Efficacy of intravenous sedation and oral nifedipine in dental implant patients with preoperative hypertension - a retrospective study of 516 cases

International audienceThis paper proposes a first attempt to define a two scales kinetic theory to describe concentrated suspensions involving short fibers, nano-fibers or nanotubes. In this case, fiber-fiber interactions can not be neglected and rich microstructures issued from these interactions can be observed, involving a diversity of fibers clusters or aggregates with complex kinematics, and different sizes and shapes. These clusters can interact to create larger clusters and also break because the flow induced hydrodynamic forces. In this paper we propose a double-scale model to describe such microstructure: at the finest scale we study the cluster kinematic based on the behaviour of the rods that constitute it, at a coarser scale, we use clusters distribution to derive the effect of the clusters presence on the suspensions properties

Hypersensitivity caused by suppression of descending inhibitory pathways following lumbar intrathecal injection of lidocaine in rats

Although the etiology of neural blockrelated transient neurological sequelae following spinal anesthesia, such as transient neurological symptoms (TNS) and less serious sensory disturbances, is still unclear, previous reports have described the facilitation of ascending nociceptive pathways as the source of complications resulting from local anesthetic toxicity, needle trauma, and patient positioning. We hypothesized that, in addition to the facilitation of ascending nociceptive pathways, the intrathecal injection of local anesthetics might interrupt descending inhibitory pathways, leading to hypersensitivity. To test this hypothesis, changes in tail flick (TF) latency were evaluated under lidocaine blockade of descending inhibitory pathways at the thoracic spinal cord level and under lumbar intrathecal lidocaine injection in rats. Furthermore, the effects of lumbar intrathecal lidocaine injection on cerebrospinal fluid (CSF) concentrations of neurotransmitters related to nociceptive transmission were investigated. The results revealed that thoracic intrathecal lidocaine shortened TF latency immediately after injection, while lumbar intrathecal lidocaine injection initially prolonged TF latency to the cut-off point and subsequently reduced TF latency compared to the baseline. Lumbar intrathecal lidocaine caused a significant reduction in norepinephrine concentrations in the CSF. These results indicate that the reduction of TF latency following lumbar intrathecal lidocaine injection was caused by the suppression of nor adrenergic descending inhibitory pathways. We concluded that the enhanced activity of dorsal horn neurons due to the suppression of descending inhibitory pathways by intrathecal lidocaine injection is one of the possible mechanisms of transient neurological sequelae

Role of tube size and intranasal compression of the nasotracheal tube in respiratory pressure loss during nasotracheal intubation: a laboratory study

Abstract Background Small nasotracheal tubes (NTTs) and intranasal compression of the NTT in the nasal cavity may contribute to increasing airway resistance. Since the effects of size, shape, and partial compression of the NTT on airway resistance have not been investigated, values of airway resistance with partial compression of preformed NTTs of various sizes were determined. Methods To determine the factors affecting the respiratory pressure loss during the nasotracheal intubation, physical and fluid dynamics simulations were used. The internal minor axes of NTTs in the nasal cavity of intubated patients were measured using dial calipers. In physical and fluid dynamics simulations, pressure losses through the tubular parts, compressed parts, and slip joints of NTTs with internal diameters (IDs) of 6.0, 6.5, 7.0, 7.5, and 8.0 mm were estimated under partial compression. Results The median internal minor axes of the 7.0- and 7.5-mm ID NTTs in the nasal cavity were 5.2 (4.3–5.6) mm and 6.0 (4.2–7.0) mm, respectively. With a volumetric air flow rate of 30 L/min, pressure losses through uncompressed NTTs with IDs of 6.0-, 6.5-, 7.0-, 7.5- and 8.0-mm were 651.6 ± 5.7 (6.64 ± 0.06), 453.4 ± 3.9 (4.62 ± 0.04), 336.5 ± 2.2 (3.43 ± 0.02), 225.2 ± 0.2 (2.30 ± 0.00), and 179.0 ± 1.1 Pa (1.82 ± 0.01 cmH2O), respectively; the pressure losses through the slip joints were 220.3 (2.25), 131.1 (1.33), 86.8 (0.88), 57.1 (0.58), and 36.1 Pa (0.37 cmH2O), respectively; and the pressure losses through the curvature of the NTT were 71.6 (0.73), 69.0 (0.70), 64.8 (0.66), 32.5 (0.33), and 41.6 Pa (0.42 cmH2O), respectively. A maximum compression force of 34.1 N increased the pressure losses by 82.0 (0.84), 38.0 (0.39), 23.5 (0.24), 16.6 (0.17), and 9.3 Pa (0.09 cmH2O), respectively. Conclusion Pressure losses through NTTs are in inverse proportion to the tubes’ IDs; greater pressure losses due to slip joints, acute bending, and partial compression of the NTT were obvious in small NTTs. Pressure losses through NTTs, especially in small NTTs, could increase the work of breathing to a greater extent than that through standard tubes; intranasal compression further increases the pressure loss

<Originals>Gabapentin produces antinociceptive effects on the spinal cord with simultaneous activation of descending facilitation in spinal nerve-ligated rats

[Abstract] Gabapentin has been proposed as one of several first-line agents to treat neuropathic pain. Although both spinal and supraspinal neuronal mechanisms participate in the antinociceptive effects of gabapentin, the supraspinal contribution to the effects of gabapentin at the spinal level remains unclear. We evaluated the role of descending modulation in the antinociceptive effects of gabapentin at the spinal level using continuous blockade ofdescending pathways in spinal nerve-ligated (SNL) rats. Tail flick (TF) latencies following sham operation or SNL operation were measured for 2 weeks. Rats were chronically implanted with both cervical and lumber intrathecal catheters, and a continuous cervical intrathecal infusion of 1% lidocaine was utilized for suppression of descending modulation. TF latencies following intrathecal administration of normal saline or 50μg gabapentin were measuredwith/without descending modulation in SNL and sham-operated rats. TF latencies (percentage of the maximum possible effect) were significantly shortened in the 2 weeks following SNL operation. With descending modulation, intrathecal gabapentin did not prolong TF latencies in sham-operated rats, and prolonged TF latency only at the 60-min time point in SNL rats ; 28.9± 17.3％ (p＜0.05 compared with baseline). Without descending modulation, intrathecal gabapentin to shamoperated rats slightly prolonged TF latencies at 15 and 30 min compared with the saline group of sham-operated rats, but intrathecal gabapentin to SNL rats resulted in significant prolongation of TF latencies ; 41.6+39.0％ (p＜0.01) to 68.2+ 37.4％ (p＜0.001). The results of this study indicate that gabapentin causes both apparent antinociception at the spinal level and simultaneousdescending facilitation in neuropathic pain conditions