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Biomedical subjects

W Y Su

Publications and source records attributed to W Y Su.

10 recordsLinked to original sources
PubMed1992

Pulmonary effects of inhaled zinc oxide in human subjects, guinea pigs, rats, and rabbits.

Occupational exposure to freshly formed zinc oxide (ZnO) particles (less than 1.0 micron aerodynamic diameter) produces a well-characterized response known as metal fume fever. An 8-hr threshold limit value (TLV) of 5 mg/m3 has been established to prevent adverse health effects because of exposure to ZnO fumes. Because animal toxicity studies have demonstrated pulmonary effects near the current TLV, the present study examined the time course and dose-response of the pulmonary injury produced by inhaled ZnO in guinea pigs, rats, rabbits, and human volunteers. The test animals were exposed to 0, 2.5, or 5.0 mg/m3 ZnO for up to 3 hr and their lungs lavaged. Both the lavage fluid and recovered cells were examined for evidence of inflammation or altered cell function. The lavage fluid from guinea pigs and rats exposed to 5 mg/m3 had significant increases in total cells, lactate dehydrogenase, beta-glucuronidase, and protein content. These changes were greatest 24 hr after exposure. Guinea pig alveolar macrophage function was depressed as evidenced by in vitro phagocytosis of opsonized latex beads. Significant changes in lavage fluid parameters were also observed in guinea pigs and rats exposed to 2.5 mg/m3 ZnO. In contrast, rabbits showed no increase in biochemical or cellular parameters following a 2-hr exposure to 5 mg/m3 ZnO. Differences in total lung burden of ZnO, as determined in additional animals by atomic absorption spectroscopy, appeared to account for the observed differences in species responses. Although the lungs of guinea pigs and rats retained approximately 20% and 12% of the inhaled dose, respectively, rabbits retained only 5%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

[Cerebrospinal fluid rhinorrhea due to sinus surgery: a case report].

Cerebrospinal fluid rhinorrhea is an uncommon but dangerous disease. Many lethal complications, such as bacterial meningitis and pneumoencephalus, may be the result of cerebrospinal fluid rhinorrhea. Otolaryngologist, neurosurgeons and radiologists must know how to diagnose, how to localize the site of leakage and how to choose the best method of treatment. A case of cerebrospinal fluid rhinorrhea and meningitis due to improper sinus surgery is presented. Satisfactory result, such as avoidance of unnecessary brain tissue damage, can be obtained by extracranial endonasal repairing of the fistula with a composite septal flap.

Adult↗
PubMed1990

Age-dependent effect of ozone on pulmonary eicosanoid metabolism in rabbits and rats.

Acute exposures to ozone have previously been shown to cause quantitative changes in the spectrum of arachidonic acid (AA) metabolites in lung lavage fluid. Since age appears to be an important variable in the toxicity of inhaled ozone, we investigated its effect on ozone-induced changes in pulmonary eicosanoid metabolism. Rats and rabbits ranging in age from neonates to young adults were exposed either to air or to 1 ppm ozone for 2 hr. Lung lavage fluid was collected within 1 hr following exposure and analyzed for its content of selected eicosanoids. In both species, there was a pronounced effect of age on ozone-induced pulmonary eicosanoid metabolism. Ozone-exposed animals at the youngest ages examined had severalfold greater amounts of two products of the cyclooxygenase pathway, prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha), than did age-matched controls. This effect lessened and eventually disappeared as the animals grew toward adulthood. In rabbits, ozone also induced increases in 6-keto-prostaglandin F1 alpha and thromboxane B2, but these changes were of lesser magnitude and evident only in the youngest rabbits exposed. There was no observed effect of ozone on lung lavage content of leukothriene B4. Indices of nonspecific pulmonary damage, i.e., protein concentration in lung lavage fluid and total number and viability of lavaged lung cells, were affected by ozone exposure, but not in an age-dependent manner that correlated with changes in pulmonary eicosanoid metabolism. In vitro ozone exposure of lung macrophages from naive rabbits of the same age range as those exposed in vivo demonstrated that ozone is capable of stimulating the elaboration of PGF2 alpha and especially PGE2. However, the increase in lavage fluid PGE2 and PGF2 alpha caused by ozone inhalation could not be attributed to macrophage metabolism conclusively since elaboration of PGE2 and PGF2 alpha by cultured macrophages was not enhanced by prior in vivo ozone exposure. In an ancillary study it was shown that 15-hydroxyprostaglandin dehydrogenase (PGDH) activity in rabbit lung homogenates was not affected by prior exposure to ozone, indicating that the increase in lung lavage fluid eicosanoids that occurred in these animals could not be explained by inhibition of PGDH.

