic AMP independent mechanism.

Animals↗
PubMed1988

Time course of electrophysiologic effects induced by di-n-butyl-2,2-dichlorovinyl phosphate (DBCV) in the adult hen.

Previous work in our laboratory indicated that di-n-butyl-2,2-dichlorovinyl phosphate (DBCV) produced electrophysiologic changes in hen peripheral nerve that coincided with the development of histopathologic changes and neurologic signs of peripheral neuropathy. The purpose of the present study was to follow the time course for the development of the electrophysiologic changes and to determine whether pretreatment with the phosphinate analog of DBCV (DBCV-P), a nonageable organophosphorus compound, prevented these effects. Although significant electrophysiologic deficits occurred in the tibial and sciatic nerve 24 h after DBCV treatment, the most marked changes coincided with the onset of clinical signs of organophosphorus-induced delayed neuropathy (14-21 d). The sciatic and tibial nerves were equally susceptible to DBCV in producing deficits characterized by changes in the relative refractory period and an increased strength-duration threshold. Pretreatment with DBCV-P prevented the clinical signs and also attenuated the electrophysiologic deficits induced by DBCV treatment. These data suggest that electrophysiologic deficits occur before clinical signs of organophosphorus-induced delayed neuropathy (OPIDN) and may be indicative of a link between neurotoxic esterase (NTE) inhibition and onset of overt clinical toxicity.

Action Potentials↗
PubMed1988

Changes in nerve membrane polarization following repeated exposure to soman.

The purpose of this study was to determine whether the slowly developing changes in potassium-induced depolarization in nerve membrane produced by soman are due to blockade of potassium conductance or to inhibition of Na,K-ATPase. Rats were dosed daily for 20 d with soman (0.075 mg/kg, ip). In isolated sucrose gap chambers, the nerves were challenged with extracellular potassium in the presence and absence of ouabain, 4-aminopyridine, and ouabain plus 4-aminopyridine. The enhancement of potassium-induced depolarization produced individually by ouabain and 4-aminopyridine was unaffected by soman pretreatment of the nerves. However, in the presence of both ouabain and 4-aminopyridine the soman-treated nerves showed a marked enhancement of potassium-induced depolarization. This effect was not seen in nerves exposed to soman for only 1 d. These results show that soman affects a nerve-membrane process other than potassium channels or Na,K-ATPase. The role of this unidentified process apparently is important in maintaining nerve function only when potassium conductance is blocked and Na,K-ATPase is inhibited. Furthermore, the effect of soman on this process is the result of an adaptive change rather than a direct effect, since single-dose exposure produced no shift in potassium-induced depolarization.

4-Aminopyridine↗
PubMed1988

Ventricular ectopic activity with diuretic therapy.

The arrhythmogenic potential of diuretic-induced hypokalemia in patients with uncomplicated hypertension has been controversial. Thirty-two hypertensive patients with previous diuretic-induced hypokalemia, normal 24-hour ambulatory ECG monitoring, and normal exercise testing were treated with 100 mg hydrochlorothiazide (HCTZ) daily (Group 1) to induce hypokalemia or with a combination of HCTZ with amiloride (Group 2) to attempt to maintain plasma potassium levels in the normal range during diuretic therapy. Those Group 1 patients (Group 1A) with increased ventricular ectopic activity (VEA) during HCTZ therapy were subsequently potassium-repleted with amiloride and with supplemental potassium chloride to evaluate the effect of these treatments on VEA. One Group 1 patient died suddenly after 12 days of HCTZ therapy. Autopsy findings suggested an arrhythmic death. Six Group 1 patients who had increased VEA with HCTZ treatment had reductions in VEA with amiloride or supplemental potassium chloride. Group 2 patients did not have a significant increase in VEA. Thus, diuretic therapy appears to cause VEA primarily by electrolyte changes that are induced.

Adult↗
PubMed1988

Phorbol esters inhibit adenylate cyclase activity in cultured collecting tubular cells.

