ABSTRACT
Observations on the developement of pathological changes of rat brain, together with dynamic detection of CN- concentrations in blood and brain tissue and quantitive analysis of brain cytochrome oxidase activity, are carried out within 24 h after acute cyanide intoxication (4.5mg/kg i.p.) . The results indicate that in the cyanide poisoning with the dose under lethality (80%LD) , the pathological changes in rat brain appear, especially in cytochrome oxidase poorly- contained areas, including! 1 ) degeneration and necrosis of neurons and gliocytes; 2) degeneration, swelling and lysis of different cell projection components; 3) the myelinoclasis of myelinated nerve fibers. Those changes undergo a dynamic course divided into three phases: 1 ) the phase of metabolic disturbance; 2) of response to injury; and 3) of restoration. The authors consider that the acute poisoning displayed by the animal after NACN injection is directly caused by the intense inhibation of brain cytochrome oxidase; the secondary lesions of brain structure may be responsible for the manifestations such as trembling, unstable, and ataxia etc.occur later. The mechanisms of the brain pathological changes after cyanide intoxication are also disscussed.
ABSTRACT
Sixty-six rabbits were divided into 2 groups, the control group and the experimental group. The latter was subdivided into 10 groups according to the time of observation after burn injury including 2nd-hour group to 30th-day group. Each group consisted of 6 animals. Specimens from the trachea and the lungs were examined with optical microscopy, scanning electron microscopy and transmission electron microscopy.No obvious lesion was seen in the specimens from the control. In the experimental group, various pathological changes began to appear from the 6th hour after injury. In the trachea and bronchi, congestion of varying degrees, edema, leucocytic infiltration, lodging, adhesion, breaking or separation of cilia, and increase of goblet cells and Clara cells in number weie found. In. the lungs, interstitial edema of varying degrees, accumulation and infiltration of neutro-phils in capillaries, pulmonary interstitium and alveolar spaces, decrease in num ber of type II pneumocytes and their lamellar bodies, vacuolization of lamellar bodies, and phagocytosis of lamellar bodies by macrophages were seen. Most prominent changes were shown on the 3rd day postburn, and they began to alleviate on the 7th day. The number of type II pneumocytes and their lamellar bodies gradually increased number. Some lesions still existed on the 30th day postburn but no significant fibrosis could be found. The occurrence and development of the main lesions and their significance were discussed.