Abstract
Previous studies revealed persistent sodium retention in dogs with chronic pericardial tamponade (induced by injection of Freund adjuvant into pericardial sacs) and pericardiocentesis, revealed in increased sodium excretion. Three groups of dogs were studied. Group 1 was treated with indomethacin (2.5 mg/kg, iv) prior to pericardiocentesis. Compared with experiments without indomethacin, sodium excretion did not increase flowing pericardiocentesis in animals treated with indomethacin despite similar changes in arterial pressure, venous pressure, hematocrit, plasma protein concentration, and renin activity. This effect of indomethacin was presumably mediated through prostaglandin (PG) synthesis inhibition. Group 2 dogs received an infusion of arachidonic acid (AA) (to increase PG synthesis) into the left renal artery (20 micrograms.kg-1. min-1). Sodium excretion increased after AA infusion during tamponade (11.2 to 30.9 mequiv.min-1) with a further increase occurring after pericardiocentesis (84.4 mequiv.min-1). Animals in group 3 were infused with both 20 and 80 micrograms. kg-1. min-1 doses of AA. Although sodium excretion following 80 micrograms.kg-1.min-1 AA(21 mequiv.min-1) was higher than that seen during 20 micrograms.kg-1.min-1 (14.2 mequiv.min-1), a further increase in sodium excretion to 45.6 mequiv.min-1 followed pericardiocentesis. During tamponade, AA did not change any of the measured parameters other than sodium excretion, a result compatible with the proposed distal tubular site of action of PG. Absolute but not fractional cortical blood flow distribution increased during the time sodium excretion increased following pericardiocentesis in all experiments. It is proposed that increased PG synthesis may be one possible mechanism involved in the natriuresis seen following pericardiocentesis. One cannot exclude the possibility that increased absolute blood flow to the superficial cortex also contributes to the observed natriuresis. Changes in arterial pressure, venous pressure, hematocrit, plasma protein concentration, and renin activity appear to contribute to the observed natriuresis but only when PG synthesis is not blocked.
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