Effect of hip hemiarthroplasty dislocation on mortality after hip fracture surgery. / [Artículo traducido] Efecto de la luxación de la prótesis parcial de cadera en la mortalidad tras la cirugía de fractura de cadera.

INTRODUCTION: Hip arthroplasty is the treatment of choice for displaced femoral neck fractures among the older population. The hip prosthesis dislocation is one of the most pointed potential complications after hip arthroplasty, but there is a lack of updated information on the effect of dislocation on the survival of older hip fracture patients so treated by hip hemiarthroplasty. We aim to evaluate the standalone effect of hip prosthesis dislocation after hip fracture hemiarthroplasty on patients' survival outcomes. MATERIALS AND METHODS: We conducted a retrospective multicenter study, including 6631 femoral neck fracture patients over 65 surgically treated by hemiarthroplasty. We made follow-up cut-offs 30-days, 6 weeks, 90-days, and one year after hospital discharge determining hip dislocation rate and patients' survival. RESULTS: The women population represented 78.7%, and the mean age of the population was 85.2 ± 6.7 years. Hip prosthesis dislocation incidence was 1.9% in the first 90-days after discharge, representing 91.54% of primary dislocations yearly noted. We reported statistically significant increased mortality rates of patients presenting at least one hip prosthesis dislocation event (from 16.0% to 24.6% at 90-day after discharge, and 29.5% to 44.7% at one year), and also significantly decreasing patient survival function at 90-day (P = .016) and one-year follow-up (P < .001). The recurrent dislocation events (26.15%) showed even higher mortality rates (up to 60.6%, p < .001). The multivariate Cox regression model determined that prosthesis dislocation was the only significant variable (P = .035) affecting patient survival, increasing the risk of dying before one year of follow-up by 2.7 times. DISCUSSION: Our study stands for the standalone hip prosthesis dislocation entailing a higher risk of death after hip fracture hemiarthroplasty in the older population.

Effect of hip hemiarthroplasty dislocation on mortality after hip fracture surgery.

INTRODUCTION: Hip arthroplasty is the treatment of choice for displaced femoral neck fractures among the older population. The hip prosthesis dislocation is one of the most pointed potential complications after hip arthroplasty, but there is a lack of updated information on the effect of dislocation on the survival of older hip fracture patients so treated by hip hemiarthroplasty. We aim to evaluate the standalone effect of hip prosthesis dislocation after hip fracture hemiarthroplasty on patients' survival outcomes. MATERIALS AND METHODS: We conducted a retrospective multicenter study, including 6631 femoral neck fracture patients over 65 surgically treated by hemiarthroplasty. We made follow-up cut-offs 30-days, 6 weeks, 90-days, and one year after hospital discharge determining hip dislocation rate and patients' survival. RESULTS: The women population represented 78.7%, and the mean age of the population was 85.2±6.7 years. Hip prosthesis dislocation incidence was 1.9% in the first 90-days after discharge, representing 91.54% of primary dislocations yearly noted. We reported statistically significant increased mortality rates of patients presenting at least one hip prosthesis dislocation event (from 16.0% to 24.6% at 90-day after discharge, and 29.5% to 44.7% at one year), and also significantly decreasing patient survival function at 90-day (p=0.016) and one-year follow-up (p<0.001). The recurrent dislocation events (26.15%) showed even higher mortality rates (up to 60.6%, p<0.001). The multivariate Cox regression model determined that prosthesis dislocation was the only significant variable (p=0.035) affecting patient survival, increasing the risk of dying before one year of follow-up by 2.7 times. DISCUSSION: Our study stands for the standalone hip prosthesis dislocation entailing a higher risk of death after hip fracture hemiarthroplasty in the older population.

Alpha-2 adrenoceptors modulate the somatostatinergic system and G protein levels in the rat hippocampus.

