Systemic lupus erythematosus is not a risk factor for poor outcomes after total hip and total knee arthroplasty.

OBJECTIVES: Historically, arthroplasty in systemic lupus erythematosus (SLE) patients has been less successful than for patients with osteoarthritis (OA). It is not known if SLE remains an independent risk factor for poor arthroplasty outcomes or if other factors, such as avascular necrosis (AVN), continue to play a role. METHODS: A case-control study using data from a single-institution arthroplasty registry compared SLE total hip arthroplasty (THA) and total knee arthroplasty (TKA) with OA controls matched by age, gender and presence of AVN. Baseline, two-year administrative and self-report data, and diagnosis leading to arthroplasty were evaluated. RESULTS: A total of 54 primary SLE THA and 45 primary SLE TKA were identified from May 2007 through June 2011. AVN was present in 32% of SLE THA and no TKA. SLE THA had worse preoperative WOMAC pain (42.5 vs. 52.7; p = 0.01) and function (38.8 vs. 48.0; p = 0.05) compared with OA. However, at two years there was no difference in WOMAC pain (91.1 vs. 92.1; p = 0.77) or WOMAC function (86.4 vs. 90.8; p = 0.28). SLE TKA were similar to OA in both preoperative pain (42.6 vs. 48.4; p = 0.14) and function (42.1 vs. 46.8; p = 0.30) and two-year pain (85.7 vs. 88.6; p = 0.50) and function (83.7 vs. 85.1; p = 0.23). Compared to OA, SLE THA and TKA patients had more renal failure (14% vs. 1%; p = 0.007) and hypertension (52% vs. 29%; p = 0.009). In a multivariate linear regression, SLE was not predictive of either poor pain or poor function. CONCLUSIONS: While SLE patients have more comorbidities than OA, and SLE THA have worse preoperative pain and function compared with OA controls, SLE was not an independent risk factor for poor short-term pain or function after either hip or knee arthroplasty.

Comparative evaluation of anticonvulsant activity of calcium channel blockers in experimental animals.

Pentylenetetrazole (PTZ)-induced convulsions and the maximal electroshock (MES) seizure test were employed to study the anticonvulsant effects of nifedipine (2, 3.5 and 5 mg kg-1), flunarizine (10, 20 and 40 mg kg-1) and diltiazem (10, 15 and 30 mg kg-1). Nifedipine and flunarizine prolonged the latent period and reduced the mean duration of PTZ induced seizures. They also reduced the severity of convulsions and the number of deaths due to PTZ significantly. Nifedipine was more potent in this regard (P < 0.01). All these drugs prolonged the latent period and reduced the duration of tonic extensor phase of MES seizures in a significant manner. Flunarizine was most potent in this test. Complete protection from tonic extensor phase was observed in 10-50% animals pretreated with nifedipine and flunarizine in a dose dependent manner. The response of diltiazem was weak in both these tests. It is concluded that all three calcium channel blockers possess an important but different anticonvulsant effect and their significant clinical use can be made while keeping in view the characteristics of their pharmacological action.

Effect of nifedipine, a calcium channel inhibitor, on sedation produced by reserpine, clonidine and propranolol in mice.

Spontaneous motor activity, rotarod test and observational rating of sedation were employed to study effect of nifedipine on sedation produced by reserpine, clonidine and propranolol. Reserpine (2 mg kg-1), clonidine (4 mg kg-1), and propranolol (40 mg kg-1) significantly reduced spontaneous motor activity and staying capacity of animals on accelerating rotarod (P < 0.01). Observational sedation was also caused significantly as indicated by a higher score in test. Nifedipine (2 mg kg-1) produced no sedation or excitation on its own. Reduction in spontaneous motor activity produced by reserpine and clonidine was partially reversed in animals treated with nifedipine (P < 0.01). A similar effect of nifedipine was also evident on the observational sedation induced by reserpine and clonidine. Effect of these drugs on rotarod times was nearly totally antagonised by nifedipine. Nifedipine did not oppose the sedation produced by propranolol which actually became significantly greater in the animals pretreated with nifedipine in all three tests. It is concluded that nifedipine antagonizes the sedation produced by reserpine and clonidine, probably by blocking central alpha 2-adrenoceptors. The sedative effect of propranolol can be potentiated by nifedipine possibly because of a pharmacokinetic interaction.

Possible role of dopamine in the growth inhibitory effect of pentazocine.

Growth inhibitory effect of pentazocine was studied in young rats for a duration of 4 weeks. The animals were subjected to various drug treatments, namely (1) distilled water 0.5 ml/kg s.c.; (2) pentazocine 10 mg/kg s.c.; (3) pentazocine 10 mg/kg s.c. plus metoclopramide 10 mg/kg s.c., and (4) pentazocine 10 mg/kg s.c. plus l-dopa 100 mg/kg s.c. Body weight was taken as a measure for the assessment of growth rate. The results of group 2 were compared with group 1 and that of groups 3 and 4 were compared with group 2. Pentazocine alone markedly inhibited the growth from the second to fourth weeks of treatment. Dopamine antagonist metoclopramide has almost completely prevented the growth inhibitory effect of pentazocine. Combination of l-dopa with pentazocine produced a significant growth inhibition in the first week but subsequently this effect was significantly less marked as compared to that of pentazocine alone. The growth inhibitory effect of pentazocine may possibly be mediated through alterations in dopaminergic mechanisms which are known to exert controlling influence on the release of several of the pituitary hormones.

The effect of beta-adrenergic stimulation and blockade on the efflux of PGE1-like material from the isolated perfused rabbit heart.

Prostaglandin (PG) release was measured from the isolated perfused rabbit heart. The effects of beta-adrenergic stimulation and blockade suggest that PG synthesis is regulated in part by adrenergic mechanisms.

beta-adrenoceptor blockade with diphenylhydantoin (DPH).

Diphenylhydantoin (DPH) (20 x 10(-6) to 80 x 10(-6) M/kg) blocked the depressor responses to isoproterenol in spinal, bilaterally vagotomized and atropine pretreated cats; depressor responses to histamine were unaffected; DPH shifted the isoproterenol concentration-response curve to the right in isolated guinea pig tracheal chain preparation, isolated rabbit ileum and isolated perfused heart of frog. The results suggest that DPH has a specific beta-adrenoceptor blocking action and the blockade appears to be competitive in nature as shown by PA2 and PA10 values.

A study of some beta-adrenoceptor blocking agents on skeletal muscle.

The effect of three recently introduced beta-adrenoceptor blockers practolol, USVC 6524 and Inpea was studied on various skeletal muscle preparations. Practoloo, USVC 6524 and Inpea produced a dose related inhibition of acetylcholine induced contractions of rectus abdominis muscle of frog. These drugs also blocked neuromuscular transmission when tested on in vitro rat phrenic nerve diaphragm preparation; the blockade was partially reversed by physotigmine, KCl and adrenaline and was potentiated by d-tubocurarine. In gastrocnemius sciatic muscle-nerve preparation only Inpea exhibited neuromuscular blocking activity, while practolol and USVC 6524 did not show any effect up to a dose of 10 mg/kg (intraarterially). The apparent discrepancies between the results of in vitro and in vivo experiments could not be adequately explained. It has been discussed that the neuromuscular blockade caused by presently investigated beta-adrenoceptor blocking agents is essentially due to curare-like activity and to a small extent may be due to local anaesthetic activity.