ABSTRACT
Our investigations have demonstrated on 10 volunteers receiving either 500 mg or 100 mg acetylsalicylic acid (ASA) that a low collagen concentration (1 microgram/ml) can best detect the aggregation defect caused by ASA. With the impedance aggregometry the mean inhibition reaches 82% and 52% with 500 mg and 100 mg ASA, respectively. Collagen at higher concentration (3 micrograms/ml) as well as ADP 10 and 25 mumol/l are less sensitive, less than 25% inhibition was recorded. These results suggest that a 1 microgram/ml concentration of collagen is adequate for the control of the ASA effect up to 6 days after intake of 100 mg. Furthermore, the von Willebrand factor (vWF) dependent platelet aggregation induced by 0.6 and 1.0 mg/ml ristocetin was clearly diminished after ASA. Therefore, a ristocetin screening test in whole blood for vWF disorder is possibly distorted when the test is performed within 6 days from ASA administration.
Subject(s)
Aspirin/pharmacology , Platelet Aggregation Inhibitors/pharmacology , Platelet Aggregation/drug effects , Adult , Aged , Collagen/pharmacology , Female , Humans , Male , Middle Aged , Ristocetin/pharmacologyABSTRACT
The present study was undertaken to evaluate the effects of Plasmodium berghei infection on the development of liver tumors induced in male Buffalo rats by aflatoxin B1 (AFB1). Intraperitoneal (i.p.) injection of 10(6) parasitized red blood cells (pRBC) into the rat 12 days prior to administration of 2 ppm dietary AFB1 for 10 weeks diminished hepatocellular carcinoma (HCC) induction compared to that observed in rats given AFB1 alone at weeks 60-82. No animals in a control group developed HCC lesions, while only 1 of 22 rats treated with P. berghei alone developed a neoplastic nodule at week 82. These data suggest a reducing effect of P. berghei on the development of liver tumors induced by AFB1 in male Buffalo rats.
Subject(s)
Aflatoxins/toxicity , Liver Neoplasms, Experimental/prevention & control , Malaria/complications , Aflatoxin B1 , Animals , Hematocrit , Liver/pathology , Liver Neoplasms, Experimental/blood , Liver Neoplasms, Experimental/pathology , Malaria/blood , Malaria/pathology , Male , Plasmodium berghei , Rats , Rats, Inbred BUFABSTRACT
The interaction between aflatoxin and malaria was tested for its usefulness as a model for hepatic tumor induction in rats. Male Buffalo rats which received aflatoxin B1 (AFB1) followed by Plasmodium berghei infection developed more preneoplastic lesions in the liver compared to those given AFB1 alone. No preneoplastic lesions were found in the liver of control and malarial-treated animals. These findings suggest that the malarial parasite facilitates liver tumor development initiated by AFB1 in rats.
