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When a rapidly reexpanding lung has been in a state of collapse for more than several days, pulmonary edema sometimes occurs in it. This is called reexpansion pulmonary edema (RPE). In this article, I present my views on the history, clinical features, morphophysiological features, pathogenesis, and treatment of RPE. Histological abnormalities of the pulmonary microvessels in a chronically collapsed lung will cause RPE, as well as mechanical stress exerted during reexpansion. Although the most effective treatment method is to treat the histological abnormalities of the pulmonary microvessels formed in a chronically collapsed lung, the cause of these abnormalities is not clear, making it difficult to put forward a precise treatment method. However, reasonably good effects can be expected from a symptomatic therapy that reduces the level of mechanical stress during reexpansion. In the future, it is expected that the cause of histological changes of the pulmonary microvessels in a chronically collapsed lung will be revealed, and appropriate therapies will therefore be developed according to this cause.

Acute pulmonary edema, a potentially fatal clinical condition, represents a serious complication of so-called "Acute mountain sickness". The overt clinical picture of high altitude pulmonary edema (HAPE) includes clinical signs, serious hypoxemia, pulmonary hypertension, and alveolar edema on chest radiography. The first case of HAPE, documented by postmortem, is probably that of doctor Jacottet, who died during the building of an observatory on Mont Blanc in 1891. In 1913, TH Ravenhill, a pioneer in mountain medicine, wrote a fundamental paper that provided a first diagnostic framework for HAPE, and, in the course of the twentieth century, H Hultgren, among his various observations on HAPE, some of which documented through cardiac catheterization, hypothesized an acute failure of the left ventricle as the cause of HAPE. Hultgren also reported, during the sixties, clinical cases in which the left atrial pressure was normal, even in the presence of an increase in pulmonary pressure. Acute pulmonary hypertension has since then been considered a basic pathophysiological factor in the genesis of HAPE, and recently Swiss Authors have provided evidence that elevated arterial pressure extends to pulmonary microcirculation, so as to determine a fluid overload in the pulmonary district. Current views of HAPE indicate that it is a kind of hydrostatic acute pulmonary edema with a modification of alveolar-capillary permeability, even if it is still not known what is the precise mechanism leading to the pathological vasoconstriction in some individuals and not in others. The potential seriousness of HAPE needs preventive and therapeutic measures whose relevance was long ago recognized and documented by different physicians, as our historical survey shows.

This article describes the events leading to the discovery of the fumonisins in South Africa in 1988 and highlights the first 10 years (1988-1998) of fumonisin research. The predominant fungus isolated from moldy corn implicated in a field outbreak of equine leukoencephalomalacia (ELEM) in South Africa in 1970 was Fusarium verticillioides (F. moniliforme). This fungus was also prevalent in moldy home-grown corn consumed by people in high-incidence areas of esophageal cancer (EC) in the Transkei region of South Africa. Culture material on corn of F. verticillioides strain MRC 826, which was isolated from moldy corn in Transkei, was shown to cause ELEM in horses, porcine pulmonary edema (PPE) syndrome in pigs, and liver cancer in rats. A short-term cancer initiation/promotion assay in rat liver was used to purify the carcinogen(s) in the culture material. These efforts finally met with success when fumonisins B1 and B2 novel mycotoxins with cancer-promoting activity in rat liver, were isolated from culture material of F. verticillioides MRC 826 at the Programme on Mycotoxins and Experimental Carcinogenesis of the Medical Research Council in Tygerberg, South Africa. Following the elucidation of the chemical structure of the fumonisins, these carcinogenic mycotoxins were shown to occur naturally in moldy corn in Transkei. Shortly thereafter, high levels of fumonisins in the 1989 U.S. corn crop resulted in large-scale field outbreaks of ELEM and PPE in horses and pigs, respectively, in the United States. Subsequently the fumonisins were found to occur naturally in corn worldwide, including corn consumed as the staple diet by people at high risk for EC in Transkei and China. These findings, together with the fact that the fumonisins cause field outbreaks of mycotoxicoses in animals, are carcinogenic in rats, and disrupt sphingolipid metabolism, have resulted in much worldwide interest in these compounds during the first 10 years after the discovery of the fumonisins in 1988.

Herbert Hultgren, a cardiologist who kept a careful diary all his career, arrived in Peru at the beginning of 1959 to study the occurrence of pulmonary hypertension in children at high altitude with patent ductus arteriosus. There, he was told about a strange condition, high altitude pulmonary edema (HAPE), and found that to Peruvian physicians looking after mine employees and their families, its occurrence was almost routine. With his Peruvian colleagues, Herb immediately began a systematic study of the condition, including catheter studies. Though the absence of left ventricular enlargement suggested a non-cardiac form of pulmonary edema, and though this is what he suggested in his first publication, in two subsequent papers, one written with Charles Houston, who contributed cases occurring in mountaineers, Herb wrote that the most probable cause was left ventricular failure. What is extraordinary is that before he finally submitted the two papers, he had certain knowledge that in one case of HAPE at least, left atrial pressure had been shown to be normal. Herb's contributions, then and later, to the elucidation of HAPE were enormous.

William Osler described the first reported case of narcotic-induced pulmonary edema in 1880. The description is that of autopsy findings of a patient who died of narcotic poisoning. Since that time, noncardiogenic pulmonary edema has come to be known to accompany overdose with a number of drugs, most notably heroin. Clinical manifestations and radiographic findings vary. The exact pathogenesis is unclear, although the mechanism is known to involve increased alveolar capillary permeability. Treatment consists of reversal of respiratory depression, oxygenation, and respiratory support. Rapid improvement with treatment is the rule.