Calcium oscillation may regulate gene transcription in a frequency-decoding manner during agonist stimulation,which provides an indicator of transcription level in cells. To determine whether persistent exposure to hypoxia may sensitize or blunt cell response to histamine, the effects of 24 h subacute mild hypoxia on histamine-stimulated calcium oscillation frequency were examined in pulmonary artery endothelial cells (PAECs). The results are: (1) 24 h subacute mild hypoxia significantly increased the histamine-stimulated calcium oscillation frequency in PAECs. The averaged frequency of calcium oscillation in posthypoxic PAECs was significantly higher than that in normoxic ones. (2) NADPH oxidase inhibitor, diphenylene iodonium chloride (DPI, 10 μmol/L), abolished histamine-stimulated calcium oscillations both in normoxic and posthypoxic PAECs. (3) Xanthine oxidase inhibitor, oxypurinol (100 μmol/L), did not affect the calcium oscillation kequency in normoxic PAECs. However, it significantly decreased the elevation of calcium oscillation frequency in posthypoxic PAECs. These results demonstrated that, during pulmonary disease related to persistent hypoxia,PAECs become more sensitive to histamine. During histamine stimulation, NADPH oxidase plays a critical role in generating calcium oscillations, while xanthine oxidase may contribute to, at least in part, the increase of calcium oscillation frequency in posthypoxic PAECs.

Roles of sympathicus, sensory neuropeptides (SNP), metabolites of cyclooxygenase, metabolites of lipoxygenase, endothelium derived relaxing factor (EDRF), reactive oxygen (ROS) and potassium channels (PC) in the hypoxic pulmonary vasoconstriction (HPV) and hypoxic cerebral vasodilation (HCVD) were studied in intact rats, rabbits and dogs. Results were as follows: during hypoxia, the excitation of sympathicus results in a constriction of both pulmonary and cerebral vessels; SNP, EDRF and the opening of 4-AP sensitive PC caused the dilation of both of them; metabolites of lipoxygenase mediated HPV and HCVD, whereas metabolites of cyclooxygenase were their modulators; hypoxia induced blockade of the ATP sensitive PC mediated HPV, but had no effect on HCVD; reduction of O_2~+ in the lung might potentiate HPV, but had no effect on HCVD. It is suggested that the alteration of lipoxygenase metabolites, ROS and ATP sensitive PC are factors accounting for the difference in response of pulmonary and cerebral vassels to hypoxia.

AIM:To investigate the role of potassium channel expression alteration in chronic cigarette smoking-induced increase in pulmonary vascular responsiveness,the effect of chronic cigarette smoking on large-conductance calcium-activated potassium channel(BKCa) and voltage-dependent delayed rectifier potassium channel(Kv1.5) expression in rat pulmonary smooth muscle cells were investigated in vivo.METHODS: HE staining,immuno-histochemistry and in situ hybridization techniques were used.RESULTS:(1) Chronic cigarette smoking downregulates the protein and mRNA expression of BKCa in pulmonary arterial smooth muscles.(2) Chronic cigarette smoking downregulated the protein and mRNA expression of Kv1.5 in pulmonary arterial smooth muscles.(3) In big artery,BKCa decreased more makedly than Kv1.5,but in small artery,both of them decreased equally.CONCLUSION: Chronic cigarette smoking downregulates the levels of BKCa and Kv1.5 in rat pulmonary arterial smooth muscle cells in vivo,which maybe contribute to the mechanism of cigarette smoking-induced increase in pulmonary vascular responsiveness.

Primary cell culture, techniques of gene transfection, gelatin zymography, and Western blot were used to investigate the effect of hypoxia on the secretion of MMP-2 and MMP-9 in pulmonary artery endothelial cells (PAEC) and smooth muscle cells (PASMC), and the role of HIF-1. Our results showed that (1) after exposure to hypoxia for 24 h, the protein content and activity of MMP-2 in the PAEC medium as well as these of MMP-2 and MMP-9 in PASMC medium (P<0.01) decreased significantly in contrast to those in normoxic group (P<0.05); (2) after transfection of wild type EPO3'-enhancer, a HIF-1 decoy, the content and activity of MMP-2 and MMP-9 in hypoxic mediums became higher than those in normoxic group (P<0.01), while transfection of mutant EPO3'-enhancer didn't affect the hypoxia-induced down-regulation. It is concluded that hypoxia could inhibit the secretion and activity of MMP-2 and MMP-9 in PAEC and PASMC, which could be mitigated by the transfection of EPO3'-enhancer and that HIF-1 pathway might contribute to hypoxia-induced down-regulation of MMP-2 and MMP-9.

