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M Ye

Publications and source records attributed to M Ye.

At least 91 records · Page 5Linked to original sources
PubMed1995

Cyst fluid from a murine model of polycystic kidney disease stimulates fluid secretion, cyclic adenosine monophosphate accumulation, and cell proliferation by Madin-Darby canine kidney cells in vitro.

Cyst fluids from subjects with autosomal dominant polycystic kidney disease (ADPKD) cause polarized monolayers of MDCK cells to secrete fluid toward the apical compartment in vitro. To determine the extent to which secretagogue accumulation may be a general feature of polycystic diseases, cyst fluid from mice with a slowly progressive form of hereditary PKD (DBA/2FG-pcy/pcy) was added to polarized MDCK monolayers. Basolateral application of cyst fluids (diluted with culture medium to 15% final concentration) from 13 different animals 16 to 35 weeks old increased the fluid secretion rate from a baseline of 0.023 +/- 0.003 to 0.111 +/- 0.017 microL/cm2/h (P < 0.005). There was a direct relation between the concentration of cyst fluid and the rate of net fluid secretion. The secretory activity of cyst fluid was not altered by pronase treatment or boiling. Cyst fluid (10%) added to the basolateral surfaces of polarized MDCK monolayers for 24 hours increased cell cyclic adenosine monophosphate (AMP) levels from a baseline of 6.3 +/- 0.2 to 17.3 +/- 0.3 pmoles/monolayer (n = 3, P < 0.05). The capacity of cyst fluid to increase cyclic AMP levels was not changed by pronase treatment or boiling. There was a direct relation between the level of cellular cyclic AMP and the rate of transepithelial fluid secretion caused by cyst fluid. Cyst fluid increased thymidine incorporation by Madin-Darby canine kidney (MDCK) cells to an extent equal to that caused by epidermal growth factor and caused MDCK cells to form cysts in collagen matricies.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Na+/H+ antiporter (NHE-1 isoform) in cultured vascular smooth muscle from the spontaneously hypertensive rat.

An increase in Na+/H+ antiporter activity may be involved in hyperproliferation of vascular smooth muscle cells (VSMC) and possibly in the vascular hyperplasia characteristic of hypertension. The present study was designed to examine cell proliferation, Na+/H+ exchange activity, and mRNA levels of the NHE-1 isoform of the Na+/H+ antiporter in cultured aortic VSMC derived from the spontaneously hypertensive rat (SHR) and from normotensive controls, the Wistar/Kyoto rat (WKY). VSMC derived from the SHR grown in early (2 to 6), but not in later (7 to 10) sub-passages, exhibited an increase in [3H]-thymidine incorporation and shorter doubling times as compared to those derived from WKY rats. Na+/H+ exchange activity assayed in the nominal absence of HCO3-/CO2, as the rate of intracellular pH (pHi) recovery after cell acidification was significantly higher in cells from SHR than in those from WKY rats when cells were studied in early sub-passages, but not in cells studied in later sub-passages. In cells grown in early sub-passage, Na+/H+ exchange activity assessed as the initial rate of Na+i accumulation following acute cell acidification was also significantly higher in SHR than WKY cells both in the nominal absence (10.22 +/- 1.15 and 6.98 +/- 1.17 mmol Na+i/90 seconds, P < 0.05, respectively) and in the presence of HCO3-/CO2 (9.94 +/- 1.02 and 5.59 +/- 0.86 mmol Na+/90 seconds, P < 0.01, respectively). There were no detectable differences in the level of steady-state Na+/H+ antiporter (NHE-1) mRNA between VSMC from SHR and WKY rats. Our findings indicate that Na+/H+ exchange activity is increased in cultured aortic VSMC derived from SHR as compared to those derived from WKY rats. The higher functional activity of the Na+/H+ antiporter in VSMC from the SHR is due to a post-transcriptional event(s) and may be related to enhanced growth in culture.

Animals↗
PubMed1995

Anion secretion drives fluid secretion by monolayers of cultured human polycystic cells.

