Pseudoaneurisma gigante de fístula arteriovenosa humeral autóloga: reparación quirúrgica / Gigant pseudoaneurysm of an autologous arteriovenous fistula in the forearm: surgical repair

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Methylprednisolone-induced hypertension in the rat: evidence against the role of plasma volume changes, vasopressin and renal prostaglandin E2.

The purpose of the study was to clarify the mechanism(s) of glucocorticoid-induced hypertension. Hypertension was induced in rats by single i.m. injection of methylprednisolone (MP) 20 mg/kg. In normal Wistar rats, systolic blood pressure (SBP) increased by 30 mmHg from days 2 to 10 after MP. Urinary sodium excretion increased transiently and sodium balance was negative. Plasma volume (PV; ml/100 g body weight) increased on day 5, but was unchanged on day 2 after MP, at a time when SBP had already increased. In rats with chronic renal failure (CRF) and low sodium intake, SBP increased more than in control rats (48 versus 22 mmHg on day 10). Hypertension was not accompanied by a significant drop in urinary excretion of prostaglandin E2 (PGE2; measured by radio-immunoassay). In normal MP-injected rats, PGE2 excretion decreased slightly and then increased; in CRF rats, basal PGE2 excretion was too low to evaluate the effect of MP. In homozygous Brattleboro rats lacking antidiuretic hormone (ADH), MP increased SBP by 28 mmHg (day 10). Similar changes were obtained in heterozygous Brattleboro rats. The changes in PV were identical to those found in Wistar rats. We conclude that increase in PV, change in PGE2 and vasopressin do not play a key role in MP hypertension. Direct effect of glucocorticoid on vascular receptors is likely to be involved in this model.

Effects of antiglucocorticoids on glucocorticoid hypertension in the rat.

The early phase of hypertension induced in rats by a glucocorticoid agonist RU 26988 was studied. Systolic blood pressure increased by 35 mm Hg. Water and sodium urinary excretion increased transiently, and plasma volume decreased. Total and ouabain-sensitive sodium efflux, as well as rubidium efflux, were enhanced by glucocorticoid administration. Low salt intake did not prevent hypertension. Pretreatment with RU 38486, a steroid with antiglucocorticoid properties, largely prevented the rise in blood pressure (+10 mm Hg) and suppressed transient natriuresis and the decrease in plasma volume. Changes in total and ouabain-sensitive sodium efflux were completely prevented, whereas changes in rubidium efflux were only partly reversed. Similarly, administration of progesterone, a steroid with antiglucocorticoid effects, prevented glucocorticoid hypertension (+11 mm Hg) and vascular ionic changes. In contrast administration of RU 28318, an antimineralocorticoid agent, was without effect on glucocorticoid hypertension (+38 mm Hg). Progesterone or RU 38486 administered after glucocorticoid also decreased blood pressure. Present data indicate that glucocorticoid hypertension may be prevented or reversed in its early phase by steroid drugs with antiglucocorticoid properties. These drugs also appeared to prevent the sodium and rubidium flux abnormalities induced by glucocorticoid. We suggest that activation of the vascular glucocorticoid receptors may be involved in the pathophysiology of glucocorticoid hypertension.

[Effect of an antiglucocorticoid steroid on the arterial hypertension induced by glucocorticoids in the rat]. / Effet d'un stéroïde antiglucocorticoïde sur l'hypertension artérielle induite par les glucocorticoïdes chez le rat.

Hypertension was induced in male rats by administration of a glucocorticoid agonist, RU 26988. Systolic blood pressure (SBP) increased by 35 mmHg. Administration of an antimineralocorticoid derivative, RU 28318, did not modify hypertension. In contrast administration of a steroid derivative with antiglucocorticoid properties, RU 38486, prevented glucocorticoid-induced hypertension in a large part. SBP augmented only by 10 mmHg. The glucocorticoid increased total and active, ouabain-sensitive, 22Na efflux, as measured from caudal arteries, whereas concomitant administration of the antiglucocorticoid derivative prevented these changes. It is suggested that glucocorticoid-induced hypertension may be related to vascular Na pump activation and to the subsequent ionic changes. These changes, as well as hypertension, are antagonized by steroid derivatives with antiglucocorticoid properties.

Papillary plasma flow in rats. II. Hormonal control.

Papillary plasma flow (PPF) was measured by the albumin accumulation technique in Wistar rats. PPF was significantly lower in male (293 +/- 5 microliter X min-1 X g-1) than in female (499 +/- 17) rats. Castration in male rats increased PPF; testosterone administration in gonadectomized rats returned PPF to control. Acute indomethacin administration equalized PPF in both sexes to low values close to those found in normal males (320 +/- 5 in males, 326 +/- 17 in females). Conversely, captopril administration equalized PPF in both sexes by raising PPF in males (505 +/- 21) without significant change in females (526 +/- 88). Dehydration decreased PPF slightly in males (255 +/- 28) but more markedly in females (349 +/- 11). This decrease was prevented by captopril administration (520 +/- 34 and 609 +/- 61 in males and females, respectively). In captopril-treated male rats, angiotensin II (AII) was continuously infused by osmotic minipumps at a rate of 5 micrograms/h. This did not restore PPF (405 +/- 12) to basal values. In contrast, AII infusion together with indomethacin administration completely restored PPF (322 +/- 22) in captopril-treated rats whereas indomethacin alone did not normalize PPF (425 +/- 18). We suggest that male sex hormones and AII decrease PPF, and account for the low PPF measured in male rats. Vasodilator PGs are involved in the high PPF found in female rats. The vasodilator action of captopril on papillary circulation is explained by both decreased AII formation and increased PG synthesis.

Increased severity of the acute renal failure induced by HgCl2 on rats with reduced renal mass.

In rats unilaterally nephrectomized 2 days before and sham operated controls, an acute fenal failure (ARF) has been induced by subcutaneous HgCl2 injection. The uninephrectomized animals showed a more severe ARF than the sham operated, 60% of the former and 10% of the controls became anuric 48 hours after ARF induction. The increased diuresis and natriuresis produced by acute saline overload did not improve the severity of the ARF. The marked difference in the evolution of this model of ARF with respect to the glycerol induced ARF, which is ameliorated by reduction of renal mass, emphasizes the different pathogenetic mechanism of these two experimental models.