Clarias batrachus具有兩種呼吸機制,分別可在水中(經由鰓、皮膚以及輔助呼吸器官)及空氣中(經由空氣呼吸器官,ABO)呼吸。牠們居住於沼澤或荒野水域,遇到突來的乾旱時能埋在泥中數日且直接呼吸空氣。當暴露在空氣中,特別是在初期階段時,其鰓蓋會進行快速地開闔運動,由大氣中吸入空氣。魚在離水時約可存活31小時,在此期間其呼吸器官會逐漸損壞。三種呼吸器官中的黏液細胞(MCs)之密度及染色性質在不同時期會有變動;在空氣中時,它們表現出對硫酸鹽分子的較大親和力,這使得呼吸表面可以保持較長期濕潤以維持呼吸。大量的硫酸化黏多醣和脂肪存在於皮下疏鬆結締組織亦有助於防止乾燥。 當魚體暴露空氣中時,ABO表面的微血管(BLCs)普遍地膨脹,降低了血液和空氣間的阻隔;之後會出血,使得紅血球密度降低。接著由梯狀的柱狀細胞(PLC)和微血管所組成的次級呼吸層(SL)會崩潰,在呼吸皮膜(RE)表面有硫酸化黏液薄膜蓋住。在另一方面,鯰魚的體表因磨損、撕裂及泥濘的環境而脫落導致出血;皮膚表面亦被覆一層薄硫酸化黏液。之後,真皮層顯出嚴重損傷,並伴隨結締組織纖維的鬆脫,這些造成具保持水份以維持皮膚呼吸功能的硫酸黏蛋白有較強的反應。長期暴露於空氣,會阻止正常鰓呼吸,並使鰓中SL層之微血管阻塞,且磨損及撕裂也造成體表出血。很快地,鰓中PLC-BLC構造亦失去其梯狀排列而使鰓破壞、最後造成魚體死亡。
Clarias batrachus has acquired a bimodal respiratory mechanism for exploitation of water (via gills and skin, an accessory respiratory organ) as well as air (through an air-breathing organ, ABO). It inhabits swamps and derelict waters and can subsist on aerial respiration when it faces acute drought, at which time it remains burrowed for days in the mud. When exposed to air the fish shows quick ventilatory movements of the operculum and inhales air from the atmosphere especially in the initial stages. Out of water, the fish can survive for about 31 h. During this period, the respiratory organs become progressively damaged. The density and staining properties of mucous cells (MCs) of all three respiratory organs show periodic fluctuations. They exhibit a greater affinity for sulfate moieties that keep respiratory surfaces moist for longer periods in order to maintain respiration during air exposure. The large quantities of sulfated mucopolysaccharides and/or lipids present in their subepithelial loose connective tissues also help in prevention of desiccation. The blood capillaries (BLCs) of the ABO extensively bulge out onto the surface to reduce the blood-air barrier distance. Later, hemorrhage causes decreased density of the RBCs. Subsequently the ladder-like PLC (pillar cell)-BLC components of the respiratory (secondary) lamellae (SL) collapse. A thin layer of sulfated slime often covers the respiratory epithelia (RE). The skin of the exposed fish also shows severe wear and tear and sloughing leading to hemorrhage. A thin layer of sulfated slime covers the skin surface. Furthermmore, the dermis shows severe damage with loosening of the connective tissue fibers, which give stronger reactions for sulfated mucin that retains additional quantities of water for continued skin respiration. Air exposure prevents normal branchial respiration, and the BLCs in the SL of the gills show congestion. Wear and tear causes hemorrhage. Soon, the PLC-BLC components of the gills also lose their ladder-like arrangement with ultimate gill degeneration prior to death of the fish.