We investigated the histopathologic pulmonary changes induced by mechanical pulmonary ventilation (MV) with a high peak airway pressure and a large tidal volume in healthy baby pigs. Eleven animals were mechanically ventilated at a peak inspiratory pressure (PIP) of 40 cm H2O, a respiratory rate (RR) of 20 min-1, a positive end-expiratory pressure (PEEP) of 3 to 5 cm H2O, and an FIO2 of 0.4. High airway pressure MV was terminated in 22 +/- 11 h because of severe hypoxemia in the animals. Five of the baby pigs were killed for gross and light microscope studies. The pulmonary changes consisted of alveolar hemorrhage, alveolar neutrophil infiltration, alveolar macrophage and type II pneumocyte proliferation, interstitial congestion and thickening, interstitial lymphocyte infiltration, emphysematous change, and hyaline membrane formation. Those lesions were similar to that seen in the early stage of the adult respiratory distress syndrome (ARDS). The remaining six animals were treated for 3 to 6 days with conventional respiratory care with appropriate ventilator settings. Prominent organized alveolar exudate in addition to lesions was also found in the five animals. These findings were indistinguishable from the clinical late stage of ARDS. Six control animals were mechanically ventilated at a PIP of less than 18 cm H2O, a RR of 20 min-1, a PEEP of 3 to 5 cm H2O, and an FIO2 of 0.4 for 48 h. They showed no notable changes in lung functions and histopathologic findings. Aggressive MV with a high PIP is often applied to patients with respiratory distress to attain adequate pulmonary gas exchange.(ABSTRACT TRUNCATED AT 250 WORDS)

We investigated the kinetics of macrophage subpopulations and the expression of monocyte chemoattractant protein 1 (MCP-1) in a rat model of bleomycin-induced lung injury. Rat macrophage subpopulations were examined by immunohistochemistry using various anti-rat macrophage monoclonal antibodies (mAbs) and their proliferative capacity by [3H]thymidine (3HTdR) autoradiography. To detect the localization of expressed MCP-1, we generated an mAb against rat MCP-1 for immunohistochemical staining. Expression of MCP-1 messenger RNA (mRNA) was detected by Northern blot hybridization. Shortly after intratracheal instillation of bleomycin, the number of exudate macrophages recognized by mAb TRPM-3 increased in the injured lungs, peaked 3 days later, and decreased thereafter, whereas tissue macrophages identified by mAb ED2 increased slowly and peaked 2 weeks after instillation. Northern blot analysis disclosed that the expression of MCP-1 mRNA in the lung was most prominent 1 day after instillation and declined thereafter, preceding the numerical change of the TRPM-3-positive exudate macrophages. Immunohistochemistry with anti-rat MCP-1 revealed that the main sources of MCP-1 production were alveolar and interstitial macrophages and polymorphonuclear leukocytes. Based on these results, MCP-1 produced by polymorphonuclear leukocytes and by alveolar and interstitial macrophages is thought to induce the infiltration of blood monocytes, and infiltrated exudate macrophages produce MCP-1 to enhance subsequent accumulation of macrophages. In contrast, the expression of MCP-1 did not correlate with the numerical changes of the ED2-positive macrophages.

This study aims to develop and validate prediction models for the number of all heatstroke cases, and heatstrokes of hospital admission and death cases per city per 12 h, using multiple weather information and a population-based database for heatstroke patients in 16 Japanese cities (corresponding to around a 10,000,000 population size). In the testing dataset, mean absolute percentage error of generalized linear models with wet bulb globe temperature as the only predictor and the optimal models, respectively, are 43.0% and 14.8% for spikes in the number of all heatstroke cases, and 37.7% and 10.6% for spikes in the number of heatstrokes of hospital admission and death cases. The optimal models predict the spikes in the number of heatstrokes well by machine learning methods including non-linear multivariable predictors and/or under-sampling and bagging. Here, we develop prediction models whose predictive performances are high enough to be implemented in public health settings.

We have previously demonstrated by in situ hybridization and Northern blot analysis that alveolar type II cells and nonciliated bronchiolar epithelial (Clara) cells in lungs of rats with diabetes have decreased surfactant protein A (SP-A) but increased mRNA. In the present study, we have examined the mRNA expression and localization of two hydrophobic surfactant proteins, SP-B and SP-C, and have compared them with SP-A mRNA levels and cellular localization in streptozotocin-induced diabetic lungs. Localization and level of expression were analyzed by in situ hybridization using type-specific, surfactant cDNA probes. Diabetes was induced in adult rats by an intraperitoneal injection of 60 mg/kg streptozotocin. Ten weeks after injection, higher numbers of silver grains representing SP-A and SP-B mRNAs were observed in alveolar type II cells of diabetic lungs, compared with control lungs. Moreover, the number of silver grains representing SP-C mRNA decreased in alveolar type II cells from diabetic lungs compared with controls, and no silver grains for SP-C mRNA were present in bronchiolar epithelial cells from either control or diabetic groups. In contrast, in bronchiolar epithelial cells of diabetic lungs, the relative abundance of silver grains for SP-A mRNA increased approximately 2-fold above controls, while SP-B mRNA decreased slightly. Taken together, there is differential expression in the level of SP-A, SP-B, and SP-C mRNAs in both alveolar and bronchiolar epithelial cells from diabetic lungs when compared with control lungs.(ABSTRACT TRUNCATED AT 250 WORDS)

We compared the cardiovascular responses between nasal and oral intubation with a fiberoptic bronchoscope under the combination of neuroleptic analgesia (NLA) and topical anesthesia. The 16 patients studied were divided into 2 groups: the nasal intubation group (N group: 8 patients) and the oral intubation group (0 group: 8 patients). There were significant changes in systolic, diastolic and mean arterial pressures in the N group and in the pressure rate quotient in the o group. Diastolic arterial pressure and heart rate were significantly higher in the N group than in the 0 group before induction of general anesthesia. The rate pressure product (RPP) was significantly higher in the N group than in the 0 group at some points during the procedure. The individual RPP in both groups was relatively stable except for one patient in the N group, who had a marked increase in RPP during the procedure. We conclude that, under the combination of NLA and topical anesthesia, the cardiovascular responses to oral flberopt.ic, intubation are less severe than those to the nasal approach. The oral approach is recommended, especially in patients with coronary artery disease, taking into consideration of the cardiovascular responses to fiberoptic intubation. (Key words: cardiovascular responses, fiberoptic intubation, orotracheal intubation, nasotracheal intubation) (Shibata Y, Okamoto K, Matsumoto M, et al.: Cardiovascular resporses to fiberoptic intubation: a comparison of orotracheal and nasotracheal intubation.