buprenorphine and Brain-Injuries

To examine the levels of thromboxane B2 (TXB2) and 6-keto prostaglandin F1alpha (6-keto PGF1alpha) production in arterial and internal jugular bulb sera in patients with traumatic brain injury (TBI). TBI is associated with arachidonate release and may be associated with an imbalance of vasoconstricting and vasodilating cyclooxygenase metabolites.. A prospective, randomized study.. The intensive care unit of a medical university hospital.. Twenty-six ventilated TBI patents (Glasgow Coma Scale score on admission, < or = 8 points) were divided randomly into two groups: a hypothermic group (n = 15), in which the patients were cooled to 32 to 33 degrees C after being giving vecuronium, midazolam, and buprenorphine; and a normothermic group (n = 11), in which the patients' body temperature was controlled at 36 to 37 degrees C by surface cooling using the same treatment as the hypothermic group. Body temperature control including normothermia was started 3 to 4 hrs after injury. The duration of hypothermia usually lasted for 3 to 4 days, after which the patients were rewarmed at a rate of approximately 1 C per day.. Blood sampling for TXB2 and 6-keto PGF1alpha was started shortly after admission in both groups. Arterial TXB2 levels on admission in both groups were elevated remarkably, but not 6-keto PGF1alpha, thereby causing an imbalance of the prostanoids after injury. In the normothermic group, TXB2 decreased transiently, but this prostanoid increased again 3 days after the injury. In the hypothermic group, such prostanoid differences disappeared shortly after therapy, and the condition was sustained for 10 days. Hypothermia attenuated differences in TXB2 levels between arterial and internal jugular bulb sera, which may reflect reduced cerebral prostanoid production. The Glasgow Outcome Scale score 6 months after the insult in the hypothermic group was significantly higher than that in the normothermic group (p = .04).. The current results from a limited number of patients suggest that moderate hypothermia may reduce prostanoid production after TBI, thereby attenuating an imbalance of thromboxane A2 and prostaglandin I2. However, it must be clarified whether the changes in the prostanoid after moderate hypothermia are a secondary effect of other mediator changes or whether they simply represent an epiphenomenon that is mechanistically unrelated to damage in TBI.

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Adult; Aged; Analgesics, Opioid; Arachidonic Acid; Brain Injuries; Buprenorphine; Child; Child, Preschool; Female; Glasgow Coma Scale; Glasgow Outcome Scale; Humans; Hypnotics and Sedatives; Hypothermia, Induced; Jugular Veins; Male; Midazolam; Middle Aged; Neuromuscular Nondepolarizing Agents; Prospective Studies; Prostaglandin-Endoperoxide Synthases; Thromboxane A2; Time Factors; Treatment Outcome; Vecuronium Bromide

Balance and bispectral index metrics were evaluated in piglets following focal and diffuse brain injury. A significant decrease in bispectral index existed at 24 hours after diffuse brain injury, but not after focal injury. Postural sway increased at 1-6 hours after both focal and diffuse injuries.

Topics: Animals; Brain Injuries; Buprenorphine; Conscious Sedation; Electroencephalography; Injections, Intramuscular; Postural Balance; Psychomotor Performance; Reaction Time; Swine

Meloxicam is a cyclo-oxygenase-2 (COX-2) preferential non-steroidal anti-inflammatory drug with very effective analgesic and anti-inflammatory effects in swine. Previous reports in piglets have demonstrated that meloxicam also inhibits COX-1 and reduces production of thromboxane significantly. We use preinjury analgesia in our immature swine (3-5-day-old piglets) model of brain injury using rapid head rotations without impact. In 23 consecutive subjects we found that premedication with meloxicam (n = 6) produced a significantly higher mortality rate (5/6 or 83%) than buprenorphine (n = 17, 1/17 or 6%, P < 0.02). On gross neuropathological examination of the meloxicam-treated swine, we observed massive subdural and subarachnoid bleeding which were not present in buprenorphine-premedicated animals. To our knowledge there are no previous reports in swine of increased bleeding or platelet inhibition associated with meloxicam administration and further research is needed to define mechanisms of action in piglets. We caution the use of meloxicam in swine when inhibition of platelet aggregation might adversely affect refinement of experimental research protocols, such as in stroke, trauma and cardiac arrest models.

Topics: Amyloid beta-Protein Precursor; Animals; Animals, Newborn; Brain; Brain Injuries; Buprenorphine; Cyclooxygenase 2 Inhibitors; Disease Models, Animal; Hematoma, Subdural; Injections, Intramuscular; Meloxicam; Premedication; Subarachnoid Hemorrhage; Survival Rate; Swine; Thiazines; Thiazoles