McCaffrey, Thomas V.

Nasal secretory activity was measured in seven dogs in response to topical stimulation by histamine and methacholine. The methacholine response was blocked by atropine but not by chlorpheniramine. The histamine response was blocked by chlorpheniramine but not by atropine. These results suggest that there are two independent mechanisms of nasal secretion in the dog.

Septic necrosis of the internal carotid artery is a major complication of peritonsillar abscess. Although once a common complication, its occurrence is rare since the introduction of antibiotics. A 12‐year‐old girl was referred to our institution after a false aneurysm of the internal carotid artery had been entered during routine tonsillectomy for a peritonsillar abscess. Review of the literature and features of the present case demonstrate the following findings suggestive of erosion of the internal carotid artery as a result of peritonsillar abscess: (1) spontaneous hemorrhage from a peritonsillar abscess, (2) persistent peritonsillar swelling after resolution of symptoms of peritonsillar abscess, (3) ipsilateral Horner's syndrome, and (4) otherwise unexplained cranial nerve palsies (nerves IX, X, XI, and XII).

The response of laryngeal airway resistance to chemoreceptor stimulation was measured before and after vagotomy in ten anesthetized dogs. With the vagus nerves intact, stimulation of chemoreceptors produced a decrease in both inspiratory and expiratory laryngeal resistance. After bilateral vagotomy below the origin of the recurrent laryngeal nerves, stimulation of chemoreceptors produced a smaller decrease in inspiratory laryngeal resistance and an increase in expiratory laryngeal resistance. We concluded that pulmonary afferent input to the respiratory neurons maintains a low airway resistance during chemoreceptor stimulation.

Giant cell granuloma is a benign lesion that generally involves the mandible and maxilla. It may be locally aggressive and result in extensive tissue destruction in advanced cases. A retrospective analysis of giant cell granuloma during the Interval 1970 to 1990 revealed 18 cases of advanced disease, as defined by bone destruction and a greatest dimension of 2.0 cm or more. Epidemiologic factors, physical findings, Imaging studies, pathologic specimens, treatment modalities, and outcome were reviewed for each case. Eight lesions were treated by local excision and curettage, and 10 were treated by partial mandibulectomy. Five mandibular defects were reconstructed with lilac bone grafts and one with a free flap. Only one patient with maxillary giant cell granuloma who underwent curettage had regrowth of what is suspected to have been residual disease. Individualized treatment, tailoring the extent of resection to the extent of disease, provided excellent results.

Seventy‐five cases of laryngotracheal stenosis treated between 1981 and 1991 were reviewed to determine the effectiveness of surgical treatment on the basis of site and severity of stenosis. Decannulation and absence of exertional dyspnea were the criteria of successful management. The treatment methods used were endoscopic laser incision and dilatation, expansion laryngotracheoplasty, and segmental resection. Endoscopic procedures were effective in treating thin (< 1 cm) stenoses in the subglottis and trachea. Laryngotracheoplasty was most effective in treating thick stenoses of the glottis and subglottis. Tracheal stenoses were most effectively treated by segmental resections. The probability for decannulation decreased with longer narrower stenoses and with increasing clinical stage. (OTOLARYNGOL HEAD NECK SURG 1993;109:468‐73.)

This study investigated the direct effects of substance P (SP) on ciliary beat frequency of human upper airway mucosa. Human adenoid explant tissue was maintained in serum free culture media, MCDB153. Ciliated epithelial cells were observed with phase‐contrast microscopy and ciliary activity was measured using a photometric technique. Oscillations in transmitted light caused by ciliary beating were recorded and modal ciliary beat frequency was determined by fast Fourier transformation. Specimens were treated with SP at concentrations of 10−4, 10−5, 10−6, and 10−7 mol/L and with equal molar solutions of SP and (D‐Pro2, D‐Trp7,9)‐SP, a SP antagonist. Substance P was found to increase ciliary beat frequency in a dose‐dependent manner with a maximum increase of 12.1%. This effect was not seen with solutions containing (D‐Pro2, D‐Trp7,9)‐SP. This suggests that SP exerts a direct stimulatory effect on ciliated cells of the upper airway. Because SP is known to be released in the upper airway in response to chemical irritation, it is presumed that the stimulatory effect of SP on mucosal cells provides a protective mechanism against inhaled irritants.

