The role of leukocytes (WBCs) and platelets (PLTs) in the pulmonary circulation may be important in the development of monocrotaline (MCT)-induced pulmonary hypertension in rats. We investigated the changes in WBCs and PLTs in the pulmonary microvasculature during the development of chronic pulmonary hypertension in MCT rats by real-time confocal scanning laser microscopy. The number of WBCs sequestered in the pulmonary microvasculature increased significantly from day 7 after MCT injection, but no further increase occurred from days 14-28. The number of PLTs sequestered in the pulmonary microvasculature increased significantly from day 7 after MCT injection, and reached a peak on day 14. However, the number of PLTs sequestered on days 21 and 28 after MCT injection was significantly lower than on day 14. These findings suggest that PLTs mainly contribute to the initial and middle stages of the development of MCT-induced pulmonary hypertension in rats, while WBCs mainly contribute to the middle and late stages.
Background: We have developed a system to monitor, simultaneously and continuously, ambulatory SaO2 measured using a pulse‐oximeter and ECG data for 24 hours.
Methods: The ambulatory SaO2‐ECG monitoring system consisted of a portable monitoring device (SM50) with two channels for ECG data and one channel for SaO2 data input; a sensor for SaO2 recording; and a pulse‐oximeter. An ambulatory monitoring analyzer was used. The SaO2 report from the present analyzer included two types of data (i.e., a profile of heart rate [HR], pulse rate [PR], and SaO2 value per min), and a trend graph of HR, arrhythmia, ST level and slope, PR, and SaO2 per minute. We also designed and produced an analytical program to automatically remove noise errors relating to the SaO2 measurement.
Results: Using this system, we performed a clinical study on ten healthy volunteers (Group N) and seven patients with chronic pulmonary diseases (Group CPD) to evaluate the usefulness of the system as a diagnostic means for respiratory failure and arrhythmia. Group N showed a stable value of 90% or over in SaO2 during the 24‐hour monitoring while Group CPD showed values under 90% SaO2 in all patients at rest during the night or after a 15‐minute walk. Transient atrial tachycardia (TAT) was observed in 3 of 7 CPD patients, and each episode was preceded by a decrease of SaO2. The occurrence of a single or double ventricular extrasystole was high in Group CPD compared with Group N (1.21 ± 0.89 vs 0.6%± 0.3%, P < 0.05), its occurrence was not associated with a decrease in SaO2.
Conclusions: In outpatients, especially patients who are taken care of at home, the present system will certainly contribute greatly to the diagnosis of respiratory failure and arrhythmia as well as to evaluate the effects on these diseases of therapy. In addition it is suggested that in CPD, patients’hypoxemia may induce TAT.
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