Changes in blood flow in the tracheal mucosa of the dog caused by the pressure exerted by high volume, low-pressure cuffs were measured with the hydrogen clearance method. Before inflating the cuffs, the blood flow of the tracheal mucosa was measured as a control for 12 h in order to confirm that the procedures of the hydrogen clearance method itself had little or no influence on the blood flow in the tracheal mucosa. After inflating the cuffs to create a tracheal wall pressure (TWP) of 1.3 kPa (10 mmHg), 2.6 kPa (20 mmHg), 3.9 kPa (30 mmHg) or 6.0 kPa (45 mmHg), local blood flows of tracheal mucosa (TBF) corresponding to each TWP were measured every hour for 12 h. No significant changes in blood flow were observed in the tracheal mucosa with the hydrogen clearance method before inflating the cuffs. In the groups with TWP of 1.3 and 2.6 kPa, the TBF rose 1 h after inflation of the cuffs, and then returned to the baseline values. In the group with TWP of 6.0 kPa, the TBF decreased markedly already 1 h after inflation of the cuffs, and continued to decrease severely thereafter. In the group with TWP of 3.9 kPa, the TBF followed an intermediate course between the groups with TWP of 2.6 kPa and 6.0 kPa. From the results of the present study, it was found that TBF was significantly impaired by a TWP of more than 3.9 kPa. Therefore, in prolonged intubation, TWP should be kept at or below 2.6 kPa.
Mechanosensitive (MS) neurons in the periodontal ligament (PDL) pass information to the trigeminal ganglion when excited by mechanical stimulation of the tooth. During occlusal tooth trauma of PDL tissues, MS neurons are injured, resulting in atrophic neurites and eventual degeneration of MS neurons. Nerve growth factor (NGF), a neurotrophic factor, serves important roles in the regeneration of injured sensory neurons. In the present study, the effect of pro‑inflammatory cytokines, including interleukin 1β (IL‑1β) and tumor necrosis factor α (TNF‑α), on transforming growth factor β1 (TGF‑β1)‑induced NGF expression was evaluated in rat PDL‑derived SCDC2 cells. It was observed that TGF‑β1 promoted NGF expression via Smad2/3 and p38 mitogen‑activated protein kinase (MAPK) activation. IL‑1β and TNF‑α suppressed the TGF‑β1‑induced activation of Smad2/3 and p38 MAPK, resulting in the abrogation of NGF expression. NGF secreted by TGF‑β1‑treated SCDC2 cells promoted neurite extension and the expression of tyrosine hydroxylase, a rate‑limiting enzyme in dopamine synthesis in rat pheochromocytoma PC12 cells. These results suggested that pro‑inflammatory cytokines suppressed the TGF‑β‑mediated expression of NGF in PDL‑derived fibroblasts through the inactivation of TGF‑β‑induced Smad2/3 and p38 MAPK signaling, possibly resulting in the disturbance of the regeneration of injured PDL neurons.
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