Objective To study the protective effects of adenovirus-mediated human beta-nerve growth factor gene (hNGFβ) transfer combined with iron fortified nutrition on blast hearing damage in guinea pigs. Methods Deafness was induced by blast (172dB SPL) in 35 healthy guinea pigs. Seven days after noise exposure, 10 guinea pigs were inoculated with adenovirus-mediated hNGFβ (Ad-hNGFβ) into the perilymphatic space (the gene group), another 10 guinea pigs were given hNGFβ combined with iron fortified nutritional diet (the combination group), still another 10 guinea pigs were inoculated with artificial perilymphatic fluid (APF), and 5 guinea pigs served as control, given neither medicine nor noise exposure. Auditory brainstem response (ABR) threshold shifts were monitored in the guinea pigs before blast exposure and after gene transfer. Changes in cochlear morphology were examined with immunohistochemical and HE staining. Results One week after successful inoculation of hNGFβ, it was noted that Ad-hNGFβ protein was expressed in each turn of the cochlea, and its intensity was almost equal. After gene transfer in the combination group and the gene group, ABR threshold shifts at week 1 and 4 were significantly smaller than those of the APF group. HE staining showed that the number of the spiral ganglion cells in the combination group and the Ad-hNGFβ group was significantly higher than that of the control group after 4 weeks (P<0.01). Conclusions Ad-hNGFβ combined with iron fortified nutritional diet was effective in the prevention and treatment of blast hearing damage of cochlear hair cells. 相似文献
Background: As in inhaled isoflurane anesthesia, when isoflurane lipid emulsion (ILE; 8%, vol/vol) is intravenously administered, the primary elimination route is through the lungs. This study was designed to determine the minimum alveolar concentration (MAC) and the time course of washout of isoflurane for intravenously infused ILE by monitoring end-tidal isoflurane concentration.
Methods: Twelve healthy adult mongrel dogs were assigned randomly to an intravenous anesthesia group with 8% ILE or to an inhalation anesthesia group with isoflurane vapor. An up-and-down method and stimulation of tail clamping were used to determine MAC of 8% ILE by intravenous injection in the intravenous anesthesia group and MAC by the inhaled approach in the inhalation anesthesia group, respectively. Isoflurane concentration and partial pressure in end-tidal gas, femoral arterial blood, and jugular venous blood were measured simultaneously just before each tail clamping and during washout.
Results: The induction time in the intravenous anesthesia group (105 +/- 24 s) was shorter than that in the inhalation anesthesia group (378 +/- 102 s; P < 0.01). MAC of 8% ILE by intravenous injection (1.12 +/- 0.18%) was significantly less than MAC by the inhaled approach (1.38 +/- 0.16%; P < 0.05). No significant difference was found between the two groups in the time course of washout of isoflurane. 相似文献