Pulmonary hemodynamic response to exercise in subjects with prior high-altitude pulmonary edema.

Individuals with a prior history of (susceptible to high altitude pulmonary edema (HAPE-S) have high resting pulmonary arterial pressures, but little data are available on their vascular response to exercise. We studied the pulmonary vascular response to exercise in seven HAPE-S and nine control subjects at sea level and at 3,810 m altitude. At each location, both normoxic (inspired PO2 = 148 Torr) and hypoxic (inspired PO2 = 91 Torr) studies were conducted. Pulmonary hemodynamic measurements included pulmonary arterial and pulmonary arterial occlusion pressures. A multiple regression analysis demonstrated that the pulmonary arterial pressure reactivity to exercise was significantly greater in the HAPE-S group. This reactivity was not influenced by altitude or oxygenation, implying that the response was intrinsic to the pulmonary circulation. Pulmonary arterial occlusion pressure reactivity to exercise was also greater in the HAPE-S group, increasing with altitude but independent of oxygenation. These findings suggest an augmented flow-dependent pulmonary vasoconstriction and/or a reduced vascular cross-sectional area in HAPE-S subjects.

Exercise-induced VA/Q inequality in subjects with prior high-altitude pulmonary edema.

Ventilation-perfusion (VA/Q) mismatch has been shown to increase during exercise, especially in hypoxia. A possible explanation is subclinical interstitial edema due to high pulmonary capillary pressures. We hypothesized that this may be pathogenetically similar to high-altitude pulmonary edema (HAPE) so that HAPE-susceptible people with higher vascular pressures would develop more exercise-induced VA/Q mismatch. To examine this, seven healthy people with a history of HAPE and nine with similar altitude exposure but no HAPE history (control) were studied at rest and during exercise at 35, 65, and 85% of maximum 1) at sea level and then 2) after 2 days at altitude (3,810 m) breathing both normoxic (inspired Po2 = 148 Torr) and hypoxic (inspired Po2 = 91 Torr) gas at both locations. We measured cardiac output and respiratory and inert gas exchange. In both groups, VA/Q mismatch (assessed by log standard deviation of the perfusion distribution) increased with exercise. At sea level, log standard deviation of the perfusion distribution was slightly higher in the HAPE-susceptible group than in the control group during heavy exercise. At altitude, these differences disappeared. Because a history of HAPE was associated with greater exercise-induced VA/Q mismatch and higher pulmonary capillary pressures, our findings are consistent with the hypothesis that exercise-induced mismatch is due to a temporary extravascular fluid accumulation.

[Pulmonary alveolar proteinosis with reverse ventilation/perfusion mismatch; a case report].

Generally, non-ventilated segments are not perfused on lung scans (V/Q match). Now we report a very rare case with pulmonary alveolar proteinosis whose scintigraphy shows the decreased ventilation, but well perfused (reverse V/Q mismatch).

[A case of the Hallermann-Streiff syndrome].

The Hallermann-Streiff Syndrome has been characterized and established according to 7 positive and 5 negative signs, which were described by François. We encountered an 11 year, 5 months old boy who had 7 positive symptoms of this syndrome in our clinic. In this study, we reported on this typical patient focusing on his dental view. 1) Prolonged retention of the primary teeth which involved microdontia were noted. Congenitally missing teeth were also seen. 2) The occlusal relationship indicated open bite, and also the mandibular function was impaired. 3) The measurements of the length and width of the dental arch were smaller than that of a normal subject, and the dental arch of the maxilla was V-shaped. 4) According to X-ray cephalometric analysis, (a) the dental calculus and the alveolar bone absorption were very evident. (b) abnormal morphologic of the glenoid fossa, mandibulars condyle and the neck of mandibula were seen. These conditions were very evident on the left side. 5) The growth obstade of the maxilla and mandibla and the left shift of the mandible were found. 6) According to histological study, enamel hypoplasia was noted.

[Inhibitory effect of amlexanox on asthmatic attacks in an aspirin sensitive asthmatic].

The anti-allergic action of amlexanox is reported to be associated with inhibition of the release of LTC4, LTD4 and histamine, and with antagonistic activity on leukotrienes. The patient was a 18-year-old female who had suffered from bronchial asthma since the age of fifteen. We diagnosed the case as aspirin sensitive asthma because of development of a severe asthmatic attack with syncope after oral administration of an analgesic for treatment of a common cold at the age of seventeen. She also had sensitivity to toothpaste. Three-minute aerosol inhalation challenge with 0.1, 1 and 10% solution of sulpyrine was performed as a stepwise increment at 20 minutes intervals. This inhalation test was positive and it evoked simultaneous increases of LTC4, LTD4 and histamine in the peripheral blood. Since the commencement of oral administration of 150 mg per day of amlexanox, the patient has had no attacks for about 8 months. In the second inhalation test, premedication with amlexanox elevated the threshold of sulpyrine and inhibited the release of LTC4, LTD4 and histamine. We report that amlexanox was of use to control asthmatic attacks in this aspirin-sensitive asthmatic patient.