Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.10.2 (focal adhesion kinase)
 44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate whether the addition of epinephrine would enhance postoperative pain relief by intrathecal morphine, we studied 36 patients scheduled to have spinal anesthesia for gynecologic surgery. Patients were randomly allocated to one of three groups: the first received epinephrine 0.12 mg, morphine 0.2 mg, and hyperbaric tetracaine 12 mg intrathecally (EMT group, n = 11); the second received morphine 0.2 mg and hyperbaric tetracaine 12 mg intrathecally (MT group, n = 13); and the third received epinephrine 0.12 mg and hyperbaric tetracaine 12 mg intrathecally (ET group, n = 12). The time to the first request for supplemental analgesics was longest (2182 +/- 251 min, mean +/- SEM) and the injection number of supplemental analgesics was least in the EMT group (P < 0.05). The percentage of patients who received supplemental analgesics in the EMT group (45.5%) was less than the other two groups (P < 0.05). Six patients in the EMT group and one in the MT group needed no additional analgesics during 48 h (P < 0.05 versus the MT and ET groups). The visual analog scale (VAS) pain score was larger in the ET group than the EMT group (P < 0.05), but was similar in the EMT and MT groups. There were no differences among groups in the incidence of nausea and pruritus. Our data show that the addition of epinephrine enhances postoperative analgesia by intrathecal morphine without increasing the incidence of adverse effects as compared with intrathecal morphine alone.
 ...
PMID:The addition of epinephrine enhances postoperative analgesia by intrathecal morphine. 765 13

Recent studies suggested that the L-arginine/nitric oxide (NO)/cyclic GMP pathway is involved in the modulation of pain perception. The present experiments were undertaken to find out the role of this pathway in the antinociception induced by oxotremorine administration. Male mice of the CD-1 strain were injected with different doses of the muscarinic agonist oxotremorine (0.005, 0.01, 0.02, 0.03 mg/kg i.p.) 5 min after the administration of saline solution or the inhibitors of NO synthase NG-nitro-L-arginine methyl ester (L-NAME: 10 and 20 mg/kg, i.p.) or NG-nitro-L-arginine (N-ARG: 10 and 20 mg/kg i.p.). Oxotremorine induced a dose- and time-dependent analgesic effect in mice, which was significantly increased by L-NAME and N-ARG administration. Either doses of the NO inhibitors given alone had no effect on the nociceptive threshold. The present results show a role of NO in the antinociception mediated by the muscarinic receptor stimulation and suggest that it exerts an inhibitory action on cholinergic analgesia.
 ...
PMID:Nitric oxide synthase inhibitors enhance the antinociceptive effects of oxotremorine in mice. 943 49

Despite opioids are routinely used for analgesia in head injured patients, the effects of such drugs on ICP and cerebral hemodynamics remain controversial. Cerebrovascular autoregulation (CAR) could be an important factor in the ICP increases reported after opioid administration. In order to describe the effects on intracranial pressure of fentanyl and correlated such effects with autoregulation status, we studied 30 consecutive severe head injury patients who received fentanyl (2 micrograms/kg) intravenously over one minute. Prior to study, CAR was assessed. Monitoring included MAP, HR, SaO2, ETCO2, SjO2 and ICP. Changes in cerebral blood flow (CBF) were estimated from relative changes in AVDO2. Patients mean GCS was 5.7 +/- 1.7 (mean +/- STD) and mean ICP on admission was 23.8 +/- 16.3 mmHg. Fentanyl caused significant increases in ICP and decreases in MAP and CPP, but CBF remained unchanged when estimated by AVDO2. In patients with preserved CAR (34.5%), opioid-induced ICP increase was greater (but not statistically significant) than in those with impaired CAR (65.5%). We conclude than fentanyl moderately increased ICP and decreased MAP and CPP. Our data suggests that in patients with preserved CAR, potent opioids could cause greater increases of ICP, probably due to activation of the vasodilatadory cascade.
 ...
PMID:Effects on intracranial pressure of fentanyl in severe head injured patients. 977 29