Normal mucociliary flow is a significant defense mechanism in the prevention of acute sinusitis. We have undertaken a study to examine the early sinus mucosal and mucociliary changes that occur in response to acute infection. Twenty rabbits were evaluated for 5 days after an obstructed maxillary sinus was inoculated with either Streptococcus pneumoniae, Hemophilus influenzae, Pseudomonas aeruginosa, or a sterile saline solution. Data collected included measurements of sinus mucosal ciliary beat frequency, quantitation of ciliated cell losses, and electron microscopic observations. Results demonstrate statistically significant (p < 0.05) changes in mucosal ciliary beat frequency that were either excitatory or inhibitory, depending both on the length of the infection and the specific organism. No changes in ciliary beat frequency were observed in the control animals (p > 0.55). Control animals likewise demonstrated no loss of ciliated cells from mucosal epithelium; however, dramatic losses of ciliated cells from the sinus mucosa of the experimental groups were observed. These losses occurred at different rates, depending on the infecting organism, but all infected groups demonstrated a >86% decrease in the number of viable ciliated cells from the sinus mucosa after sinusitis of 5 days duration. We conclude that a significant loss of ciliated cells from sinus mucosa and a corresponding disruption of normal mucociliary flow occurs early after exposure to pathogenic organisms and is a significant predisposing factor in the development of acute sinusitis.

Assessment of laryngeal framework surgery requires an awareness of the effect of vocal fold mass, stiffness, and position on voice production. The vibratory pattern of the vocal folds during phonation depends on the subglottic pressure as well as the mass and stiffness of the folds. To assess the effect of variations in vocal fold tension with contraction of the cricothyroid muscle on phonation, eight mongrel dog larynges were studied in vivo. Photoglottography, electroglottography, and subglottic pressure were simultaneously recorded as airflow rate and superior laryngeal nerve (SLN) stimulation were varied. Stimulation of the SLN was modified by varying the frequency and voltage of the stimulating electrical signal. Multiple regression analysis of the data revealed a direct relationship between the voltage of SLN stimulation and frequency of vibration (P < 0.001) at constant subglottic pressure. Increases in the stimulating voltage to the SLN also led to an increase in open quotient (p < 0.001), but no statistically significant change in speed quotient, subglottic pressure, or sound intensity. Changing the frequency of SLN stimulation had only a modest effect on the frequency of vibration. These results are consistent with the reported findings of an increase in frequency and open quotient with increased tension in an in vitro canine model. The glottographic measurement open quotient appears to be an estimator of cricothyroid contraction and longitudinal vocal fold tension, and may be clinically applicable to the assessment of superior laryngeal nerve injuries and laryngeal framework procedures.

Two groups of rats were used to evaluate the results of nerve repair using fibrin tissue adhesive. In one group of 10 rats, a simple neurotomy of the sciatic nerve was performed. In the second group of 10 rats, a 1‐cm segment of sciatic nerve was excised bilaterally and used as an autogenous nerve graft. The neurotomy and the nerve graft were repaired on one side by microsurgical suture technique using 10‐0 nylon suture. The opposite side was repaired using fibrin adhesive. The results of the repair were assessed at 12 weeks. Functional assessment of nerve regeneration was performed in those rats with intact repair sites. Nerve‐muscle twitch strengths were not significantly different (p > 0.05) between nerves repaired using suture and fibrin adhesive; however, compound active potential parameters were significantly better in nerve grafts repaired using suture technique (p < 0.05).

Substance P is a neuropeptide released by afferent neurons in the respiratory tract during inflammatory reactions. It produces effects on blood vessels, bronchial smooth muscle, nasal glands, and respiratory cilia. We studied the in vitro effect of substance P on the ciliary beat frequency of human adenoid explants and its mechanism of action. Substance P was added to cultured adenoid at concentrations of 10−10, 10−8, 10−6, and 10−4 mol/L. Ciliary beat frequency was determined with phase‐contrast microscopy and microphotometry. Substance P increased ciliary beat frequency a maximum of 11.9% ± 3.8% (p < 0.01). Diclofenac (10−6 mol/L) significantly blocked the ciliostimulatory effects of SP (p < 0.022), indicating that prostaglandin synthesis is an intermediate step in the action of substance P on ciliary beat frequency. The L‐arginine analogs, NG‐nitro‐L‐arginine methyl ester and NG‐monomethyl‐L‐arginine, inhibit nitric oxide synthesis from L‐arginine. L‐Arginine analogs (10−4 to 10−2 mol/L) inhibited the effect of substance P (p < 0.02 at the higher concentration). This inhibition was reversed by adding L‐arginine, demonstrating that nitric oxide production is a required step in substance P‐induced ciliostimulation. Substance P stimulates ciliary activity in human nasal mucosa as a result of secondary production and release of endogenous prostaglandins and nitric oxide. It is likely that inflammatory disease processes that stimulate release of substance P and subsequent prostaglandin and nitric oxide production modify mucociliary transport. Pharmacologic modification of substance P and its second messengers may eventually permit regulation of this important defense mechanism and control of neurogenic inflammation.