Objective To determine whether rizatriptan has an effect on cortical spreading depression (CSD) and c-Fos expression within periaqueductal grey (PAG) induced by CSD in rats. Methods The experimental SD rats were randomly divided into group A injected with KCl, group B KCl plus rizatriptan and group C NaCL The number and amplitude of CSD were recorded after KCl or NaCl injection. C-Fos positive neurons of different layer were identified by the immunohistochemical technique 2 hours after the first injection of KCl or NaCl. Results There was no CSD in group C. The number of CSD in group A ( 10.70±3.23 ) was significantly more than that in group B (6.10±2.56, t = - 3.528, P < 0.01 ). The amplitude of CSD in group A ( 17.33 (95% CI 11.45--23.11 ) mV) was significantly greater than that in group B (11.82 (95%CI 9.24--14.70) mV, Z= -4.360, P< 0.01). There were more cFos-like immnoreactive neurons in every layer in group A than in group C (P < 0.01 ) and in group B (P < 0.05 ). Conclusion Rizatriptan has an inhibitory effect on CSD, which might induce the headache through exciting the neurons in PAG.

OBJECTIVE: To investigate the influence of buried thread nasal augmentation on dorsal soft tissue of nose and revision rhinoplasty. METHODS: A clinical data of 29 patients requesting revision rhinoplasty after buried thread nasal augmentation, who were admitted between July 2017 and July 2019 and met the selection criteria, was retrospectively analyzed. All patients were female with an average age of 26.8 years (range, 18-43 years). The patiens were admitted to the hospital at 3-48 months after buried thread nasal augmentation (median, 15 months). Among them, there were 18 cases of insufficient nasal tip projection, 22 cases of insufficient nasal root projection, 7 cases of threads ectasia, 5 cases of threads exposure, 3 cases of infection, and 10 cases with two or more conditions. There were 9 cases of combined short nose deformity, 1 case of spherical hypertrophy of the nasal tip, 3 cases of deviation of the nasal columella, 3 cases of excessive width of the nasal base, and 1 case of nasal hump. Three infected patients only underwent threads removal and debridement. The rest patients underwent revision rhinoplasty, and the dorsum of the nose was made with polytetrafluoroethylene expansion; the tip of the nose was reshaped by taking autologous rib cartilage and alar cartilage in 16 cases, and by taking autologous septal cartilage and alar cartilage in another 10 cases. The threads and surrounding tissue specimens removed during operation were subjected to histologic observation. Nasal length and nasal tip projection were measured after revision rhinoplasty and the ratio was calculated to evaluate the nasal morphology; patient satisfaction was evaluated using the Likert 5-grade scale. RESULTS: Patients were followed up 12-48 months (mean, 18 months). Inflammation was controlled in 3 patients with infections caused by buried thread nasal augmentation. The remaining 26 patients had satisfactory results immediately after revision rhinoplasty. Before revision rhinoplasty and at 7 days and 6 months after revision rhinoplasty, the nasal length was (4.11±0.34), (4.36±0.25), and (4.33±0.22) cm, respectively; the nasal tip projection was (2.34±0.25), (2.81±0.18), and (2.76±0.15) cm, respectively; and the nasal tip projection/nasal length ratio was 0.57±0.08, 0.65±0.05, and 0.64±0.04, respectively. There were significant differences in the nasal length and the nasal tip projection between time points ( P<0.05). There was a significant difference in the nasal tip projection/nasal length ratio between pre- and post-operation ( P<0.05), but there was no significant difference between 7 days and 6 months after operation ( P>0.05). The Likert score for satisfaction ranged from 1.5 to 5.0 (mean, 4.05). During follow-up period of 26 patients, no nasal prosthesis was exposed, and the shape of the nose was stable, and the nasal skin of 5 patients with exposed threads could be seen with different degrees of scarring; there was no infection, cartilage resorption, and no cartilage deformation, displacement, or exposure. Histological observation showed that absorbable threads were not only absorbed after implantation, but also with the prolongation of time, the inflammatory changes in the surrounding tissues caused by decomposition and absorption of the threads showed a gradual aggravation of the first, the heaviest inflammatory reaction in 6 to 12 months, and then gradually reduce the trend. CONCLUSION After implantation of the absorbable thread into the subcutaneous tissue of the nasal dorsum, the nature of the thread is different from the body's own tissue, which will affect the soft tissue compliance of the nasal dorsum. The degradation and absorption of the thread will stimulate the infiltration of inflammatory cells and the proliferation of fibroblasts in the surrounding tissue and then form scar tissue, which will affect the design and effect of revision rhinoplasty.
Humans ; Female ; Adult ; Male ; Rhinoplasty ; Retrospective Studies ; Reoperation ; Nasal Cartilages ; Nasal Septum ; Cicatrix