Injection Of Hypertonic Saline Research Articles

Kinesthetic illusions attenuate experimental muscle pain, as do muscle and cutaneous stimulation

In the present study, muscle pain was induced experimentally in healthy subjects by administrating hypertonic saline injections into the tibialis anterior (TA) muscle. We first aimed at comparing the analgesic effects of mechanical vibration applied to either cutaneous or muscle receptors of the TA or to both types simultaneously. Secondly, pain alleviation was compared in subjects in whom muscle tendon vibration evoked kinesthetic illusions of the ankle joint. Muscle tendon vibration, which primarily activated muscle receptors, reduced pain intensity by 30% (p<0.01). In addition, tangential skin vibration reduced pain intensity by 33% (p<0.01), primarily by activating cutaneous receptors. Concurrently stimulating both sensory channels induced stronger analgesic effects (−51%, p<0.01), as shown by the lower levels of electrodermal activity. The strongest analgesic effects of the vibration-induced muscle inputs occurred when illusory movements were perceived (−38%, p=0.01). The results suggest that both cutaneous and muscle sensory feedback reduce muscle pain, most likely via segmental and supraspinal processes. Further clinical trials are needed to investigate these new methods of muscle pain relief.

Reorganised motor control strategies of trunk muscles due to acute low back pain

This study assessed how the low back motor control strategies were affected by experimental pain. In twelve volunteers the right m. longissimus was injected by hypertonic and isotonic (control) saline. The pain intensity was assessed on a visual analog scale (VAS). Subjects were seated on a custom-designed chair including a 3-dimensional force sensor adjusted to the segmental height of T1. Electromyography (EMG) was recorded bilaterally from longissimus, multifidus, rectus abdominis, and external oblique muscles. Isometric trunk extensions were performed before, during, and after the saline injections at 5%, 10%, and 20% of maximum voluntary contraction force. Visual feedback of the extension force was provided whereas the tangential force components were recorded. Compared with isotonic saline, VAS scores were higher following hypertonic saline injections (P<.01). Experimental low back pain reduced the EMG activity bilaterally of the rectus abdominis muscles during contractions at 10% and 20% MVC (P<.01) although force accuracy and tangential force variability was not affected. Increased variability in the tangential force composition was found during pain compared with the non-painful condition (P<.05). The immediate adaptation to pain was sufficient to maintain the quality of the task performance; however the long-term consequence of such adaptation is unknown and may overload other structures.

Tonic modulation of central CRF circuits by oxytocin in response to peripheral salt loading

Central oxytocinergic neurons can likely modulate stress-related circuits through both paracrine and synaptic release of oxytocin (OT). One classic hallmark of a stress response is the activation of the HPA axis by corticotrophin releasing factor (CRF) positive neurons in the paraventricular nucleus of the hypothalamus (PVN). However, OT neurons in the PVN may also contribute via a synaptic pathway to the modulation of CRF neurons in the central amygdala (CeA), an area that helps integrate neuroendocrine and autonomic responses to stress. Prior studies have shown that peripheral salt loading activates OT neurons in the PVN but reduces anxiety-like behavior and the HPA response to restraint stress. In the present study, we examined a possible crosstalk between OT-mediated signaling and CRF neurons following peripheral salt loading using a Cre-lox based mouse model that selectively expresses red fluorescent protein in CRF neurons. The CRF-reporter mice received an injection of either isotonic or hypertonic saline one hour prior to euthanasia. Whole-cell patch clamp recordings were then made from identified CRF neurons in acute PVN and CeA slices. Compared with mice that received isotonic saline, hypertonic mice showed a significant OT receptor (OTR) mediated inhibitory tone on CRF neurons within the PVN and the CeA. Interestingly, within the PVN, this inhibitory tone was independent of activity-mediated release of classic excitatory and inhibitory neurotransmitters. Together, these data reveal novel ways by which OT can impact CRF microcircuitry to curb stress responsiveness, and furthers our understanding of the neuromodulatory role of endogenous OT with regard to complex social behaviors. Support: 13PRE17100047 (DP), HL096830 (EGK)

Acute experimental hip muscle pain alters single-leg squat balance in healthy young adults