Aging↗
PubMed1988

Distribution of noradrenergic nerve fibers in canine nasal mucosa following selective neurectomies.

In this study, we have used noradrenergic histofluorescence and selective neurectomies of the vidian, ethmoid and caudal nasal nerves to evaluate the distribution of postganglionic sympathetic fibers in the canine nasal mucosa. In conjunction with the histochemical localization of the noradrenergic fibers in the nasal mucosa after vidian neurectomy, the norepinephrine content of the mucosa was also evaluated using high-performance liquid chromatography. Unilateral neurectomy of the superior cervical ganglion (SCG) resulted in the unilateral disappearance of all noradrenergic histofluorescence in the nasal mucosa, while no morphological changes in noradrenergic fibers could be identified after neurectomy of the cervical sympathetic trunk 1 cm below the SCG. Ethmoid neurectomy caused the disappearance of noradrenergic fibers of the upper third of the nasal mucosa, while vidian neurectomy resulted in a partial loss of noradrenergic fibers in the lower two-thirds of the nasal mucosa. The loss was chiefly in the area adjacent to venous sinusoids and was responsible for 50% of the norepinephrine content of this tissue. We concluded that all the postganglionic sympathetic fibers are from the ipsilateral SCG. Some of them travel via the ethmoid nerve and innervate the upper third of the nasal mucosa. The remaining fibers travel via the vidian nerve and perhaps the vessel walls of the supplying arteries and innervate the lower two-thirds of the nasal mucosa. The vidian nerve chiefly innervates the venous sinusoids of the lower two-thirds of the nasal mucosa.

Adrenergic Fibers↗
PubMed1987

Retrograde axonal transport of true blue dye by the peripheral autonomic nerves in canine nasal mucosa.

In this study we employed retrograde axonal transport of (E)-2,2'-vinylendi-benzofuran-5-carboxamidin-diaceturate+ ++ or true blue (TB) to study the peripheral autonomic innervation of the canine nasal mucosa. After injection of TB into the nasal mucosa, labeled neurons were found in the ipsilateral sphenopalatine ganglion (SPG) and the superior cervical ganglion (SCG). There were no labeled neurons in the middle cervical or stellate ganglia. This indicated that the origin of the postganglionic sympathetic fibers of the nasal mucosa was only from the ipsilateral SCG. When TB was injected into the nasal mucosa of dogs following a caudal or ethmoidal neurectomy, labeled neurons could still be found in the SPG and SCG. When TB was injected into the nasal mucosa of dogs following ethmoidal and vidian neurectomies or with maxillary neurectomy added, some labeled neurons could still be found in both the ipsilateral SPG and SCG. These results support the concept that another pathway--perhaps perivascular--exists for postganglionic sympathetic fibers other than the vidian and ethmoidal nerves. Labeled neurons were still observed in SPG when TB was applied to the canine nasal mucosa following neurectomy of either the ethmoidal or the caudal nasal nerve. However, retrograde labeled neurons could not be found in SPG following simultaneous neurectomies of the ethmoidal and caudal nasal nerves. These results show that the postganglionic parasympathetic fibers originating in the SPG travel along the ethmoidal and caudal nasal nerves.

Animals↗