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I graduated from the University of Hamburg Faculty of Medicine in 1972. In 1973, as a second-year resident in Internal Medicine at the University Hospital in Hamburg-Eppendorf, I experienced a night on call that remains vivid in my memory. My pager sounded in the middle of a warm June night—about two o'clock in the morning. In those days, there were no direct communication pagers; the call came through the telephone central, and the operator informed me that I was needed on the Cardiology floor. As I rode the elevator to the 8th floor, my mind raced through possible emergencies: acute chest pain, a dangerous arrhythmia, or acute heart failure. The ward was dark, except for the softly lit nurses' station. I introduced myself to the night nurse, who apologized, “I'm sorry to have to call you, but I need you to pronounce a patient dead. She just passed away a few minutes ago.” I entered the room and found a young woman, pulseless and still. The quiet in the room was striking. The nurse gave me the time of death, and I signed the certificate—sudden death of a young woman on the Cardiology ward. All that remained was to read her medical record. The diagnosis was primary pulmonary hypertension, caused by the appetite suppressant Menocil (aminorex), an amphetamine derivative prescribed in Germany, Austria, and Switzerland in 1969 and 1970. The drug had been withdrawn in 1971 after it was discovered that the incidence of primary pulmonary hypertension had increased a thousand-fold, with aminorex as the common factor. According to her record, the patient had taken the drug after her second pregnancy, hoping to fit into her bikini again. Primary pulmonary hypertension? I had no idea what that was. All I knew was that this patient was my age, and she had died from a drug-induced disease. Back in the call room, I opened Harrison's Textbook of Medicine. There, under primary pulmonary hypertension, were just two and a half pages—a rare disease of young women, with an unknown cause, leading to death. The bottom line: nothing was known. The next morning, after my shift, I knocked on the door of a cardiology attending and said, “Last night I had to pronounce dead a patient with primary pulmonary hypertension—who takes care of these patients?” He looked up briefly from his EKG strip and replied, “These patients are being cared for by the pulmonologists, because this is a lung vascular disease.” I thanked him and went to see a senior pulmonologist, asking the same question. The answer was quick: “These patients all die from heart failure; they belong to cardiology.” So there it was: we knew nothing about this disease, and no one wanted to take care of these patients1. In London, pathologist Lynn Reid, originally from Australia, worked with rats exposed to chronic hypoxia, leading to pulmonary hypertension. Her angiography described “a loss of the background haze, pruning of the lung vascular tree, and muscularization of the precapillary arteries.” When asked whether there was also hyperplasia, she replied, “Oh my gosh, I don't know!” In Denver, Colorado, the Cardiovascular Pulmonary Research Laboratory (CVP lab) was prolific, publishing a new paper almost every month, mainly in the Journal of Applied Physiology. In Sheffield, England, Gwenda Barer ran a lab, also working with hypoxic rats. Every 4 years, a Lung Circulation Conference was held in Prague, Czechoslovakia, organized by Jiří Widimský. In San Francisco, the CVRI lab, led by pediatric cardiologist Abe Rudolph, focused on neonatal pulmonary hypertension. The field was small, progress was slow, and I wondered if the CVP lab in Denver was the Mecca of pulmonary circulation research. Early in my training, I found lung function studies uninspiring—lung circulation alone seemed challenging enough. That changed in my third year, thanks to the guidance of my clinical teacher and mentor, Volker Sill. He pointed out that the Physiology Institute on the Eppendorf campus had an unused hypobaric hypoxia chamber, complete with a dedicated technician. Inspired by Volker Sill, I joined him in successfully applying for a research grant from the German Volkswagen Foundation. This support enabled me to establish a modest research lab—a small room I shared with a technician who had previously worked in the University's Biochemistry Department. Together, we focused on hypoxia models and the measurement of histamine in body fluids and tissue extracts, influenced by the work of Michael Kay, whose paper had shaped my direction [1]. Over the next few years in that small lab, I managed to publish several basic research papers [2, 3]. I look forward to sharing more about these studies in future vignettes and monographs. The author has nothing to report. The author has nothing to report. The author has nothing to report. The author declares no conflicts of interest.