We have investigated the hypothesis that active anion transport drives fluid secretion by the cystic epithelium in autosomal dominant polycystic kidney disease (ADPKD). We prepared monolayers of a primary culture derived from cystic tissue removed from ADPKD patients. The monolayers were grown on permeant supports, and fluid secretion was initiated by forskolin. The results were compared with those obtained with monolayers of Madin-Darby canine kidney (MDCK) cells, known to secrete Cl-. In the absence of the agonist, ADPKD monolayers absorbed fluid (0.20 +/- 0.02 microliter.cm surface area-2.h-1). Forskolin reversed this to secretion (0.60 +/- 0.03 microliter.cm-2.h-1). Control MDCK monolayers did not transport fluid in either direction, but forskolin induced secretion (0.48 +/- 0.03 microliter.cm-2.h-1). The electrical properties of the monolayers were monitored in Ussing chambers. Forskolin increased the transepithelial potential difference (Vte) of ADPKD monolayers (-0.9 +/- 0.1 to -1.1 +/- 0.1 mV) and the short-circuit current (Isc) (6.6 +/- 0.7 to 9.2 +/- 0.8 microA/cm2). The transepithelial resistance (Rte) fell (156 +/- 9 to 138 +/- 10 omega.cm2). Similar results were obtained with MDCK monolayers. The polarity of Vte and the direction of the Isc are compatible with the hypothesis that active secretion of anion drives fluid secretion. Basolateral application of the Na-K-2Cl cotransporter, bumetanide, reduced forskolin-stimulated fluid secretion by ADPKD monolayers (0.56 +/- 0.05 to 0.28 +/- 0.03), depolarized Vte, and inhibited Isc without affecting Rte. Apical application of the Cl- channel blocker, diphenylamine-2-carboxylate, also inhibited fluid secretion by ADPKD monolayers (0.65 +/- 0.03 to 0.27 +/- 0.02 microliter.cm-2.h-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

In vitro fluid secretion by epithelium from polycystic kidneys.

The size of the kidneys in patients with autosomal dominant polycystic kidney disease (ADPKD) is due in large measure to the accumulation of secreted fluid within thin-walled epithelial sacs. We measured the net transepithelial movement of liquid in response to forskolin in isolated, intact cysts excised from the surface of human ADPKD kidneys and in cultured, polarized monolayers of epithelial cells derived from ADPKD cysts. 10 excised cysts bathed symmetrically in control culture medium secreted fluid at a rate of 0.19 +/- 0.03 microliter/cm2 per hour after stimulation with forskolin (10 microM). Ouabain (100 microM) addition to the cavity fluid did not change the rate of fluid secretion of 10 forskolin-treated cysts, but addition of the glycoside to the external bathing medium fluid of nine cysts decreased secretion to -0.004 +/- 0.05 microliter/cm2 per hour. 24 monolayers absorbed fluid (range -0.029 to -0.412 microliter/cm2 per hour); by contrast, fluid was secreted (range 0.074 to 1.242 microliters/cm2 per hour) after stimulation with forskolin (10 microM). Ouabain (0.1 microM) in the basolateral but not in the apical medium inhibited fluid secretion. Forskolin increased the intracellular cyclic AMP content of ADPKD and MDCK monolayers by 236 and 196%, respectively. Six ADPKD monolayers had stable lumen negative transepithelial electrical potential differences (PDte) of -1.4 +/- 0.3 mV, positive short circuit currents (SCC) of 11.9 +/- 2.1 microAmp/cm2 and a tissue resistance (Rte) of 116 +/- 14 ohm.cm2. Forskolin increased SCC to 15.5 +/- 1.9 microAmp/cm2 (P < 0.005) and decreased Rte to 95 +/- 13 ohm.cm2 (P < 0.05); PDte remained stable at -1.4 +/- 0.3 mV. Ouabain (10 microM) had no effect when added to the apical medium, but in the basolateral medium decreased SCC to 1.7 +/- 0.3 microAmp/cm2 and PDte to -0.2 +/- 0.1 mV. We conclude that ADPKD cells in surface cysts have the potential to absorb or to secrete solutes and fluid. cAMP-mediated fluid secretion from the basolateral medium into the lumen of surface ADPKD cysts may be driven by anion transport.

Biological Transport↗
PubMed1995

Intracellular acidification associated with changes in free cytosolic calcium. Evidence for Ca2+/H+ exchange via a plasma membrane Ca(2+)-ATPase in vascular smooth muscle cells.