BackgroundClinical musculoskeletal pain commonly accompanies hip pathology and can impact balance performance. Due to the cross-sectional designs of previous studies, and the multifactorial nature of musculoskeletal pain conditions, it is difficult to determine whether pain is a driver of balance impairments in this population. This study explored the effects of experimentally induced hip muscle pain on static and dynamic balance. MethodsTwelve healthy adults (4 women, mean[SD]: 27.1[3] years) performed three balance tasks on each leg, separately: single-leg standing (eyes closed), single-leg squat (eyes open), forward step (eyes open); before and after hypertonic saline injection (1ml, 5% NaCl) into the right gluteus medius. Range, standard deviation (SD), and velocity of the centre of pressure (CoP) in medio-lateral (ML) and anterior–posterior (AP) directions were considered. ResultsDuring the single-leg squat task, experimental hip pain was associated with significantly reduced ML range (−4[13]%, P=0.028), AP range (−14[21]%, P=0.005), APSD (−15[28]%, P=0.009), and AP velocity (−6[13]%, P=0.032), relative to the control condition, in both legs. No effect of pain was observed during single-leg standing and forward stepping. Significant between-leg differences in ML velocity were observed during the forward stepping task (P=0.034). DiscussionPain is a potentially modifiable patient-reported outcome in individuals with hip problems. This study demonstrates that acute hip muscle pain alone, without interference of musculoskeletal pathology, does not lead to the same impairments in balance as exhibited in clinical populations with hip pathologies. This is the first step in understanding how and why balance is altered in painful hip pathologies.

Impaired anticipatory postural adjustments due to experimental infrapatellar fat pad pain.

Anticipatory postural adjustments (APAs) are motor responses generated to stabilize balance prior to voluntary movement. This study investigated how infrapatellar fat pad pain induces reorganization of APAs during reaction time tasks. It has been hypothesized that knee pain may cause insufficient APAs, thereby impairing the balance. While standing, 12 healthy men performed two reaction time tasks (shoulder flexion of the dominant side and bilateral heel lift, respectively) before, during and after experimental infrapatellar fat pad pain induced in the dominant side by injections of hypertonic saline. Isotonic saline was injected as control. The reaction time task performance was assessed by peak angle and peak angular velocity. Timing and intensity of the postural muscle activity were recorded by surface electromyography. The reaction time task performance was not significantly affected by experimental pain. The onset of muscle activity in vastus medialis, vastus lateralis and tibialis anterior muscles on the dominant side during the bilateral heel lift task was significantly delayed during pain, and their muscle activity was reduced when compared with non-painful sessions (p<0.05). The contralateral vasti muscles demonstrated early onset during pain compared with the non-painful session of the same task (p≤0.05). This study demonstrates that knee pain reorganizes the APAs which may destabilize the balance control. The knee pain-related reorganization of postural muscle activity during APA may be a part of the central modulation to maintain posture and protect the painful limb while preserving the reaction task movement performance.

The Effect of Experimental Neck Pain on Pressure Pain Sensitivity and Axioscapular Motor Control

Clinical neck pain affects pain sensitivity and coordination of neck muscles, but the impact on the shoulder muscles is unclear. This study investigated the effect of experimental neck pain on the activity of the axioscapular muscles during arm movements and changes in pain sensitivity. Experimental neck pain was induced in 24 healthy volunteers by injecting hypertonic saline into the splenius capitis. Isotonic saline was injected as control. Before, during, and after injections, electromyography was recorded bilaterally from 8 muscles during standardized arm movements (140° scapular plane elevation), and the root mean square amplitude was extracted. Likewise, pressure pain thresholds were assessed bilaterally on 3 sites. The root mean square electromyography was decreased for the ipsilateral upper trapezius (P < .01) and increased for the ipsilateral middle deltoid (P < .03) during upward movements. The root mean square electromyography was reduced for the ipsilateral upper trapezius (P < .01) during downward movement, whereas an increase was recorded in the contralateral external oblique (P < .02). At the injection site, the pressure pain threshold increased during pain compared with the post condition (5 minutes after potential pain had subsided; P < .03). In this study, trunk and axioscapular muscle activities were reorganized in response to localized and referred pain evoked by hypertonic saline injection into an intrinsic neck muscle with no direct attachments to the trunk or shoulder girdle. PerspectiveReorganized activity of the axioscapular muscles has been shown previously in neck pain patients and is believed to happen during the transition from acute to chronic pain. The present study demonstrates for the first time that such reorganization may happen acutely, adding to our understanding of the effects of acute neck pain.

Dynamic mechanical assessment of muscle hyperalgesia in humans: the dynamic algometer.

