Accelerometry May be Superior to EMG for Early Evaluation of Vocal Cord Function After Nerve Injury in a Pig Model.

OBJECTIVE: Vocal cord (VC) movement has been demonstrated by the use of accelerometry (ACC) to decrease in parallel with the electromyographic amplitude (EMG) during ongoing traction injury to the recurrent laryngeal nerve (RLN). When RLN function recovers, discrepancies between EMG and VC movement have been reported in clinical and experimental studies. The present study was conducted to clarify the actual relationship between EMG and VC movement measured by ACC during nerve recovery. METHODS: EMG obtained by continuous nerve monitoring (C-IONM) was compared with ACC during traction injury to the RLN, and throughout 40-min nerve recovery. A three-axis linear accelerometer probe was attached to the VC, and ACC data were registered as described. Traction damage was applied to the RLN until there was a 70% amplitude decrease from baseline EMG, or until loss of signal (LOS), that is, EMG values ≤100 µV. RESULTS: Thirty-two RLN from 16 immature pigs were studied. Correlation between EMG and ACC were calculated during nerve injury and nerve recovery. The mean correlations were for the 70% and LOS group from start to end of traction: 0.82 (±0.17) and 0.87 (±0.17), respectively. Corresponding correlation coefficients during 40-min recovery was 0.50 (±0.48) in the 70% group and 0.53 (±0.33) in the LOS group. CONCLUSION: There is a high correlation between EMG and VC movement during nerve injury, and a moderate correlation during early nerve recovery. EMG recovery after RLN injury ensures sufficient VC function as assessed by ACC. LEVEL OF EVIDENCE: N/A Laryngoscope, 134:1485-1491, 2024.

Fluid filtration and vascular compliance during cardiopulmonary bypass: effects of two volatile anesthetics.

BACKGROUND: As intraoperative fluid accumulation may negatively impact post-operative organ function, strategies minimizing edema generation should be sought for. During general anesthesia, isoflurane in contrast to sevoflurane has been associated with increased fluid extravasation and edema generation. In this study, we tested sevoflurane against isoflurane with focus on vascular compliance and fluid shifts in an experimental cardiopulmonary bypass (CPB) model. METHODS: Sixteen pigs underwent 120 min of cardiopulmonary bypass with isoflurane or sevoflurane anesthesia. Net fluid balance, plasma volume, serum-electrolytes, serum-albumin, serum-protein, colloid osmotic pressures in plasma and interstitial fluid, hematocrit levels, and total tissue water content were recorded. Intra-abdominal and intracranial pressures were measured directly, and fluid extravasation rates were calculated. RESULTS: Fluid extravasation rate increased dramatically in both groups during initiation of cardiopulmonary bypass, with no group differences. The animals of the sevoflurane group needed significantly more fluid supplementation to maintain a constant reservoir volume in the CPB circuit during bypass. Plasma volumes prior to bypass were 56.5 ± 7.9 ml/kg (mean ± SD) and 58.7 ± 3.8 ml/kg in the isoflurane group and sevoflurane group, respectively. During bypass, plasma volumes in the isoflurane group decreased about 25%, and remained significantly lowered when compared to the sevoflurane group, where the values remained stable. CONCLUSIONS: No differences in fluid extravasation rates were observed between sevoflurane and isoflurane. The increased net fluid balance in the sevoflurane group during cardiopulmonary bypass was not associated with edema generation. Plasma volume was retained in the sevoflurane group, in contrast to the isoflurane group.

Increased interstitial protein because of impaired lymph drainage does not induce fibrosis and inflammation in lymphedema.