The purpose of this study was to define the mechanism whereby agonists that increase free cytosolic calcium (Cai2+) affect intracellular pH (pHi) in smooth muscle. Rat aortic vascular smooth muscle cells grown on coverslips were loaded with BCECF/AM or fura-2/AM for continuous monitoring of pHi or Cai2+, respectively, in a HCO3-/CO2- containing medium. Recovery from rapid increases in Cai2+ produced by 1 microM angiotensin (Ang) II (delta Cai2+ -229 +/- 43 nM) or 1 microM ionomycin (delta Cai2+ -148 +/- 19 nM) was accompanied by a fall in pHi (delta pHi, -0.064 +/- 0.0085 P < 0.01, and -0.05 +/- 0.012 pH units, P < 0.01, respectively). Neither the fall in pHi nor the rise in Cai2+ elicited by Ang II was prevented by pretreatment with agents which block the action of this agonist on pHi via the stimulation of the Cl/HCo3 exchangers (DIDS, 50 microM) or the Na+/H+ antiporter (EIPA, 50 microM). In the presence of DIDS and EIPA, Ang II produced a fall in pHi (delta pHi, -0.050 +/- 0.014, P < 0.01) and a rise in Cai2+ (delta Ca2+ 252 +/- 157 nM, P < 0.01). That the change in pHi was secondary to changes in Cai2+ was inferred from the finding that, when the rise in Cai2+ elicited by Ang II was prevented by preincubation with a Ca2+ buffer, BAPTA (60 microM), the fall in pHi was abolished as well (delta pHi, 0.0014 +/- 0.0046). The pHi fall produced by Ang II and ionomycin was prevented by cadmium at a very low concentration (20 nM) which is known to inhibit plasma membrane Ca(2+)-ATPase activity (delta pHi -0.002 +/- 0.0006 and -0.0016 pH units, respectively). Cadmium also blunted Cai2+ recovery after Ang II and ionomycin. These findings suggest that the fall in pHi produced by these agents is due to H+ entry coupled to Ca2+ extrusion via the plasma membrane Ca(2+)-ATPase. Our results indicate that agonists that increase Cai2+ cause intracellular acidification as a result of Ca2+/H+ exchange across the plasma membrane. This process appears to be mediated by a plasma membrane Ca(2+)-ATPase which, in the process of extruding Ca2+ from the cell, brings in [H+] and thus acidifies the cell.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1995

Relation of recurrent laryngeal nerve compound action potential to laryngeal biomechanics.

This study was designed to investigate the compound action potential (CAP) of the recurrent laryngeal nerve (RLN) and to correlate this electrophysiologic signal to laryngeal biomechanics and phonatory function. Four adult mongrel canines were anesthetized. The RLN was isolated and stimulated, and recording electrodes were applied. The electromyographic (EMG) electrode was placed in the thyroarytenoid (TA) muscle. The RLN CAP and the EMG of the TA muscle were recorded and compared to the stimulation intensity, subglottic pressure (Psub), and each other. The CAP peak-to-peak and EMG peak-to-peak amplitudes demonstrated a sigmoidal relation to stimulus intensity and a linear relation to Psub and to each other. On the basis of these findings, the RLN CAP appears to be a reliable physiologic measure of laryngeal function.

Action Potentials↗
PubMed1995

Evidence for a potent lipid secretagogue in the cyst fluids of patients with autosomal dominant polycystic kidney disease.

Transepithelial fluid secretion appears to be an important factor in the progressive enlargement of cysts in autosomal dominant polycystic kidney disease. Evidence indicates that the fluid within cysts harbors an autocrine, paracrine, or endocrine secretagogue with the capacity to modulate the rate of cyst expansion. Fluids from five patients with autosomal dominant polycystic kidney disease were studied to determine the chemical nature and the physiologic function of the putative secretagogue. The secretory activity of cyst fluid assayed with polarized monolayers of Madin Darby canine kidney cells could be ascribed to a lipophilic substance of molecular weight < 3,500 d that was not destroyed by freezing, boiling, or proteolytic digestion. This lipid stimulated the production of intracellular cAMP and increased the rate of fluid secretion when added to either surface of cultured renal epithelial cells. Anion exchange chromatography revealed biologic secretory activity to a greater extent in the neutral lipid than in the fatty acid and phospholipid fractions separated from cyst fluid. More extensive chromatographic separation showed preferential appearance of the secretagogue in a fraction of neutral lipids enriched in monoglycerides. Among several candidate lipids, 1-mono-arachidonyl glyceride and arachidonic acid were found to mimic the effect of the cyst fluid to stimulate fluid secretion by Madin Darby canine kidney cells; however, their abundance in cyst fluid was insufficient to account for the degree to which secretion was stimulated by cyst fluid. Moreover, the effect of the arachidonic acid species to stimulate fluid secretion was inhibited by treatment with indomethacin, whereas the effect of the cyst fluid was not. On the basis of this study, it was concluded that human autosomal dominant polycystic kidney disease cyst fluid contains an anonymous lipid with the capacity to stimulate fluid secretion in renal epithelia. This potent endogenous modulator of fluid transport may have an important role in determining the rate at which cysts expand in autosomal dominant polycystic disease.