Musculoskeletal pain is often associated with a nonhomogeneous distribution of mechanical hyperalgesia. Consequently, new methods able to detect this distribution are needed. To develop and test a new method for assessing muscle hyperalgesia with high temporal and spatial resolution that provides complementary information compared with information obtained by traditional static pressure algometry. The dynamic pressure algometer was tested bilaterally on the tibialis anterior muscle in 15 healthy subjects and compared with static pressure algometry. The device consisted of a wheel that was rolled over the muscle tissue with a fixed velocity and different predefined forces. The pain threshold force was determined and pain intensity to a fixed-force stimulation was continuously rated on a visual analogue scale while the wheel was rolling over the muscle. The pressure pain sensitivity was evaluated before, during, and after muscle pain and hyperalgesia induced unilaterally by either injection of hypertonic saline (0.5 mL, 6%) into the tibialis anterior or eccentric exercise evoking delayed-onset muscle soreness (DOMS). The intraclass correlation coefficient was >0.88 for the dynamic thresholds; thus, the method was reliable. Compared with baseline, both techniques detected hyperalgesia at the saline injection site and during DOMS (P<0.05). The dynamic algometer also detected the widespread, patchy distribution of sensitive loci during DOMS, which was difficult to evaluate using static pressure algometry. The present study showed that dynamic pressure algometry is a reliable tool for evaluating muscle hyperalgesia (threshold and pain rating) with high temporal and spatial resolution. It can be applied as a simple clinical bed-side test and as a quantitative tool in pharmacological profiling studies.

Thermoregulatory consequences of salt loading in the lizard Pogona vitticeps.

Previous research has demonstrated that dehydration increases the threshold temperature for panting and decreases the thermal preference of lizards. Conversely, it is unknown whether thermoregulatory responses such as shuttling and gaping are similarly influenced. Shuttling, as an active behavioural response, is considered one of the most effective thermoregulatory behaviours, whereas gaping has been proposed to be involved in preventing brain over-heating in lizards. In this study we examined the effect of salt loading, a proxy for increased plasma osmolality, on shuttling and gaping in Pogona vitticeps. Then, we determined the upper and lower escape ambient temperatures (UETa and LETa), the percentage of time spent gaping, the metabolic rate (V̇O2 ), the evaporative water loss (EWL) during gaping and non-gaping intervals and the evaporative effectiveness (EWL/V̇O2 ) of gaping. All experiments were performed under isotonic (154 mmol l(-1)) and hypertonic saline injections (625, 1250 or 2500 mmol l(-1)). Only the highest concentration of hypertonic saline altered the UETa and LETa, but this effect appeared to be the result of diminishing the animal's propensity to move, instead of any direct reduction in thermoregulatory set-points. Nevertheless, the percentage of time spent gaping was proportionally reduced according to the saline concentration; V̇O2 was also decreased after salt loading. Thermographic images revealed lower head than body surface temperatures during gaping; however this difference was inhibited after salt loading. Our data suggest that EWL/V̇O2 is raised during gaping, possibly contributing to an increase in heat transfer away from the lizard, and playing a role in head or brain cooling.

Radiation pretreatment does not protect the rat optic nerve from elevated intraocular pressure-induced injury.

Optic nerve injury has been found to be dramatically reduced in a genetic mouse glaucoma model following exposure to sublethal, head-only irradiation. In this study, the same radiation treatment was used prior to experimental induction of elevated intraocular pressure (IOP) to determine if radiation is neuroprotective in another glaucoma model. Episcleral vein injection of hypertonic saline was used to elevate IOP unilaterally in two groups of rats: (1) otherwise untreated and (2) radiation pretreated, n > 25/group. Intraocular pressure histories were collected for 5 weeks, when optic nerves were prepared and graded for injury. Statistical analyses were used to compare IOP history and nerve injury. The density of microglia and macrophages in two nerve head regions was determined by Iba1 immunolabeling. Mean and peak IOP elevations were not different between the two glaucoma model groups. Mean optic nerve injury grades were not different in glaucoma model optic nerves and were equivalent to approximately 35% of axons degenerating. Nerves selected for lower mean or peak IOP elevations did not differ in optic nerve injury. Similarly, nerves selected for lower injury grade did not differ in IOP exposure. By multiple regression modeling, nerve injury grade was most significantly associated with mean IOP (P < 0.002). There was no significant effect of radiation treatment. Iba1+ cell density was not altered by radiation treatment. In contrast to previous observations in a mouse genetic glaucoma model, head-only irradiation offers the adult rat optic nerve no protection from optic nerve degeneration due to chronic, experimentally induced IOP elevation.

