Comparison of cardiac output and hemodynamic responses of intubation among different videolaryngoscopies in normotensive and hypertensive patients / 华中科技大学学报（医学）（英德文版）

Tracheal intubation with Macintosh laryngoscope (MAC) might result in severe cardiovascular complications. The results of conducted studies investigating the effects of videolaryngoscopies on hemodynamic response of tracheal intubation are conflicting. We know little about the effects of videolaryngoscopies on cardiac output changes during tracheal intubation. We compared cardiac output (COP) and hemodynamic responses in normal blood pressure (n=60) and hypertensive patients (n=60) among 3 intubation devices: the MAC, the UE videolaryngoscopy ® (UE), and the UE video intubation stylet ® (VS). Cardiac index (CI), stroke volume index (SVI), heart rate (HR), systolic blood pressure (SBP) and diastolic blood pressure (DBP) were recorded using LidcoRapid (V2)® preinduction, preintubation, and every minute for the first 5 min after intubation. We assessed oropharyngeal and laryngeal structures injury as well. Intubation time was significantly shorter than MAC groups (P<0.001) only in UE group of normotensive and hypertensive patients. In normotensive patients, there were no significant differences in any of COP variables or hemodynamic variables among the three devices. In hypertensive patients, SBP and DBP in the MAC group were significantly higher (P<0.05 or <0.01) than the UE and VS groups at 1, 2 and 3 min after intubation, but there were no significant differences in CI, SVI and HR among the three devices. There was no significant difference in oropharyngeal and laryngeal structures injury among all groups. It was concluded that both the UE and VS attenuate only the hemodynamic response to intubation as compared with the MAC in hypertensive patients, but not in normotensive patients.

Comparison of cardiac output and hemodynamic responses of intubation among different videolaryngoscopies in normotensive and hypertensive patients / 华中科技大学学报（医学）（英德文版）

Tracheal intubation with Macintosh laryngoscope (MAC) might result in severe cardiovascular complications. The results of conducted studies investigating the effects of videolaryngoscopies on hemodynamic response of tracheal intubation are conflicting. We know little about the effects of videolaryngoscopies on cardiac output changes during tracheal intubation. We compared cardiac output (COP) and hemodynamic responses in normal blood pressure (n=60) and hypertensive patients (n=60) among 3 intubation devices: the MAC, the UE videolaryngoscopy ® (UE), and the UE video intubation stylet ® (VS). Cardiac index (CI), stroke volume index (SVI), heart rate (HR), systolic blood pressure (SBP) and diastolic blood pressure (DBP) were recorded using LidcoRapid (V2)® preinduction, preintubation, and every minute for the first 5 min after intubation. We assessed oropharyngeal and laryngeal structures injury as well. Intubation time was significantly shorter than MAC groups (P<0.001) only in UE group of normotensive and hypertensive patients. In normotensive patients, there were no significant differences in any of COP variables or hemodynamic variables among the three devices. In hypertensive patients, SBP and DBP in the MAC group were significantly higher (P<0.05 or <0.01) than the UE and VS groups at 1, 2 and 3 min after intubation, but there were no significant differences in CI, SVI and HR among the three devices. There was no significant difference in oropharyngeal and laryngeal structures injury among all groups. It was concluded that both the UE and VS attenuate only the hemodynamic response to intubation as compared with the MAC in hypertensive patients, but not in normotensive patients.