Animals↗
PubMed1995

Function of the interarytenoid(IA) muscle in phonation: in vivo laryngeal model.

Thyroarytenoid(TA), lateral cricoarytenoid(LCA), and IA muscles are referred to as the adductors of the vocal fold. The TA is known to shorten the vocal folds and to adduct the membranous vocal fold, and the LCA adducts the inter-vocal process region and IA adducts the posterior commissure. Even though IA has an important role for the positioning of the vocal folds during respiration and phonation together with the action of the posterior cricoarytenoid muscle, little is known about the effect of IA on voice parameters during phonation. An in vivo canine model was used in five mongrel dogs to examine the role of the IA muscle in controlling phonation. In two out of five dogs, sound could not be elicited without stimulating the IA branches of the recurrent laryngeal nerves. When the IA was dynamically and statistically stimulated, subglottic pressure, vocal intensity and fundamental frequency were increased. However, open quotient was not changed markedly. These results suggest that the IA affects the voice parameters mainly by controlling subglottic pressure during phonation.

Animals↗
PubMed1995

[Effect of scopolamine on the contents of beta-endorphin and oxytocin in hypothalamus, pituitary and plasma in morphine dependent rats].

Male Sprague-Dawley rats weighing 180-220 g were rendered dependent on morphine by repeated injections of morphine in increasing doses for 14 days. 0.3 mg/kg of scopolamine was injected intraperitoneally bid for 3 and 4 days. Control rats were similarly injected with saline. The contents of beta-endorphin (beta-EP) and oxytocin (OT) in hypothalamus, pituitary and plasma were measured by radioimmunoassay. The results showed that both beta-EP and OT in hypothalamus and plasma increased but both were decreased in pituitary in morphine dependent rats (P < 0.01). After scopolamine treatment, the contents of beta-EP increased but OT decreased in hypothalamus (P < 0.01), and both elevated significantly in pituitary (P < 0.01). The results suggested that scopolamine might modulate hypothalamus-pituitary system to affect the release or synthesis of beta-EP and OT in the brain.

Animals↗
PubMed1995

[Production and characterization of monoclonal antibody against aflatoxin B1].

Two hybridoma cell lines 1B5 and 2F1 capable of secreting specific monoclonal antibodies (McAbs) against aflatoxin B1 (AFT B1) were obtained. BALB/c mice were immunized by intrasplenic injection of AFT B1-human serum albumin conjugate (AFT B1-HSA) containing 9 AFT B1 residue per molecule. Spleen cells of BALB/c mouse with high serum antibody titer were fused with SP 2/0 myeloma cells in the presence of polyethylene glycol. Hybridoma cell lines were selected by using an indirect ELISA with AFT B1-keyhole limpet haemocyanin as coating antigen and grown as ascite tumour cells in BALB/c mice which previously had received an intraperitoneal injection with Freund's incomplete adjuvant. The McAbs were found to have strong reaction with AFT B1-bovine serum albumin conjugate (AFT B1-BSA) and no reaction with HSA or BSA. The reactivity of the McAbs with AFT analogs was determined by an indirect inhibition ELISA and the concentrations (ng/ml) required to inhibit 50 binding of McAb to AFT B1-BSA conjugate solid phase were AFT B1 4.0ng/ml, B2 36.9ng/ml, G1 23.3ng/ml and G2 403.3ng/ml for 1B5 McAb, and AFT B1 2.4ng/ml, B2 2.6ng/ml, G1 2.8ng/ml and G2 4.7ng/ml for 2F1 McAb.