Modulation of motor variability related to experimental muscle pain during elbow-flexion contractions

Experimental muscle pain typically reorganizes the motor control. The pain effects may decrease when the three-dimensional force components are voluntarily adjusted, but it is not known if this could have negative consequences on other structures of the motor system. The present study assessed the effects of acute pain on the force variability during sustained elbow flexion when controlling task-related (one-dimensional) and all (three-dimensional) contraction force components via visual feedback. Experimental muscle pain was induced by bolus injection of hypertonic saline into m. biceps brachii, and isotonic saline was used as control. Twelve subjects performed sustained elbow flexion at different levels of the maximal voluntary contraction (5–30% MVC) before, during, and after the injections. Three-dimensional force components were measured simultaneously with surface electromyography (EMG) from elbow flexors and auxiliary muscles. Results showed that force variability was increased during pain compared to baseline for contractions using one-dimensional feedback (P<.05), but no significant differences were found for three-dimensional feedback. During painful contractions (1) EMG activity from m. trapezius was increased during contractions using both one-dimensional and three-dimensional feedback (P<.05), and (2) the complexity of EMG from m. triceps brachii and m. deltoid was higher for the three-dimensional feedback (P<.05). In conclusion, the three-dimensional feedback reduced the pain-related functional distortion at the cost of a more complex control of synergistic muscles.

Serotonin, glutamate and glycerol are released after the injection of hypertonic saline into human masseter muscles - a microdialysis study.

BackgroundChronic myalgia is associated with higher muscle levels of certain algesic biomarkers. The aim of this study was to investigate if hypertonic saline-induced jaw myalgia also leads to release of such biomarkers and if there were any sex differences in this respect.MethodsHealthy participants, 15 men and 15 aged-matched women (25.7 ± 4.3 years) participated. Intramuscular microdialysis into masseter muscles was performed to sample serotonin (5-HT), glutamate, lactate, pyruvate, glucose and glycerol. After 2 hours 0.2 mL hypertonic saline (58.5 mg/mL) was injected into the masseter on one side and 0.2 mL isotonic saline (9 mg/mL) into the contralateral masseter close to the microdialysis catheter. Microdialysis continued for 1 hour after the injections. Pressure pain thresholds (PPT) and pain were assessed before and after injections.ResultsThe median (IQR) peak pain intensity (0–100 visual analogue scale) after hypertonic saline was 52.5 (38.0) and after isotonic saline 7.5 (24.0) (p < 0.05). 5-HT, glutamate and glycerol increased after hypertonic saline injection (p < 0.05). Lactate, pyruvate and glucose showed no change. PPT after microdialysis was reduced on both sides (p < 0.05) but without side differences. Pain after hypertonic saline injection correlated positively to 5-HT (p < 0.05) and negatively to glycerol (p < 0.05).Conclusions5-HT, glutamate and glycerol increased after a painful hypertonic saline injection into the masseter muscle, but without sex differences. Since increased levels of 5-HT and glutamate have been reported in chronic myalgia, this strengthens the validity of the pain model. Glycerol warrants further investigations.

The dynamics of the pain system is intact in patients with knee osteoarthritis: An exploratory experimental study

