For decades clinicians have believed that many of the grave symptoms and a large number of the deaths in pneumonia were directly due to failure of the circulation. In 1889 Romberg1 and his associates studied the problem and reached the conclusion that, while fatal circulatory failure did occur in rabbits inoculated with lethal doses of pneumococci, the failure was not of myocardial origin as had been supposed, but was invariably caused by the exhaustion of the vasomotor center in the bulb.
Since that time physicians have tried to combat the failure of the vasomotor mechanism in pneumonia by administering drugs which would augment the activity of the vasomotor center.
The results have been sufficiently confusing to make a re-investigation desirable. The present communication deals only with the blood-pressure in pneumonia. Other phases of the subject will appear in later papers.
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