Activators of protein kinase C, a calcium- and phospholipid-dependent protein kinase, inhibit vasopressin-stimulated water flow in toad bladder. To determine the biochemical mechanisms of this inhibition, we examined the effects of activators of protein kinase C on arginine vasopressin (AVP)-stimulated adenylate cyclase activity in cultured rabbit cortical collecting tubular cells. The phorbol ester, 4 beta-phorbol 12-myristate 13-acetate (PMA), the diacylglycerol, 1-oleyl-2-acetyl glycerol (OAG), and the diacylglycerol kinase inhibitor, R59022, all rapidly activate protein kinase C in collecting tubular cells. Pretreatment with PMA produces a delayed inhibition (greater than or equal to 4 h) of AVP-stimulated adenylate cyclase activity. The 4-h time lag suggests that the effects of protein kinase C are mediated indirectly, possibly as a consequence of stimulating cell proliferation. PMA does not inhibit cholera toxin- or forskolin-stimulated adenylate cyclase activity, suggesting an effect on the vasopressin receptor or coupling of the receptor to the stimulatory guanine nucleotide regulatory protein. Neither prostaglandins nor the inhibitory guanine nucleotide regulatory protein appear to mediate this effect. In contrast, treatment with either OAG or R59022 produces a rapid inhibition of both AVP- and forskolin-stimulated adenylate cyclase activity suggesting a prominent distal site of action, presumably at the catalytic subunit of adenylate cyclase. The results demonstrate that different activators of protein kinase C inhibit AVP-stimulated adenylate cyclase activity by distinctly different mechanisms possibly by altering the substrate specificity or activating multiple forms of the kinase. These results have important implications when using different activators to study the biological effects of protein kinase C.

Adenylyl Cyclase Inhibitors↗
PubMed1988

Cyclic guanosine monophosphate increases hydraulic conductivity in rabbit and rat CCT.

Although guanosine 3',5'-cyclic monophosphate (cGMP) is present in renal nephron segments, there is no information on the role of cGMP as a mediator of renal tubular transport events. We found that an activator of guanylate cyclase (nitroprusside) and 8-bromocGMP (8-BrcGMP) significantly increased hydraulic conductivity in rabbit and rat cortical collecting tubules (CCT) perfused in vitro. The effect of 10(-4) M 8-BrcGMP to increase CCT hydraulic conductivity was reversible and comparable in magnitude and time course to that produced by maximal concentrations of arginine vasopressin. In rabbit CCT, cGMP increased hydraulic conductivity in the presence of phosphodiesterase inhibition with methylisobutylxanthine and in the presence of supramaximal concentrations of arginine vasopressin. Neither nitroprusside nor 8-BrcGMP stimulated adenylate cyclase activity in microdissected CCT. These data demonstrate that cGMP can act independently of either stimulation of adenylate cyclase activity or inhibition of phosphodiesterase activity to increase hydraulic conductivity in the mammalian CCT.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Human platelet thermostable phenol sulfotransferase from blacks and whites: biochemical properties and variations in thermal stability.

Phenol sulfotransferase (PST) catalyzes the sulfate conjugation of catecholamines and of phenolic drugs. Human platelet PST exists in at least a thermolabile form (TL PST) and a thermostable form (TS PST). The mean basal level of platelet TS PST activity in samples from American blacks is significantly higher than the basal activity in samples from whites. We carried out the studies reported here to determine whether the higher basal TS PST activity in platelet homogenates from blacks was biochemically similar to the lower basal activity in samples from whites. We also characterized variations in TS PST thermal stability. Platelet TS PST activities in samples from the two groups were almost identical with respect to pH optima, Michaelis-Menten constant values for substrates, and susceptibilities to inhibition by 2,6-dichloro-4-nitrophenol and sodium chloride. Thermolabile and thermostable TS PST were present in samples from both blacks and whites. Thermal stabilities of TS PST in samples from 167 volunteers (104 blacks, 63 whites) were expressed as heated sample-to-control sample ratios. Bimodal frequency distribution histograms of the heated-to-control ratios revealed subgroups of samples with thermolabile TS PST activities from 13.5% of blacks (heated-to-control ratio less than 0.32) and 12.7% of whites (heated-to-control ratio less than 0.27). The mean heated-to-control ratio for thermostable TS PST from blacks was significantly higher than that from whites (0.52 +/- 0.01 vs 0.43 +/- 0.01, respectively, mean +/- SEM; p less than 0.0001). Our studies demonstrated the similarity of biochemical properties of platelet TS PST at the extremes of basal activity. They also showed equivalent subgroups of blacks and whites with thermolabile TS PST. The results are an important initial step toward testing the hypothesis that inheritance may be one factor in the regulation of basal levels of activities and thermal stabilities of platelet TS PST from American blacks.