Aflatoxin B1↗
PubMed1995

[Missed diagnosis in prostate incidental carcinoma].

522 cases of benign prostate hyperplasia from 1980 to 1994 were reviewed. Prostate incidental carcinoma (PIC) was identified in 26 cases (4.98%). In order to study the pathomorphological features and to study the causes for missed diagnosis of this entity, the authors observed and analysed the numbers of carcinomatous foci their distribution, classification, staging and differentiation, morphological features and prostate specific antigen (PSA) markers. It was found that 23 cases exhibited a pathological structure of uniform pattern and 3 cases with pluriform pattern. Adenocarcinoma was most common. 17 cases were A1 stage and 9 cases were A2 stage. Isolated multiple foci of invasion and alterations of architecture are important pathological features of these cases. Missed diagnosis of prostate cancer is related to the small amount of biopsy tissue, contrast between benign and malignant prostate epithelial tissue not distinct, scarce nuclear anaplasia, careless microscopic observation, or observer lacks the ability to differentiate between pathologic types and pluriform patterns. Different PSA reactions may be related to tumor differentiation and classification.

Adenocarcinoma↗
PubMed1994

HLA-DQ and TAP2 genes in patients with insulin-dependent diabetes mellitus.

We examined the prevalence of HLA-DRB1, DQB1, DQA1 and TAP2 genes in children with insulin-dependent diabetes mellitus (type 1 diabetes). These HLA and TAP2 alleles were identified by dot-blot analysis of polymerase chain reaction (PCR)-amplified genomic DNA with sequence-specific oligonucleotide probes. The results show that those DQB1 alleles, which carry non-aspartic acid at position 57, in conjunction with DQA1 alleles carrying arginine at position 52, are strongly associated with susceptibility to type 1 diabetes. The prevalence of the TAP2* 0201 allele in diabetic patients was significantly lower than that in normal controls. Analysis of the data suggests that DQ alleles have the primary association with type 1 diabetes and that the association of TAP2 alleles with the disease is secondary.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1994

Rat kidney glutamyl aminopeptidase (aminopeptidase A): molecular identity and cellular localization.

Glutamyl aminopeptidase [aminopeptidase A (EAP), EC 3.4.11.7] is an ectoenzyme that selectively hydrolyzes acidic amino acid residues from the amino terminus of oligopeptides. EAP activity is highest within the kidney and small intestine. The murine pre-B cell BP-1/6C3 and the human kidney glycoprotein gp160 differentiation antigens have been reported to have biochemical properties indistinguishable from EAP. It is not known, however, if rat kidney EAP is a homologue of these antigens or molecularly distinct. Using the reverse transcription-polymerase chain reaction method with oligonucleotide primers based on the BP-1/6C3 nucleotide sequence, we isolated a 450-bp partial cDNA from rat kidney poly(A)+ RNA. The partial cDNA encoded a predicted protein that was 92% and 86% identical to the murine BP-1/6C3 and human gp160 antigens, respectively; the amino acid sequence within the zinc-binding domain was completely conserved. Purification of EAP from rat kidney and microsequence analysis of a tryptic digest peptide fragment (18-mer) indicated that the fragment was highly similar to a region within the BP-1/6C3 and gp160 proteins. Northern blot hybridization and immunoblot analyses were also consistent with labeling of products the same size as reported for the BP-1/6C3 and gp160 antigens. There was a good correlation between the cellular distribution of EAP mRNA and EAP immunoreactivity, with proximal tubules and glomerular mesangial cells having the highest densities. These results indicate that rat kidney EAP is a species homologue of the murine BP-1/6C3 and human gp160 antigens. Furthermore, on the basis of its cellular localization, rat kidney EAP is likely to be involved in degradation of oligopeptides within the glomerulus and the glomerular filtrate. Since cells that express EAP also express receptors for angiotensin II, an intrarenal vasoactive hormone that is a substrate for EAP, these results further suggest that EAP may play a role in modulating the activity of intrarenal angiotensin II.

Amino Acid Sequence↗
PubMed1994

Changes in glottal area associated with increasing airflow.

