Eficácia e efeitos hemodinâmicos da anestesia raquidiana com ropivacaína isobárica, hipobárica ou hiperbárica em cães anestesiados com isofluorano

The aim of the study was to assess hemodynamic changes and complications of spinal anesthesia with ropivacaine at different baricities. Six beagle dogs aged four years. The dogs were anesthetized with isoflurane and subjected to the following treatments: Ghypo = spinal anesthesia with hypobaric ropivacaine (0.5mL of 0.9[%] NaCl+0.5mL ropivacaine at 0.75[%]); Giso = isobaric spinal anesthesia (0.5mL of 0,906[%] NaCl+0.5mL ropivacaine at 0.75[%]); Ghyper = hyperbaric spinal anesthesia (0.5mL of 10[%] glucose+0.5mL ropivacaine at 0.75[%]). After induction to anesthesia and maintenance with isoflurane, animals were positioned in right lateral recumbency for pulmonary artery catheterization through the left jugular vein. Spinal anesthesia was carried out with injection of 1mL of local anesthetic using a 22G Quincke tip needle in the L5-L6 space along 1 minute. Dogs were maintained under inhalation anesthesia for 60 minutes in ventral recumbency. HR, FR, MAP, CO, mPAP and body temperature progressively increased in all groups, whereas PCWP increased only in GHYPO at all time points. The TPRI showed significantly higher values in GISO at M1, M5 and M10 compared to the other groups, except for M5, during which GISO differed only from GHYPER. The PVRI increased at M5 compared to MB in GISO. Side effects such as unilateral motor deficit, bladder atony, excitation, acute pain and chemosis were observed. The hemodynamic changes were not relevant, although inhalation anesthesia with isoflurane might have influenced the results. The changes observed in the study demonstrate that motor blockade is likely to be obtained with isobaric and hyperbaric ropivacaine, thereby confirming the influence of baricity on the type of nerve fibers on the spinal cord. The isobaric solution results in a mixed blockade (motor and sensory blockade). Hemodynamic changes such as hypotension and bradycardia were not evidenced in this study, although local anesthetics were administered in low volumes and resultatogether with isoflurane anesthesia. Regarding complications, post-anesthetic observation is warranted in order to identify and treat possible changes. Spinal anesthesia in the conditions studied did not cause hemodynamic changes in isoflurane-anesthetized dogs and is thus considered safe for routine practice, although a few complications are prone to occur.Doutor em Ciência Animal Faculdade de Medicina Veterinária de Araçatuba (FMVA) Universidade Estadual Paulista (Unesp), Rua Clóvis Pestana 793, Dona AméliaPrograma de Pós-Graduação em Ciência Animal FMVA-Unesp, Rua Clóvis Pestana 793, Dona AméliaDocente do Curso de Medicina Veterinária Hospital Universitário Centro Universitário de Rio Preto (Unirp), Rodovia BR-153 Km 69Large Animal Department College of Veterinary Medicine University of Florida, 2015 SW 16th AvenueDepartamento de Clínica Cirurgia e Reprodução Animal (DCCRA). FMVA- -Unesp, Rua Clóvis Pestana 793, Dona AméliaDoutor em Ciência Animal Faculdade de Medicina Veterinária de Araçatuba (FMVA) Universidade Estadual Paulista (Unesp), Rua Clóvis Pestana 793, Dona AméliaPrograma de Pós-Graduação em Ciência Animal FMVA-Unesp, Rua Clóvis Pestana 793, Dona AméliaDepartamento de Clínica Cirurgia e Reprodução Animal (DCCRA). FMVA- -Unesp, Rua Clóvis Pestana 793, Dona Améli

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)