1. The Lung and Large Intestine Are Internally Connected

1. The Lung and Large Intestine Are Internally Connected

In recent years, domestic researchers have conducted several experimental studies on the internal connection between the lung and large intestine, consistently concluding that this traditional TCM organ theory has a material basis. First, it has been observed that severe intestinal dysfunction—such as various types of paralytic ileus, mechanical ileus, and necrotizing enteritis—is often accompanied by respiratory failure. A classic example of concurrent intestinal and respiratory disorders is adult respiratory distress syndrome (ARDS). Why do severe intestinal diseases lead to respiratory complications? Modern medicine still struggles to provide a complete answer. However, from a traditional TCM perspective, the recognition of the lung–large intestine relationship—from classics like the "Inner Canon" and "Difficult Classics" to works like "Shanghan Lun" and "Jingui Yaolue," as well as all subsequent Tang and Song dynasty texts—seems self-evident. This principle has guided clinical practice and frequently yielded effective results. To uncover the essence of this theory, domestic researchers conducted a systematic study on 48 ARDS patients, finding that among them, 25 had pre-existing intestinal dysfunction prior to ARDS onset, while 23 did not. The term "intestinal dysfunction" does not refer to ordinary gastrointestinal disturbances; among the 25 cases, 21 were paralytic ileus, 3 were mechanical ileus, and 1 was mesenteric artery embolism, with 16 subsequently developing toxic shock. All 25 patients with severe intestinal dysfunction experienced acute respiratory failure 1–3 days after the onset of intestinal symptoms, characterized by rapid breathing—often exceeding 28 breaths per minute—and a drop in arterial oxygen partial pressure, with PaO2<8kPa. Simultaneously, A------aDO2 increased, reaching over 4kPa during inhalation and exceeding 13.3kPa even when breathing pure oxygen, clearly indicating that severe intestinal dysfunction can damage lung function. Building on this understanding, some researchers created animal models by clamping the superior mesenteric artery, inducing ischemic intestinal dysfunction. As a result, the lungs of the same animals exhibited lesions of grade II or higher, whereas the lungs of unclamped animals showed no similar changes. At the same time, equal numbers of animals were subjected to clamping of the renal artery or the lower limb arteries, but no lung changes were observed in any of these groups. Additionally, comparing animals subjected to clamping of the superior mesenteric artery with those that underwent no clamping at all, the clamped group tested positive for endotoxins in their blood after 90 minutes of exposure, while the unclamped group remained negative. These experiments demonstrate that intestinal dysfunction leads to lung lesions, confirming the material basis of the TCM theory that the lung and large intestine are internally connected. Preliminary assessments also suggest that this causal relationship may be linked to the production of endotoxins in the bloodstream. Currently, in addition to the aforementioned experiments, some researchers have induced permanent semi-ligation at the rectal outlet, resulting in lung lesions. Others have refined these clamping and permanent semi-ligation methods, employing external ligation to create reversible narrowing at the rectal outlet, thereby triggering a series of pathological changes in the lungs. The results indicate that this improved model essentially achieves the intended purpose—namely, the occurrence of a series of lung lesions. Beyond confirming the "lung–large intestine internal connection," this outcome demonstrates that external ligation can effectively induce lung lesions.

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Narrow, allowing the model to return to normal. This not only makes it possible to reuse the model but also provides better conditions for in-depth research into the essence of this theory. Under the conditions of this improved animal model, artificially induced dry stool accumulation in the large intestine leads to the manifestation of Yangming Fu-organ excess syndrome in the animal model, thereby resulting in specific pulmonary lesions. These lesions include pulmonary congestion, pulmonary hemorrhage, and pulmonary necrosis. Electron microscopy reveals swelling and necrosis of the alveolar epithelium as well as swelling and necrosis of macrophages, while no abnormalities are observed in other organs. Experimental results indicate that after administering Dachengqi Tang to the model animals, pulmonary symptoms show significant improvement.