Laryngeal resistance varies inversely with airflow during phonation. This study evaluated the morphological changes in the glottis that accompany decreases in laryngeal resistance at higher levels of airflow. An in vivo canine model of phonation and a video analysis system were used to assess changes in area. Four animals were examined stroboscopically as airflow increased, with constant recurrent laryngeal nerve stimulation. Glottal dynamics were evaluated by means of photoglottography, electroglottography, and measures of subglottic pressure. Analysis of digitized stroboscopic images indicated that increasing airflow had no obvious effect on the glottal chink (vocal process contact). Increasing airflow was associated with an increase in the area of peak opening and an increase in the glottal area integral.

Analysis of Variance↗
PubMed1994

Acid-base status and intracellular pH regulation in lymphocytes from rats with genetic hypertension.

This article reviews work from this laboratory dealing with acid-base status and intracellular pH (pHi) regulation in rat genetic models of hypertension. With freshly isolated thymic lymphocytes, pHi and its regulation were examined in the spontaneously hypertensive rat (SHR). In this rat model, pHi was found to be reduced as compared with that of lymphocytes from normotensive Wistar-Kyoto (WKY) rats. The activity of the Na+/H+ antiporter assessed after stimulation by acute cell acidification was similar in lymphocytes from SHR and WKY rats both in the nominal absence of HCO3- and in media containing HCO3- (22 mM). The kinetic properties of the Na+/H+ antiporter, examined as a function of pHi with the Hill kinetic model, revealed no significant differences between lymphocytes from SHR and WKY rats. The kinetic properties of the Na(+)-dependent and Na(+)-independent Cl(-)-HCO3- exchangers, examined as a function of external Cl-, were also virtually identical in lymphocytes from SHR and WKY rats. Unlike the Na(+)-H+ exchanger and the Na(+)-independent Cl(-)-HCO3- exchanger, which had their highest activities at extremes of pHi (low pHi, Na(+)-H+ exchanger; high pHi, Na(+)-independent Cl(-)-HCO3- exchanger), the Na(+)-dependent Cl(-)-HCO3- exchanger had its maximal activity near steady-state pHi. In Dahl/Rapp salt-sensitive rats with hypertension, the pHi of thymic lymphocytes was also reduced as compared with that of normotensive salt-resistant animals. In this model, renal net acid excretion in salt-sensitive rats was augmented as compared with that of salt-resistant rats. The increase in renal acid excretion was due to an increase in both ammonium and titratable acid excretion and was observed while animals were placed on high, normal and low salt diets. The findings of intracellular acidosis and enhanced renal acid excretion suggest that cellular acid overproduction is augmented in salt-sensitive hypertension.

Acid-Base Equilibrium↗
PubMed1994

Microprocessor-programmed infusion of theophylline rapidly attained expected steady-state level in rabbit plasma.

A self-made microprocessor-programmed (two-compartmental model) infusion controller was connected with an infusion pump, which achieved an expected steady-state plasma concentration (Cpss) rapidly (5 T1(2)alpha) and maintained the level. Theophylline was selected as an example, and its pharmacokinetic parameters of rabbits, expected Cpss, body weight (wt), and infusion time (t) were input. The programmed infusion rate (Kt) was determined by the following equation: (Kt) = Cpss.K10.Vc.wt (1 + [(K21-beta)/beta]EXP(-K21t)) and the predicted value was calculated by the formula: C(t) = Cpss X [1-EXP(-alpha t)]. The needed concentration and total volume of drug were automatically shown on the screen. The drug was automatically infused after pumping, and the plasma concentration of theophylline was measured by colorimetric method. The results showed that the median absolute value of the performance error (MAVPE) was 8.3%. Although T1(2)beta of theophylline was 6.08 h, the expected Cpss was attained in only 30 min (5 T1(2)alpha) after start of infusion and then well maintained.

Animals↗
PubMed1994

Effects of arytenoid adduction on laryngeal function following ansa cervicalis nerve transfer for vocal fold paralysis in an in vivo canine model.

Laryngeal reinnervation with the ansa cervicalis has been proposed as a treatment for human unilateral vocal fold paralysis (UVFP). This study tested the assumption that results from reinnervation could be improved if combined with medialization surgery. Six canine subjects underwent recurrent laryngeal nerve section and reinnervation with a branch of the ansa cervicalis. After reinnervation, vocal function was assessed before and after arytenoid adduction. Although laryngeal function improved significantly following reinnervation, results were significantly enhanced by the addition of medialization surgery. The implications for the treatment of human unilateral vocal fold paralysis are discussed.

Animals↗