Hemodynamic Effect of Uranyl Acetate in Male Rats

Veronika Morvai1, Éva Szakmáry2, Erzsébet Tátrai2, and György Ungváry3

1 Second Department of Medicine, Faculty of Medicine, Semmelweis University, Budapest, Hungary
2 National Institute for Occupational Health, József Fodor National Center for Public Health, Budapest, Hungary
3 József Fodor National Center for Public Health, Budapest, Hungary

Corresponding author: Veronika Morvai MD, PhD, DSc
    Second Department of Medicine
    Faculty of Medicine
    Semmelweis University
    Szentkirályi u.46
    H-1088 Budapest, Hungary
    Telephone: 36-1-266-0926
    Fax number: 36-1-266-0816
    E-mail: morvai@bel2.sote.hu

CEJOEM 2004, Vol.10. No.2.: 149–157

Key words:
Uranyl acetate, ECG-change, hemodynamic changes, tubular nephropathy

Abstract:
Several heavy metals, such as cadmium, lead, nickel, and cobalt, are known to damage the cardiovascular system. However, it had not been cleared up whether uranium exerts a similar effect or not. In the present study, experiments were performed to reveal possible uranium-induced impairments of the structure of the cardiovascular system and/or of its function and to elucidate their potential role in the mechanism of the nephrotoxic effect of uranium or uranium salts.
    Male SPRD rats were daily treated for 6 weeks with 75 mg/kg b.m. uranyl acetate dissolved in the same volume of distilled water given by gavage; the controls received similar amounts of distilled water. At the end of the 6-week treatment, the animals were anesthetized with pentobarbital-Na and 6-lead ECG was recorded. Then hemodynamic investigations were performed by means of 57Co- or 113Sn-labelled microspheres (McDevitt and Nies, 1976); cardiac output and its organ fractions (brain, heart, liver, kidneys, stomach, intestine, parietal bone, and femur) were determined. The values of total peripheral resistance, nutritive blood flow and vascular resistance of the organs were calculated.
    It was found that uranyl acetate reduced the gain of body mass, increased the cardiac index, decreased the heart rate and increased the organ fractions of the cardiac output to the heart and parietal bone along with an increase of nutritive blood flow to the heart and intestine. However, the most striking shifts were observed in the kidneys: increased vascular resistance with a concomitant fall in the fraction of cardiac output and nutritive blood flow to the organ, resulting in histologically verified tubular nephropathy of segmental localisation.
    It was concluded that the cardiovascular impact of uranyl acetate resembles that characteristic of hypoxia and the changes observed may be causative in the mechanism of uranium toxicity. At the same time, the uranyl acetate-induced systemic circulatory effects along with the marked local changes of renal hemodynamics are considered to have a decisive role in the most significant toxic effect of uranium or uranium salts, namely, in the induction of nephrotoxic damages.

Received: 12 February 2004
Accepted: 26 February 2004
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