Reduction of pulmonary inflammatory response by erythropoietin in a rat model of endotoxaemia / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Erythropoietin elicits protective effects in lung tissue injury induced by ischaemic reperfusion and hyperoxia. We investigated the protective roles of erythropoietin in pulmonary inflammation and lung injury during acute endotoxaemia.</p><p><b>METHODS</b>A total of 32 male Sprague-Dawley rats were randomly assigned to four groups: saline group, erythropoietin + saline group, saline + lipopolysaccharide group and erythropoietin + lipopolysaccharide group. Rats were treated with erythropoietin (3000 U/kg, i.p.) or saline, 30 minutes prior to lipopolysaccharide administration (6 mg/kg, i.v.). Four hours after lipopolysaccharide injection, samples of pulmonary tissue were collected. Optical microscopy was performed to examine pathological changes in lungs. Wet/dry (W/D) ratios, myeloperoxidase activity, malondialdehyde concentrations and tumour necrosis factor-alpha (TNF-alpha) as well as interleukin 1 beta (IL-1beta) levels in lungs were measured. The pulmonary expression of nuclear factor kappaB (NF-kappaB) p65 was evaluated by Western blotting. Differences between the different groups were analysed by one-way analysis of variance (ANOVA).</p><p><b>RESULTS</b>The lung tissues from the saline + lipopolysaccharide group were significantly damaged, which were less pronounced in the erythropoietin + lipopolysaccharide group. The W/D ratio increased significantly in the saline + lipopolysaccharide group (5.75 +/- 0.22) as compared with the saline group (3.85 +/- 0.20) (P < 0.01), which was significantly reduced in the erythropoietin + lipopolysaccharide group (4.50 +/- 0.35) (P < 0.01). Myeloperoxidase activity and malondialdehyde levels increased significantly in the saline + lipopolysaccharide group compared with the saline group, which was reduced in the erythropoietin + lipopolysaccharide group. The TNF-alpha level of pulmonary tissue increased significantly in the saline + lipopolysaccharide group ((9.80 +/- 0.82) pg/mg protein) compared with the saline group ((4.20 +/- 0.42) pg/mg protein, P < 0.01). However, the increase of TNF-alpha level of pulmonary tissue was significantly reduced in the erythropoietin + lipopolysaccharide group ((6.50 +/- 0.66) pg/mg protein, P < 0.01). Similarly, pulmonary IL-1beta levels were elevated markedly in the saline + lipopolysaccharide group in contrast to the saline group, whereas the elevation was much less in the erythropoietin + lipopolysaccharide group. The nuclear localization of p65 increased markedly in the saline + lipopolysaccharide group and this enhancement of nuclear p65 expression was much less in the erythropoietin + lipopolysaccharide group.</p><p><b>CONCLUSION</b>Erythropoietin attenuates pulmonary inflammation and suppresses TNF-alpha and IL-1beta overproduction during acute endotoxaemia, which is partially mediated by inhibition of NF-kappaB.</p>

Melatonin reduces acute lung injury in endotoxemic rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Treatment with melatonin significantly reduces lung injury induced by bleomycin, paraquat and ischemia reperfusion. In the present study, we investigated the possible protective roles of melatonin in pulmonary inflammation and lung injury during acute endotoxemia.</p><p><b>METHODS</b>Thirty-two male Sprague-Dawley rats were randomly assigned to four groups: vehicle + saline group, melatonin + saline group, vehicle + lipopolysaccharide group, melatonin + lipopolysaccharide group. The rats were treated with melatonin (10 mg/kg, intraperitoneal injection (i.p.)) or vehicle (1% ethanol saline), 30 minutes prior to lipopolysaccharide administration (6 mg/kg, intravenous injection). Four hours after lipopolysaccharide injection, samples of pulmonary tissue were collected. Blood gas analysis was carried out. Optical microscopy was performed to examine pathological changes in lungs and lung injury score was assessed. Wet/dry ratios (W/D), myeloperoxidase activity, malondialdehyde concentrations and tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) levels in lungs were measured. The pulmonary expression of nuclear factor-kappa B (NF-kappaB) p65 was evaluated by Western blotting.</p><p><b>RESULTS</b>PaO(2) in the vehicle + lipopolysaccharide group decreased compared with that in the vehicle + saline group. This decrease was significantly reduced in the melatonin + lipopolysaccharide group. The lung tissues from the saline + lipopolysaccharide group were significantly damaged, which were less pronounced in the melatonin + lipopolysaccharide group. The W/D ratio increased significantly in the vehicle + lipopolysaccharide group (6.1 +/- 0.18) as compared with that in the vehicle + saline group (3.61 +/- 0.3) (P < 0.01), which was significantly reduced in the melatonin + lipopolysaccharide group (4.8 +/- 0.25) (P < 0.01). Myeloperoxidase activity and malondialdehyde levels increased significantly in the vehicle + lipopolysaccharide group compared with that in the vehicle + saline group, which was reduced in the melatonin + lipopolysaccharide group. The TNF-alpha level of pulmonary tissue increased significantly in the vehicle + lipopolysaccharide group ((8.7 +/- 0.91) pg/mg protein) compared with that in the vehicle + saline group ((4.3 +/- 0.62) pg/mg protein, P < 0.01). However, the increase of TNF-alpha level of pulmonary tissue was significantly reduced in the melatonin + lipopolysaccharide group ((5.9 +/- 0.56) pg/mg protein, P < 0.01). Pulmonary IL-10 levels were elevated markedly in the vehicle + lipopolysaccharide group in contrast to that in the vehicle + saline group, whereas the elevation was augmented in the melatonin + lipopolysaccharide group. The nuclear localization of p65 increased markedly in the vehicle + lipopolysaccharide group and this enhancement of nuclear p65 expression was much less in the melatonin + lipopolysaccharide group.</p><p><b>CONCLUSION</b>Melatonin reduces acute lung injury in endotoxemic rats by attenuating pulmonary inflammation and inhibiting NF-kappaB activation.</p>