The endogenous cannabinoid anandamide, a lipid mediator, induces various physiologic events such as vascular relaxation, inhibition of gap-junctions formation, tumor proliferation, neurologic analgesia, and apoptosis. Although increased concentration of anandamide in plasma has been implicated in pathophysiologic states including endotoxin-induced hypotension, the effects of anandamide on hepatocytes still remain unclear. In this study, we present evidence that plasma anandamide concentration is highly increased in severe hepatitis and cirrhosis patients. In addition, concentrations of anandamide within the pathophysiologic range potently induced apoptosis of hepatoma cell line (Hep G2) and primary hepatocytes, suggesting a possible link between increased anandamide level and hepatocyte damage. Anandamide-induced cell death was preceded by G0/G1 cell-cycle arrest, activation of proapoptotic signaling (i.e., p38 MAPK and JNK), and inhibition of antiapoptotic signaling (i.e., PKB/Akt) pathways. Moreover, anandamide increased susceptibility to oxidative stress-induced hepatocyte damage. In this context, methyl-beta-cyclodextrin (MCD), a membrane cholesterol depletor, or mevastatin, an HMG-CoA reductase inhibitor, or N-acetyl cysteine, an antioxidant, potently inhibited the anandamide-induced proapoptotic events and cell death, whereas putative cannabinoid receptor antagonists did not exhibit an inhibitory effect on anandamide-induced cell death. Furthermore, binding assay using polymyxin beads revealed that anandamide could interact with cholesterol. In conclusion, our data suggest that cholesterol present in the cell membrane determines the fate of hepatocytes exposed to anandamide, possibly functioning as an anandamide receptor.
 ...
PMID:Membrane cholesterol but not putative receptors mediates anandamide-induced hepatocyte apoptosis. 1457 55

Prehospital analgesia can be safely provided with only three agents: fentanyl, morphine and the mixed-gas nitrous oxide/oxygen. Of these three, fentanyl is by far the best agent for general EMS analgesic therapy by paramedics. However, to initiate prehospital analgesia earlier in the EMS response time frame, EMT's should administer nitrous oxide/oxygen. This protocol can easily be added to the EMT education program or through a continuing education session. All of the other agents discussed have absolutely no role in modern prehospital care.
 ...
PMID:Simplifying prehospital analgesia. Why certain medications should or should not be used for pain management in the field. 1602 66

No validated screening tasks exist to distinguish children who can accurately use self-report pain measures from those who cannot. Children aged 3-7 years (n=108), each with a parent, provided data before and after day surgery. Parents rated how well they thought their child could understand the Faces Pain Scale-Revised (FPS-R), and children completed 4 screening tasks in counterbalanced order, such as rating pain in vignettes and selecting a middle-sized cup. Parents and children used the FPS-R to rate the children's pain intensity. Children's FPS-R ratings were scored for accuracy based on the extent to which they conformed to expected pain trajectories (e.g., pain increasing following surgery, decreasing following analgesia), and based on parent-child agreement. On average, parents rated the youngest age at which children could understand the FPS-R as 4.4 years (95% confidence interval 4.1-4.5). The youngest children provided inaccurate high pain ratings before surgery, but they became indistinguishable from the oldest in the accuracy of their pain ratings for the remainder of the 3-day study period, suggesting that direct experience with pain or with the rating task may improve accuracy. Although children's performance on the screening tasks was significantly associated with self-report accuracy, no prediction was strong enough for clinical use (all r's < 0.30). We failed to identify a screening tool that was better than chronological age in identifying which children could accurately self-report pain using the FPS-R. Future research should explore other screening tasks, training methods, and simplified approaches to pain assessment for young children. The ability to use self-report pain scales usually develops from age 3 to 7 years, but no valid screening method exists to identify this achievement.
 ...
PMID:Can we screen young children for their ability to provide accurate self-reports of pain? 2139 89