Background and aimsDespite the high prevalence of knee osteoarthritis (OA) it remains one of the most frequent knee disorders without a cure. Pain and disability are prominent clinical features of knee OA. Knee OA pain is typically localized but can also be referred to the thigh or lower leg. Widespread hyperalgesia has been found in knee OA patients. In addition, patients with hyperalgesia in the OA knee joint show increased pain summation scores upon repetitive stimulation of the OA knee suggesting the involvement of facilitated central mechanisms in knee OA. The dynamics of the pain system (i.e., the adaptive responses to pain) has been widely studied, but mainly from experiments on healthy subjects, whereas less is known about the dynamics of the pain system in chronic pain patients, where the pain system has been activated for a long time. The aim of this study was to assess the dynamics of the nociceptive system quantitatively in knee osteoarthritis (OA) patients before and after induction of experimental knee pain. MethodsTen knee osteoarthritis (OA) patients participated in this randomized crossover trial. Each subject was tested on two days separated by 1 week. The most affected knee was exposed to experimental pain or control, in a randomized sequence, by injection of hypertonic saline into the infrapatellar fat pad and a control injection of isotonic saline. Pain areas were assessed by drawings on anatomical maps. Pressure pain thresholds (PPT) at the knee, thigh, lower leg, and arm were assessed before, during, and after the experimental pain and control conditions. Likewise, temporal summation of pressure pain on the knee, thigh and lower leg muscles was assessed. ResultsExperimental knee pain decreased the PPTs at the knee (P<0.01) and facilitated the temporal summation on the knee and adjacent muscles (P<0.05). No significant difference was found at the control site (the contralateral arm) (P=0.77). Further, the experimental knee pain revealed overall higher VAS scores (facilitated temporal summation of pain) at the knee (P<0.003) and adjacent muscles (P<0.0001) compared with the control condition. The experimental knee pain areas were larger compared with the OA knee pain areas before the injection. ConclusionsAcute experimental knee pain induced in patients with knee OA caused hyperalgesia and facilitated temporal summation of pain at the knee and surrounding muscles, illustrating that the pain system in individuals with knee OA can be affected even after many years of nociceptive input. This study indicates that the adaptability in the pain system is intact in patients with knee OA, which opens for opportunities to prevent development of centralized pain syndromes.

Hydatid Cyst of Liver Presented as Obstructive Jaundice in Pregnancy; Managed by PAIR

Incidence of Hydatid disease in pregnancy ranges from 1in 20,000 to 1 in 30,000. The most common site of hydatid cysts is the liver. The diagnosis of liver hydatid cysts is not difficult but the management during pregnancy is problematic. Both medical and surgical treatments are available but there is no consensus and each case has to be individualized. We present a case of liver hydatid cyst presented with obstructive jaundice during pregnancy which was managed by Puncture of the cyst under USG guidance; Aspiration of the cystic fluid, Injection of hypertonic saline, and Re-aspiration of solution without drainage (PAIR) and albendazole therapy. Very few cases of liver hydatosis were reported previously which had been managed by PAIR.

Effects of simulated weightlessness on intramuscular hypertonic saline induced muscle nociception and spinal Fos expression in rats

We assessed the effects of simulated weightlessness, hindlimb unloading (HU) by 7 days of tail suspension, on noxious mechanically and heat evoked spinal withdrawal reflexes and spinal Fos expression during muscle nociception elicited by intramuscular (i.m.) injection of hypertonic (HT; 5.8%) saline into gastrocnemius muscle in rats. In HU rats, i.m. HT saline-induced secondary mechanical hyperalgesia was enhanced, and secondary heat hypoalgesia was significantly delayed. After 7 days of HU, basal Fos expression in spinal L4-6 segments was bilaterally enhanced only in superficial (I–II) but not middle and deep laminae (III–VI) of the spinal dorsal horn, which finding was not influenced by tail denervation. Unilateral i.m. HT saline injection increased spinal Fos expression bilaterally in both the control rats and 7 days of HU rats. The HT saline-induced bilateral increase of spinal Fos occurred within 0.5h and reached its peak within 1h, after which it gradually returned to the control levels within 8h. Spatial patterns of spinal Fos expression differed between the control group and 7 days of HU group. In superficial laminae, the HT saline-induced increases in Fos expression were higher and in the middle and deep laminae V–VI lower in the 7 days of HU than control rats. It is suggested that supraspinal mechanisms presumably underlie the effects of HU on spinally-organized nociception. Simulated weightlessness may enhance descending facilitation and weaken descending inhibition of nociception.

Acetylation preserves retinal ganglion cell structure and function in a chronic model of ocular hypertension.

