Influence of bacterial endotoxins on bone marrow and blood components

Endotoxin [Lipopolysaccharide, LPS] a component of the bacterial wall of gram-negative bacteria, has been recognized as one of the most potent bacterial products in the induction of host inflammatory responses and tissue injury and was used in this study to mimic infections. LPS induces production and release of several cytokines. In response to these cytokines, different effects of endotoxins are seen. The effect of three types of endotoxins [Escherichia coli, Klebsiella pneumoniae and Salmonella typhimurium] on bone marrow, differential counts and peripherial blood parameters were investigated in adult rats. Male spraguo Dawely albino rats weighing 220 - 250 g were used. They were injected i.p. [1 mg/kg body weight] with single dose of 3 types of endotoxins. Blood samples were collected from the experimental animals at 24 and 72 hours of the injection. At 72 hours the bone marrow aspirations were harvested from the femur of the rats for microscopic examination. Endotoxins induced different changes in the cells of bone marrow. Also, lipopolysaccharide caused significant decreases in red blood cells, white blood cells and platelets counts, hemoglobin content and hematocrit percent. Data of the present study point out to the dose of these toxins according to suitable pharmacopeia. Lemulus amebocyte lysate [LAL] test is specificly used for determination of the endotoxin limit. This recommendation should be observed to avoid the toxic effects of endotoxins

Effects of bacterial endotoxin on some metabolites and enzymes in rat serum

The effects of bacterial endotoxins [Escherichia coli, Klebsiella pneumoniae, and Salmonella typhimurium] on glucose and blood urea nitrogen [BUN] levels and aspartate aminotransferase [ASAT], alanine aminotransferase [ALAT] and lactate dehydrogenase [LDH] activities were studied. Three groups of rats were injected [1 mg/kg body weight, i.p.] with three types of bacterial endotoxins [E. coli, K. pneumoniae and S. typhimurium] as a single dose. The control group was injected i.p. [1 mg/kg] in 0.9% normal saline. Blood sampling was performed from the orbital vein plexus after 24 and 72 hr of injection. Glucose level was increased significantly after 24 hr of after each 3 solutions of endotoxin. Its level showed non-significant decrease after 72 hr post-treatment. However, endotoxins caused significant increases in BUN, ASAT and LDH at 24 and 72 hr post-treatment. On the other hand, the ALAT activity was significantly decreased after the referred observation periods of endotoxins injection. The variation in serum glucose level after 24 and 72 hr post-treatment may be referred to different reasons. On the other hand, the increase of BUN concentration may be due to the toxic effect of bacterial endotoxins resembling to that occurring in renal damage and impairment of renal function. However, the changes in serum aminotransferases and LDH activities may be due to endotoxins induced hepatic microcirculatory disturbance and to the subsequent liver injury and tissue hypoxia

Plasma beta-endorphin, adrenocorticotropin and corticosterone changes in response to acute and prolonged morphine administration in rats

The influence of morphine on the functional activity of the pituitary-adrenocortical system in the rate was studied by investigating its effect on the secretion of beta-endorphin [beta-END] and adrenocorticotropin [ACTH] by the pituitary gland and corticosterone by the adrenal gland. The acute administration of morphine [5 mg / 100 g i.p.] produces a characteristic that increases in plasma beta-END, ACTH and corticosterone after 5, 15 and 25 min, whereas decreases in beta-END, ACTH and corticosterone levels sere seen after 90 and 120 min. Saline[i.p.] produced decreases of beta-END and ACTH levels, 90 and 120 min after injection and an increase in corticosterone after 5, 15 and 25 min. It appears that, in the rat, the response of pituitary-adrenal exis to acute morphine administration could change depending upon the time of sampling. Additionally, prolonged morphine [0.5 mg/100 g i.p. daily] administration for a period of 7 days has little effect on plasma level beta-END, ACTH and corticcosterone. This may indicate that drug tolerance might have developed. Conversely, repeated daily doses of morphine [2 mg/100 g i.p.] for 7 days cause a significant lowering of plasma beta-END and ACTH contents, while non-significant decreases in plasma corticosterone level was recorded. These data suggest that the effect of morphine is dose related. Overall, the present results are consistent with an increased release of pro-opiomelanocortin - derived peptides after acute morphine treatment for a short-term, and with a decreased releae of these peptide in prolonged treatment