OBJECTIVE: The pathophysiology of lymphedema is incompletely understood. We asked how transcapillary fluid balance parameters and lymph flow are affected in a transgenic mouse model of primary lymphedema, which due to an inhibition of vascular endothelial growth factor receptor-3 (VEGFR-3) signaling lacks dermal lymphatics, and whether protein accumulation in the interstitium occurring in lymphedema results in inflammation. METHODS AND RESULTS: As estimated using a new optical-imaging technique, we found that this signaling defect resulted in lymph drainage in hind limb skin of K14-VEGFR-3-Ig mice that was 34% of the corresponding value in wild-type. The interstitial fluid pressure and tissue fluid volumes were significantly increased in the areas of visible swelling only, whereas the colloid osmotic pressure in plasma, and thus the colloid osmotic pressure gradient, was reduced compared to wild-type mice. An acute volume load resulted in an exaggerated interstitial fluid pressure response in transgenic mice. There was no accumulation of collagen or lipid in skin, suggesting that chronic edema presented in the K14-VEGFR-3-Ig mouse was not sufficient to induce changes in tissue composition. Proinflammatory cytokines (interleukin-2, interleukin-6, interleukin-12) in subcutaneous interstitial fluid and macrophage infiltration in skin of the paw were lower, whereas the monocyte/macrophage cell fraction in blood and spleen was higher in transgenic compared with wild-type mice. CONCLUSIONS: Our data suggest that a high interstitial protein concentration and longstanding edema is not sufficient to induce fibrosis and inflammation characteristic for the human condition and may have implications for our understanding of the pathophysiology of this condition.

The alpha11beta1 integrin has a mechanistic role in control of interstitial fluid pressure and edema formation in inflammation.

OBJECTIVE: Collagen-binding integrins may be involved in controlling interstitial fluid pressure (Pif), transcapillary fluid flux, and tissue fluid volume. Our aim was to explore whether the newly discovered collagen binding alpha11beta1 integrin has a mechanistic role in inflammatory edema formation. METHODS AND RESULTS: In collagen matrices seeded with a mixture of mast cells and fibroblasts, fibroblasts lacking the alpha11 integrin subunit (alpha11(-/-)) contracted collagen gels less efficiently than control fibroblasts, suggesting that the alpha11beta1 integrin is able to mediate tensile force in connective tissues. In alpha11(-/-) mice, control Pif in skin did not differ from the pressure found in wild-type mice. Whereas a reduction in Pif was found in control mice after inducing inflammation, thereby contributing to fluid extravasation and edema formation, such a reduction was not seen in alpha11(-/-) mice. That this effect is mediated through the extracellular compartment is suggested by a similar plasma protein extravasation ratio in alpha11(-/-) and wild-type mice. CONCLUSIONS: Our data suggest that alpha11beta1 integrins on dermal fibroblasts mediate collagen lattice remodeling and have a mechanistic role in controlling Pif in inflammation and thereby fluid extravasation and edema formation in vivo.

Lowered albumin extravasation rate in heart but not in other organs in beta3-integrin-deficient mice.

AIM: The vascular protein permeability is dependent on the integrity of the vascular wall. The heart capillaries in male mice lacking beta3 integrins have an immature phenotype. Previously, we have demonstrated a role for alphavbeta3 integrins in control of interstitial fluid pressure (Pif) and thereby in the fluid flux during inflammation. We wanted to explore a possible role for alphavbeta3 integrins in controlling capillary protein permeability during control situation and inflammation. METHODS: We performed double-tracer and microdialysis experiments on beta3-integrin-deficient mice and wild type control mice. We also measured blood pressure and heart rate in the two mice strains. RESULTS: We found reduced albumin extravasation (during 25 min) in the heart capillaries (0.053 +/- 0.003 vs. 0.087 +/- 0.009 mL g(-1) dw, P < 0.05), and an increased cardiac mass/body weight (5.3 x 10(-3) +/- 0.3 x 10(-3) vs. 3.8 x 10(-3) +/- 0.1 x 10(-3), P < 0.01) in the beta3-integrin-deficient mice (n = 6) compared with the controls (n = 6). Heart rate and blood pressure were the same in mice with and without beta3-integrins. No difference in permeability was found in other tissues studied, or under local inflammation. CONCLUSION: These results show a function for the alphavbeta3 integrin in the regulation of protein permeability, selective for the heart capillaries.