The current studies investigate if the histone deacetylase (HDAC) inhibitor, valproic acid (VPA), can limit retinal ganglion cell (RGC) degeneration in an ocular-hypertensive rat model. Intraocular pressure (IOP) was elevated unilaterally in Brown Norway rats by hypertonic saline injection. Rats received either vehicle or VPA (100 mg/kg) treatment for 28 days. Retinal ganglion cell function and number were assessed by pattern electroretinogram (pERG) and retrograde FluoroGold labeling. Western blotting and a fluorescence assay were used for determination of histone H3 acetylation and HDAC activity, respectively, at 3-day, 1-week, and 2-week time points. Hypertonic saline injections increased IOPs by 7 to 14 mm Hg. In vehicle-treated animals, ocular hypertension resulted in a 29.1% and 39.4% decrease in pERG amplitudes at 2 and 4 weeks, respectively, and a 42.9% decrease in mean RGC density at 4 weeks. In comparison, VPA treatment yielded significant amplitude preservation at 2 and 4 weeks and showed significant RGC density preservation at 4 weeks. No significant difference in RGC densities or IOPs was measured between control eyes of vehicle- and VPA-treated rats. In ocular-hypertensive eyes, class I HDAC activity was significantly elevated within 1 week (13.3 ± 2.2%) and histone H3 acetylation was significantly reduced within 2 weeks following the induction of ocular hypertension. Increase in HDAC activity is a relatively early retinal event induced by elevated IOP, and suppressing HDAC activity can protect RGCs from ocular-hypertensive stress. Together these data provide a basis for developing HDAC inhibitors for the treatment of optic neuropathies.

Experimental pain has a greater effect on single motor unit discharge during force-control than position-control tasks

ObjectiveWhen matching target force during pain, single motor unit (SMU) discharge is modified in a manner thought to redistribute load in painful tissue. This adaptation might not be appropriate when maintaining joint posture against an external load. We compared changes in SMU discharge rate of knee extensor muscles in a force-control and a position-control task during pain. MethodsThirteen healthy adults (31±6years) performed position- and force-control contractions using matched loads in non-pain and pain states. Pain was induced by injection of hypertonic saline into the infrapatellar fat pad. Intramuscular and surface electromyography of knee extensor and flexor muscles was recorded. ResultsWhen considering the discharge of a select population of SMUs that were recorded across all conditions performed on the same day, there was a decrease in mean discharge rate, and this was smaller in the position- than force-control task for the same SMUs. A similar tendency was observed for SMUs recorded on different days. However, gross agonist muscle activity (which incorporates SMUs that are not included in the discharge rate analysis because they were not present in all conditions) increased in both tasks during pain. Gross antagonist muscle EMG only increased in the force-control task. ConclusionThe effect of pain on muscle activity appears unique to the contraction type, with less influence during position- than force-control tasks. SignificanceSimplistic theories of pain adaptation of movement during voluntary efforts cannot be extrapolated to more postural functions. This has implications for understanding movement changes that may underpin persistence/recurrence of pain and the management of musculoskeletal pain.

Autonomic responses to exercise: cortical and subcortical responses during post-exercise ischaemia and muscle pain.

Sustained isometric contraction of skeletal muscle causes an increase in blood pressure, due to an increase in cardiac output and an increase in total peripheral resistance-brought about by an increase in sympathetically-mediated vasoconstriction. Both central command and reflex inputs from metaboreceptors in the contracting muscles have been shown to contribute to this sympathetically mediated increase in blood pressure. Occluding the blood supply and trapping the metabolites in the contracted muscle (post-exercise ischaemia) has shown that, while heart rate returns to baseline following exercise, the increase in MSNA and blood pressure persists in the absence of central command-sustained by peripheral inputs. Post-exercise ischaemia activates group III and IV muscle afferents, which are also activated during noxious stimulation. Indeed, post-exercise ischaemia is painful, so what is the role of pain in the increase in blood pressure? Intramuscular injection of hypertonic saline causes a deep dull ache, not unlike that produced by post-exercise ischaemia, and we have shown that this can cause a sustained increase in MSNA and blood pressure. We have used functional Magnetic Resonance Imaging (fMRI) of the brain to identify the cortical and subcortical sites involved in the sensory processing of muscle pain, and in the generation of the autonomic responses to muscle pain, produced either by post-exercise ischaemia or intramuscular injection of hypertonic saline. During static hand-grip exercise there were parallel increases in signal intensity in the contralateral primary motor cortex, deep cerebellar nuclei and cerebellar cortex that ceased at the end of the exercise, reflecting the start and end of central command. Progressive increases during the contraction phase occurred in the contralateral insula, as well as the contralateral primary somatosensory cortex, and continued during the period of post-exercise ischaemia. Decreases in signal intensity occurred in the perigenual anterior cingulate cortex during the contraction phase; these too were sustained during post-exercise ischaemia. That similar changes occurred with intramuscular injection of hypertonic saline suggests that much of the cortical and subcortical changes seen during post-exercise ischaemia reflect the sensory and affective attributes of the muscle pain, rather than in furnishing the cardiovascular responses per se.

