Surgeons' decision making in patients with chronic wrist pain: role of bilateral three-compartment wrist arthrography--prospective study.

PURPOSE: To determine if wrist arthrography changes surgeons' diagnoses and treatment plans for patients with chronic wrist pain. MATERIALS AND METHODS: Bilateral, three-compartment wrist arthrography was performed in 64 patients. Prospective questionnaires evaluated surgeons' diagnoses and management plans at three stages: before arthrography, after arthrography of the symptomatic wrist, and after arthrography of the asymptomatic wrist. RESULTS: Surgeons tended to plan more conservative management after receiving the results of arthrography. The number of patients for whom the reported treatment plan included surgery dropped from 28 of 64 patients (44%) to 19 of 64 patients (30%) after review of the arthrography results (P = .05). The number of patients for whom the treatment plan included treatment of any kind dropped from 55 of 64 patients (86%) to 49 of 64 patients (77%) after review of the arthrography results (P = .09). An overall change in treatment plan occurred in 29 of 64 patients (45%). CONCLUSION: Wrist arthrography influences surgeons' decision making. After reviewing the results of arthrography, surgeons tended to change treatment plans toward more conservative, less invasive treatment.

Nonsurgical management of gastric or duodenal perforation from a Wills-Oglesby-type gastrostomy tube.

PURPOSE: To describe the clinical and radiologic appearance of gastrointestinal perforation related to a Wills-Oglesby-type gastrostomy tube, as well as techniques for nonsurgical management. MATERIALS AND METHODS: Five patients with a previously placed 14-F modified Wills-Oglesby-type gastrostomy catheter experienced viscus perforation by the distal limb of the catheter during a 30-month period. RESULTS: The average interval between tube placement and perforation event was 4.3 months. Three patients had migration of the gastrostomy tube into the duodenum and subsequent duodenal perforation. One patient had posterior perforation of the stomach, and one patient developed a gastrocolic fistula. Generalized peritonitis was not present in any patient. All patients were treated successfully without surgery, and tube feedings were re-established in 4-14 days. CONCLUSIONS: Gastrostomy tube-related perforation is an uncommon, delayed complication of percutaneous gastrostomy with the modified Wills-Oglesby-type catheter. Nonsurgical management is feasible in select instances. Because of these gastrointestinal perforations, the gastrostomy tube has been modified (eliminating the distal tip), and no gastrostomy-associated gastrointestinal perforation has been experienced since.

Transfected D2 dopamine receptors mediate the potentiation of arachidonic acid release in Chinese hamster ovary cells.

A rat D2L dopamine receptor, a splice variant of the D2 receptor, has recently been cloned. When transfected into and stably expressed in Chinese hamster ovary cells, these receptors mediate the inhibition of both basal and forskolin-stimulated cAMP production, as previously described. We examined what role this receptor might play in the production of the second messenger arachidonic acid. The calcium ionophore A23187 stimulated the release of arachidonic acid, and this release of arachidonic acid was potentiated by dopamine in a concentration-dependent manner. Dopamine alone, however, had no effect on arachidonic acid release. Quinpirole, a D2-selective agonist, augmented A23187-stimulated arachidonic acid release, and sulpiride, a D2-selective antagonist, blocked this augmentation. cAMP analogs and agents that activate adenylyl cyclase were utilized in an attempt to overcome this dopamine effect. Forskolin, prostaglandin E2, dibutyryl-cAMP, 8-(4-chlorophenylthio)-cAMP, and pertussis toxin all had no appreciable effect on either A23187-stimulated arachidonic acid release or the dopamine enhancement. Inhibition of protein kinase C using long term phorbol ester desensitization and pharmacological inhibitors diminished the dopamine potentiation of arachidonic acid release. These results suggest that the D2 receptor may be increasing the release of arachidonic acid by a mechanism involving protein kinase C but independent of the D2 receptor's inhibition of adenylyl cyclase.

The rat alpha 2-C4 adrenergic receptor gene encodes a novel pharmacological subtype.

A rat gene and brain cDNA (pA2d) encoding the homologue of the human alpha-C4 adrenergic receptor subtype were isolated and characterized. RNA blots indicate that this gene is expressed in brain, heart and kidney but not in lung, liver or pancreas. Yohimbine, WB-4101 and prasozin all exhibited high affinity for this receptor in binding studies. Clonidine was more potent and efficacious than norepinephrine in inhibiting forskolin-stimulated cAMP production in CHO cells expressing pA2d. Together, these data suggest that the alpha 2-C4 gene product defines a previously undescribed pharmacological subtype of alpha 2-adrenergic receptor.

A transfected m1 muscarinic acetylcholine receptor stimulates adenylate cyclase via phosphatidylinositol hydrolysis.

The m1 muscarinic acetylcholine receptor gene was transfected into and stably expressed in A9 L cells. The muscarinic receptor agonist, carbachol, stimulated inositol phosphate generation, arachidonic acid release, and cAMP accumulation in these cells. Carbachol stimulated arachidonic acid and inositol phosphate release with similar potencies, while cAMP generation required a higher concentration. Studies were performed to determine if the carbachol-stimulated cAMP accumulation was due to direct coupling of the m1 muscarinic receptor to adenylate cyclase via a GTP binding protein or mediated by other second messengers. Carbachol failed to stimulate adenylate cyclase activity in A9 L cell membranes, whereas prostaglandin E2 did, suggesting indirect stimulation. The phorbol ester, phorbol 12-myristate 13-acetate (PMA), stimulated arachidonic acid release yet inhibited cAMP accumulation in response to carbachol. PMA also inhibited inositol phosphate release in response to carbachol, suggesting that activation of phospholipase C might be involved in cAMP accumulation. PMA did not inhibit prostaglandin E2-, cholera toxin-, or forskolin-stimulated cAMP accumulation. The phospholipase A2 inhibitor eicosatetraenoic acid and the cyclooxygenase inhibitors indomethacin and naproxen had no effect on carbachol-stimulated cAMP accumulation. Carbachol-stimulated cAMP accumulation was inhibited with TMB-8, an inhibitor of intracellular calcium release, and W7, a calmodulin antagonist. These observations suggest that carbachol-stimulated cAMP accumulation does not occur through direct m1 muscarinic receptor coupling or through the release of arachidonic acid and its metabolites, but is mediated through the activation of phospholipase C. The generation of cytosolic calcium via inositol 1,4,5-trisphosphate and subsequent activation of calmodulin by m1 muscarinic receptor stimulation of phospholipase C appears to generate the accumulation of cAMP.