Adult↗
PubMed1988

Personnel time and preparation costs for compounded versus premixed intravenous admixtures in three community hospitals.

Personnel time requirements and costs associated with the ordering, preparation, and administration of manually compounded versus premixed i.v. admixtures were determined at three for-profit community hospitals. The three hospitals, all owned by one corporation, ranged in size from 160 to 239 beds. At each hospital, pharmacists or technicians manually compounded admixtures in glass bottles or plastic bags. Work flow descriptions of the activities involved in the preparation and administration of admixtures were created, and time-motion and work-sampling techniques were used to observe three to five pharmacists or technicians in each hospital over a seven-day period. Drug waste also was monitored. At the conclusion of the baseline study, each hospital switched to the premixed products that they had chosen to evaluate; admixtures of cefazolin sodium, cefoxitin sodium, gentamicin sulfate, and potassium chloride were available. After a two-week acclimation period, the seven-day study was repeated. Average total labor time ranged from 5.6 to 9.1 minutes per compounded admixture to 4.1 to 7.7 minutes per premixed admixture. The percentage of total labor time devoted to compounding, delivering, stocking, and other physical handling of materials decreased by 64% for admixtures of gentamicin or potassium chloride and by 67% for admixtures of cefazolin or cefoxitin. The average reduction in annual costs for accessories, labor time, wasted drugs, and inventory at each hospital was +15,000. Additional savings were realized from overall lower acquisition costs for the premixed products at the study hospitals. The use of premixed i.v. admixtures reduced preparation time and labor and material costs in three small- and medium-sized community hospitals.

Costs and Cost Analysis↗
PubMed1988

DFP-induced elevation of strength-duration threshold in hen peripheral nerve.

Previous research has indicated that organophosphorus agents which induce a delayed neuropathy also elevate the strength-duration threshold during the progression of the neuropathy. To establish further the correlation between strength-duration changes and delayed neuropathy, the purpose of the present study was to investigate the biochemical and electrophysiological effects of two additional agents: diisopropylflourophosphate (DFP) and phosphonothioc acid, methyl-[2-(dimethylamino)-ethyl]O-ethyl ester (VX). DFP-treated hens exhibited clinical signs of toxicity at the time of electrophysiologic recording and biochemical analysis. DFP treatment also resulted in significantly elevated thresholds of the strength-duration curves of both the sciatic and tibial nerves. The VX-treated animals exhibited no clinical signs, despite aggressive dosing, and there were no significant changes in the electrophysiologic characteristics (conduction velocity, relative refractory period, strength-duration threshold) of either peripheral nerve. Acetylcholinesterase activities of the brain and skeletal muscle were significantly reduced in the VX- and DFP-treated hens, whereas creatine phosphokinase activities in these tissues were unaffected. These results are consistent with the view that elevation of the strength-duration threshold in peripheral nerves is among the earliest indicators of organophosphorus-induced delayed neuropathy.

Acetylcholinesterase↗
PubMed1988

Pyridostigmine-induced decrement in skeletal muscle contracture is not augmented by soman.

Previous studies have reported that pyridostigmine induces a decrement in contractile force generated during tetanic stimulation of skeletal muscle. Although our studies suggested that pyridostigmine affected release of transmitter from the motor nerve terminal, we could not exclude the possibility that the drug's action was due to depolarization blockade of the muscle brought on by excessive transmitter in the synaptic cleft. The purpose of this study was to determine whether the effect of combined treatment with pyridostigmine and an irreversible cholinesterase inhibitor (soman) would potentiate the decrement in muscle contracture observed with pyridostigmine alone. As reported previously, pyridostigmine (25 mg/kg) significantly reduced muscle contracture during tetanic stimulation (20-100 Hz), and soman (0.075 mg/kg) increased muscle contracture. Combined treatment with pyridostigmine and soman produced a decrease in muscle contracture equivalent to the effect of pyridostigmine alone. Since there was no evidence of depolarization blockade of the muscle despite aggressive treatment with two cholinesterase inhibitors, these results support the view that pyridostigmine has a significant presynaptic action to decrease neurotransmitter release. This action opposes the drug's inhibition of cholinesterase, and the net effect of combined treatment with pyridostigmine and soman is a muscle response which is largely unchanged from the effect of pyridostigmine alone.

Acetylcholinesterase↗