Involvement of central and peripheral cannabinoid receptors on antinociceptive effect of tetrahydrocannabinol in muscle pain

Cannabinoid (CB) receptors have emerged as an attractive therapeutic target for pain management in recent years and the interest in the use of cannabinoids is gradually increasing, particularly in patients where conventional treatments fail. Muscle pain is a major clinical problem and new pharmacological approaches are being studied. Recently, we have demonstrated that cannabinoid synthetic agonists are useful to reduce muscular pain in two animal models, where the local administration is effective. Now, we want to know if tetrahydrocannabinol (THC), a cannabinoid natural derivative with therapeutic use in humans, is also effective in reducing acute muscle pain. The antinociceptive effect of THC by systemic (i.p.) and local (i.m.) administration was tested in two animal models of acute muscle pain, rat masseter and gastrocnemius, induced by hypertonic saline (HS) injection. The drugs used were the non-selective agonist THC and two selective cannabinoid antagonists, AM251 (CB1) and AM630 (CB2). THC, i.p. and i.m. administered, reduced the nociceptive behaviours induced by HS in both muscular pain models. The antinociceptive effect induced by the systemic administration of THC was mediated by CB1 receptors in the masseter muscle whereas in gastrocnemius both CB1 and CB2 receptors participated. When THC was administered locally, only CB2 receptors were involved in the antinociceptive effect in both muscles. This study suggests that THC could be a future pharmacological option in the treatment of muscle pain. The local administration of THC could be an interesting option to treat this type of pain avoiding the central adverse effects.

Astrocyte processes label for filamentous actin and reorient early within the optic nerve head in a rat glaucoma model.

To determine if astrocyte processes label for actin and to quantify the orientation of astrocytic processes within the optic nerve head (ONH) in a rat glaucoma model. Chronic intraocular pressure (IOP) elevation was produced by episcleral hypertonic saline injection and tissues were collected after 5 weeks. For comparison, eyes with optic nerve transection were collected at 2 weeks. Fellow eyes served as controls. Axonal degeneration in retrobulbar optic nerves was graded on a scale of 1 to 5. Optic nerve head sections (n ≥ 4 eyes per group) were colabeled with phalloidin (actin marker) and antibodies to astrocytic glial fibrillary acidic protein and aquaporin 4, or axonal tubulin βIII. Confocal microscopy and FIJI software were used to quantify the orientation of actin bundles. Control ONHs showed stereotypically arranged actin bundles within astrocyte processes. Optic nerve head actin bundle orientation was nearly perpendicular to axons (82.9° ± 6.3° relative to axonal axis), unlike the retrobulbar optic nerve (45.4° ± 28.7°, P < 0.05). With IOP elevation, ONH actin bundle orientation became less perpendicular to axons, even in eyes with no perceivable axonal injury (i.e., 38.8° ± 15.1° in grade 1, P < 0.05 in comparison to control ONHs). With severe injury, ONH actin bundle orientation became more parallel to the axonal axis (24.1° ± 28.4°, P < 0.05 in comparison to control ONHs). Optic nerve head actin bundle orientation in transected optic nerves was unchanged. Actin labeling identifies fine astrocyte processes within the ONH. Optic nerve head astrocyte process reorientation occurs early in response to elevated IOP.

The Role of Hypertonic Saline in Monopolar Tonsillectomy in Pediatric Patients.

Looking for a simple and inexpensive method to reduce patients' pain during tonsillectomy. Bilateral tonsillectomy patients were enrolled and placed into different groups based on their admission numbers. Patients with odd numbers had electrical tonsillectomy on the right side with hypertonic saline injection into peritonsillar gap (group A) or electrical tonsillectomy on the left side without hypertonic saline injection (group B). Those with even numbers had electrical tonsillectomy on the left side with hypertonic saline injection into peritonsillar gap (group A) or electrical tonsillectomy on the right side without hypertonic saline injection (group B). Pain, operative bleeding, post-operation bleeding and operation time were evaluated. Injecting hypertonic saline into peritonsillar gap reduced pain caused by electrical tonsillectomy but did not impact operation or postoperative bleeding and operation time. While simple and economic, monopolar electrical tonsillectomy with the help of hypertonic saline injected into peritonsillar gap can effectively relieve patients from pain compared with surgeries without hypertonic saline injection.