To determine whether the intensity of dyspnea at a given level of respiratory motor output differs between bronchoconstriction and the presence of an external resistance, we compared the sensation of difficulty in breathing during isocapnic voluntary hyperventilation in six normal subjects. An external resistance of 1.9 cmH2O.1-1.s was applied during both inspiration and expiration. To induce bronchoconstriction, histamine aerosol (5 mg/ml) was inhaled until airway resistance (Raw) increased to a level approximately equal to the subject's control Raw plus the added external resistance. To clarify the role of vagal afferents on the genesis of dyspnea during both forms of obstruction to airflow, the effect of airway anesthesia by lidocaine aerosol inhalation was also examined after histamine and during external resistive loading. The sensation of difficulty in breathing was rated at 30-s intervals on a visual analog scale during isocapnic voluntary hyperpnea, in which the subjects were asked to copy an oscilloscope volume trace obtained previously during progressive hypercapnia. Histamine inhalation significantly increased the intensity of the dyspneic sensation over the equivalent external resistive load at the same levels of ventilation and occlusion pressure during voluntary hyperpnea. Inhaled lidocaine decreased the sensation of dyspnea during bronchoconstriction with no change in Raw, but it did not significantly change the sensation during external resistive loading. These results suggest that afferent vagal activity plays a role in the genesis of dyspnea during bronchoconstriction.

We examined the effects of multiple repetitive airway obstruction (RAO) on arterial oxygen saturation (SaO2) and pulmonary and systemic arterial pressure in eight anesthetized spontaneously breathing dogs. SaO2 was monitored at the tongue with a pulse oximeter. RAO created by an electrical valve that was attached to a tracheal cannula was alternated with seven consecutive spontaneous breaths until the nadir SaO2 (nSaO2) became constant or decreased to less than 35%. Tracheal occlusion durations of 15, 30, 45 and 60 s were chosen arbitrarily. In each animal nSaO2 decreased with every trial number in an exponential fashion, and the rate of nSaO2 fall was greater for the longer occlusion duration. In each animal the increases in pulmonary arterial pressure (PAP) and systemic arterial pressure (SAP) were inversely related to the nSaO2 values, and the relationship between nSaO2 and PAP or SAP was identical for all occlusion durations. Moreover, when the animals breathed pure oxygen and SaO2 did not decrease, there were no significant increases in the PAP and SAP at similar levels of pleural pressure (Ppl). In another six dogs, the effects of RAO on PAP and SAP were compared with those of intermittent hypoxic exposure without apnea, which was achieved by the inhalation of hypoxic gas (4 to 6% O2, 5% CO2 in N2) instead of RAO, to examine the effects of interruption of ventilation. The relationships between nSaO2 and both pressures did not differ significantly from those during RAO.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract

In Urayasu City, where about 85% of the city area liquefied during the 2011 Great East Japan Earthquake, water pipes were seriously damaged due to liquefaction. Joints of water pipes were pulled out at many sites. Shaking continued at a long predominant period for a long time after the occurrence of liquefaction during the earthquake. So, the long-period shaking of liquefied ground, which was a kind of sloshing must cause large cyclic compressional and tensile strain to the water pipes in horizontal direction near some boundaries, resulting in the disconnection of the pipe joints. Then seismic response analyses were carried out to demonstrate the concentration of horizontal tensile strain at 5 areas in Urayasu City under four levels of shear modulus by considering the effect of liquefaction. Analyzed results showed large tensile strain induced near the site where the water pipes were pulled out.

I . To clarify whether acute changes in the properties of baroreflexes can occur in man, we evaluated the time course of baroreflex control of heart rate and cardiopulmonary baroreflex control of forearm vascular resistance (FVR) over 240 min after intravenous administration of propranolol (0.2 mg/kg) in I3 healthy young men.2. Systolic and diastolic blood pressure remained unchanged after propranolol. Propranolol significantly decreased cardiac index and heart rate, and significantly increased total peripheral resistance. These effects remained unchanged for 240 min after propranolol.3. Baroreflex control of heart rate was significantly augmented immediately after, and at 30, 60 min after propranolol, but partly reverted to the initial level afterwards. Cardiopulmonary baroreflex control of FVR was reduced immediately after, and at 30, 60 min after propranolol, but partly reverted t o the initial level afterwards. Pressor responses to phenylephrine was reduced immediately after propranolol, but no significant differences were observed after 30 min.4. These results suggest that acute changes in the properties ofbaroreflexes occur in man after propranolol.