ABSTRACT
OBJECTIVE: Atorvastatin has been suggested to reduce hematoma volume and improve neurological outcomes in patients with chronic subdural hematoma (CSDH). However, the benefits and harms of atorvastatin use after surgery in elderly patients are not well studied. PATIENTS AND METHODS: We conducted a retrospective trial to analyze older people (> 60 years) with CSDH, those who were treated with surgical intervention. Patients were assigned to study group if they received oral atorvastatin after surgery at least 1 week, and patients without atorvastatin medication postoperatively were assigned to control group. The primary outcome was the overall rate of recurrence at 1 month after surgery. The main secondary endpoints were the scores on the modified Rankin Scale (mRS), hematoma volume, mortality, and complications after surgery. RESULTS: A total of 49 eligible patients were included - 21 in the study group and 28 in the control group. The baseline characteristics were similar between the 2 groups. At 1 month, recurrence of subdual hematoma requiring repeat surgery was reported in 4 of 21 patients (19.0%) in the study group and in 5 of 28 patients (17.9%) in the control group (p=0.915). The hematoma volume was similar between the 2 groups (p=0.979). A favorable outcome (a score of 2 or less on the mRS) occurred in 90.5% of patients in the study group and in 96.4% of those in the control group (p=0.390). CONCLUSIONS: In older people with CSDH, postoperative atorvastatin use barely reduces the incidence of recurrence and hematoma volume.
Subject(s)
Atorvastatin/therapeutic use , Hematoma, Subdural, Chronic/prevention & control , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Aged , Aged, 80 and over , Female , Hematoma, Subdural, Chronic/epidemiology , Hematoma, Subdural, Chronic/surgery , Humans , Incidence , Male , Postoperative Period , Recurrence , Retrospective Studies , Treatment OutcomeABSTRACT
Previous studies have indicated that thalamic nucleus submedius is involved in opioid-mediated antinociception in tail flick test and formalin test. The current study examined the effects of opioids microinjected into the thalamic nucleus submedius on the allodynia developed in neuropathic pain model rats, and determined the roles of different subtypes of opioid receptors in the thalamic nucleus submedius opioid-evoked antiallodynia. The allodynic behaviors induced by L5/L6 spinal nerve ligation were assessed by mechanical (von Frey filaments) and cold (4 degrees C plate) stimuli. Morphine (1.0, 2.5, and 5.0 microg) microinjected into the thalamic nucleus submedius contralateral to the nerve injury paw produced a dose-dependent inhibition of the mechanical and cold allodynia, and these effects were reversed by microinjection of the non-selective opioid receptor antagonist naloxone (1.0 microg) into the same site. Microinjection of endomorphin-1 (5.0 microg), a highly selective mu-opioid receptor agonist, and [D-Ala2, D-Leu5]-enkephalin (10 microg), a delta-/mu-opioid receptor agonist, also inhibited the allodynic behaviors, and these effects were blocked by selective mu-opioid receptor antagonist beta-funaltrexamine hydrochloride (3.75 microg). However, the [D-Ala2, D-Leu5]-enkephalin-evoked antiallodynic effects were not influenced by the selective delta-opioid receptor antagonist naltrindole (5.0 microg). Microinjection of the selective kappa-receptor agonist spiradoline mesylate salt (100 microg) into the thalamic nucleus submedius failed to alter the allodynia induced by spinal nerve ligation. These results suggest that the thalamic nucleus submedius is involved in opioid-evoked antiallodynia which is mediated by mu- but not delta- and kappa-opioid receptor in the neuropathic pain model rats.
Subject(s)
Analgesics, Opioid/pharmacology , Neuralgia/metabolism , Pain Threshold/physiology , Peripheral Nervous System Diseases/metabolism , Receptors, Opioid/metabolism , Thalamus/metabolism , Animals , Disease Models, Animal , Dose-Response Relationship, Drug , Drug Interactions/physiology , Hyperalgesia/drug therapy , Hyperalgesia/metabolism , Hyperalgesia/physiopathology , Male , Morphine/pharmacology , Narcotic Antagonists/pharmacology , Neural Pathways/physiology , Neuralgia/drug therapy , Neuralgia/physiopathology , Pain Measurement , Pain Threshold/drug effects , Peripheral Nervous System Diseases/drug therapy , Peripheral Nervous System Diseases/physiopathology , Physical Stimulation , Prefrontal Cortex/physiology , Rats , Rats, Sprague-Dawley , Receptors, Opioid/agonists , Receptors, Opioid, kappa/agonists , Receptors, Opioid, kappa/metabolism , Receptors, Opioid, mu/agonists , Receptors, Opioid, mu/antagonists & inhibitors , Receptors, Opioid, mu/metabolism , Receptors, sigma/agonists , Receptors, sigma/metabolism , Thalamus/anatomy & histology , Thalamus/drug effectsABSTRACT
This study was designed to evaluate the role of endogenous ouabain (EO) in the development of hypertension in 1ktc (one kidney, one clip) hypertensive rats. First, the EO content of the serum of 1k1c hypertensive rats and normal Sprague-Dawley (SD) rats was detected by the enzyme linked immunosorbent assay method (ELISA). Second, blood pressure changes in the 1k1c rats were recorded directly after the 1k1c rats were injected randomly with anti-ouabain antibody, normal rabbit IgG, and normal saline, respectively. The results showed that EO levels in the serum of 1k1c hypertensive rats were significantly higher than those of normal SD rats (2.25 +/-0.92 microg/l vs. 1.12 +/- 0.17 microg/l, p< 0.01), and correlated significantly with systolic blood pressure (r= 0.59, p< 0.05). Anti-ouabain antibody was able to significantly decrease the blood pressure of 1k1c hypertensive rats in a dose-dependent manner, while normal rabbit IgG or normal saline was not. These results indicate that endogenous ouabain might play an important role in the development of hypertension in 1k1c hypertensive rats.