alpha 2-Adrenoceptor agonists and somatostatin (SS) exert opposite effects on the spike discharge of pyramidal and granule cells in the rat hippocampus. We studied whether clonidine, an alpha 2-adrenoceptor agonist, and yohimbine, an alpha 2-adrenoceptor antagonist, can modulate somatostatin-like immunoreactivity (SSLI) levels, binding of 125I-Tyr11-somatostatin (125I-Tyr11-SS) to its specific receptors, SS-inhibited adenylyl cyclase (AC) activity, and the guanine-nucleotide binding regulatory proteins Gi and G(o) in the rat hippocampus. Clonidine (1 mg/kg, intraperitoneally (IP) or yohimbine (5 mg/kg, IP) injected at both 10 and 16 hours before decapitation did not affect SSLI content in the hippocampus. Clonidine administration decreased the number of specific SS receptors and increased the apparent affinity in hippocampal membranes. This change in SS binding was not the result of a direct effect of clonidine on these receptors because no effect in binding was produced by high concentrations of clonidine (10(-5) M) when added in vitro. Pretreatment with yohimbine prevented the clonidine-induced in SS binding. Yohimbine alone produced a significant increase in the number of 125I-Tyr11-SS receptors and a decrease in its apparent affinity. Clonidine decreased the ADP-ribosylation of a 41- and a 39-kDa G-protein by pertussis toxin (PTX), whereas yohimbine had no effect on the PTX-catalyzed ADP-ribosylation. No significant differences were seen for the basal or for the forskolin (FK)-stimulated AC enzyme activities in the control, clonidine- and/or yohimbine-treated groups. Somatostatin caused a significantly lower inhibition in AC activity in hippocampal membranes of clonidine-treated rats, whereas yohimbine led to an opposite effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of phenylephrine and prazosin on the somatostatinergic system in the rat frontoparietal cortex.

Somatostatin (SS) and noradrenaline (NA) are distributed in the rat cerebral cortex, and seizure activity is one of the aspects of behavior affected by both neurotransmitters. Due to the possible interaction between both neurotransmitter systems, we studied whether phenylphrine, an alpha 1-adrenoceptor agonist, and prazosin, an alpha 1-adrenoceptor antagonist, can modulate SS-like immunoreactivity (SS-LI) levels, binding of [125I][Tyr11]SS to its specific receptors, the ability of SS to inhibit adenylate cyclase (AC) activity, and the guanine nucleotide binding regulatory protein G, and G., in the Sprague-Dawley rat frontoparietal cortex. An IP dose of 2 or 4 mg/kg of phenylephrine injected 7 h before decapitation decreased the number of SS receptors and increased the apparent affinity in frontoparietal cortex membranes. An IP dose of 20 or 25 mg/kg of prazosin administered 8 h before decapitation increased the number of SS receptors and decreased their apparent affinity. The administration of prazosin before the phenylephrine injection prevented the phenylephrine-induced changes in SS binding. The addition of phenylephrine and/or prazosin 10(-5) M to the incubation medium changed neither the number nor the affinity of the SS receptors in the frontoparietal cortex membranes. Phenylephrine or prazosin affected neither SS-LI content nor the basal or forskolin (FK)-stimulated AC activities in the frontoparietal cortex. In addition, SS caused an equal inhibition of AC activity in frontoparietal cortex membranes of phenylephrine-and prazosintreated rats compared with the respective control group. Finally, phenylephrine and prazosin did not vary the pertussis toxin (PTX)-catalyzed ADP ribosylation of Gi- and/or Go-proteins. These results suggest that the above-mentioned changes are related to the phenylephrine activation of alpha 1-adrenoceptors or to the blocking of these receptors by prazosin. In addition, these data provide further support for a functional interrelationship between the alpha 1-adrenergic and somatostatinergic systems in the rat frontoparietal cortex.

Somatostatin receptors coupled to the inhibition of adenylyl cyclase in the rat frontoparietal cortex are modulated by alpha 2 adrenoceptors.

The administration of an alpha 2-adrenoceptor agonist, clonidine, increased the number of somatostatin (SS) receptors and the affinity constant in frontoparietal cortex membranes. In addition, in the clonidine group, the capacity of SS to inhibit basal and forskolin (FK)-stimulated adenylyl cyclase (AC) activity in the frontoparietal cortex was significantly higher than in the control group. Pretreatment with the alpha 2-adrenoceptor antagonist yohimbine prevented the clonidine-induced changes in SS binding and SS-inhibited AC activity. Yohimbine alone had an opposite effect from clonidine. These experiments provide further evidence that the alpha-adrenergic system modulates the rat frontoparietal cortex somatostatinergic system.

Changes in alpha 1-adrenergic neurotransmission alter the number of somatostatin receptors in the rat hippocampus.

The administration of an i.p. dose of phenylephrine (2 mg/kg) increased the number of [125I]Tyr11-somatostatin ([125I]Tyr11-SS) receptors and decreased their apparent affinity in rat hippocampal membranes 7 h after its injection. Prazosin (20 mg/kg, i.p.) administered 1 h before phenylephrine reversed effects of the latter on SS binding. Prazosin alone decreased the number of SS receptors without changing the affinity. The addition of phenylephrine or prazosin (10(-5) M) to the incubation medium did not change the SS binding characteristics. The present results support the notion that the alpha 1-adrenergic system regulates the binding of SS to its specific receptors in rat hippocampus.