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PubMed1981

Inhibition by bradykinin of the vascular action of angiotensin II in the dog kidney.

In the dog anesthetized with pentobarbital, the effect of bradykinin on the lowering of renal blood flow produced by bolus injections of angiotensin II was studied. Injection into the renal artery of angiotensin II (0.06--0.50 microgram) caused vasoconstriction and decreased blood flow to the kidney in a dose-related manner. Renal arterial infusion of bradykinin (10 ng kg-1 min-1), prostaglandin (PG) E2 (4 ng kg-1 min-1) or PGI2 (4 ng kg-1 min-1) produced renal vasodilation and inhibited the vasoconstrictor effect of angiotensin II. However, renal arterial infusion of another vasodilatory peptide, substance P (2 ng kg-1 min-1), did not alter the effect of angiotensin II on the renal vasculature. Pretreatment of dogs with an inhibitor of PG synthesis, sodium meclofenamate (5 mg/kg), abolished the inhibitory effect of bradykinin on angiotensin II-induced renal vasoconstriction. In contrast, renal arterial infusion of either PGE2 or PGI2 was equally effective in reducing the renal vascular effect of angiotensin II in animals with and without meclofenamate pretreatment. These results suggest that bradykinin reduces the reactivity of the renal vasculature to angiotensin II by a mechanism dependent upon PG synthesis.

Angiotensin II↗
PubMed1981

Bartter's syndrome: physiological and pharmacological studies.

Six siblings with Bartter's syndrome were studied. Increased urinary immunoreactive prostaglandin E (iPgE) was corrected by administration of the prostaglandin synthetase inhibitors, indomethacin, ibuprofen and meclofenamate. In addition, plasma potassium rose, plasma renin activity and angiotensin resistance decreased, and the exaggerated natriuresis following saline loading was abolished. Increased urinary iPgE also became normal following the phospholipase inhibitor, mepacrine, but the other abnormalities remained unaltered. The kallikrein inhibitor, aprotinin, did not alter urinary iPgE, plasma potassium or electrolyte balance. During hypotonic saline infusion, proximal tubular potassium or electrolyte balance. During hypotonic saline infusion, proximal tubular sodium reabsorption was normal or increased. Free water clearance and the percentage of distally delivered sodium which was reabsorbed were, however, significantly decreased. The results suggest that neither the increased renal PgE production nor the hyperbradykininemia seen in Bartter's syndrome play a major role in its pathogenesis, or manifestations, and that the effects of the prostaglandin synthetase inhibitors on the syndrome are non-specific. The results and relevant literature are analysed in an attempt to identify the initial defect in the interrelated sequence of events. The data are compatible with an intrarenal defect in sodium transport, leading to increased sodium delivery to the distal tubule, with secondary hyperreninemia, hypokalemia and elevated iPgE excretion.

Adult↗
PubMed1984

Effect of topically applied steroidal and nonsteroidal anti-inflammatory agents on skin repair and regeneration.

We studied the effects of topically applied steroidal and nonsteroidal anti-inflammatory agents on dermal and epidermal wound healing. Superficial wounds (0.3 mm deep) on the skin of domestic pigs were treated daily with either 0.1% triamcinolone acetonide (TA), 1% hydrocortisone (HC), 1% nandrolone decanoate (ND), 1% ND + 0.1% TA, 10 mg ibuprofen, 10 mg meclofenamate sodium, 3 mg indomethacin, vehicle (USP petrolatum or 70% ethanol), or control (untreated). Wounds were excised on days 2-7 after wounding and the epidermis was separated from the dermis. The dermis was assayed for collagen biosynthesis and the epidermis was evaluated for reepithelialization. A significant decrease (P less than 0.01) in relative collagen synthesis was observed in the wounded dermis in both HC- and TA-treated groups on day 3 after wounding, but there were no significant differences on days 4-7. Depressed collagen and noncollagenous protein production was also noted in vehicle-treated wounds on day 3. Topical application of ND did not affect collagen synthesis, but when combined with TA it eliminated the inhibitory effect observed as a result of TA alone. Topical ND accelerated wound reepithelialization by 12.5% compared with vehicle and by 26% compared with untreated controls. TA delayed epidermal resurfacing by 22%, but when combined with ND (ND + TA) the rate of reepithelialization was similar to vehicle-treated wounds. HC enhanced resurfacing when compared with untreated wounds but did not differ markedly from its vehicle. The nonsteroidal anti-inflammatory drugs when topically applied markedly reduced inflammation (erythema, heat, and edema) but did not influence the healing process.

Administration, Topical↗
PubMed1984

An expanded profile of cutaneous reactions to nonsteroidal anti-inflammatory drugs. Reports to a specialty-based system for spontaneous reporting of adverse reactions to drugs.

The nonsteroidal anti-inflammatory drugs are widely used in the United States and are a frequent cause of cutaneous reactions. Since December 1980, dermatologists have reported 135 of these drug reactions to a specialty-based Adverse Drug Reaction Reporting System. Reactions to piroxicam were most frequently reported; the majority of reactions to this drug were vesiculobullous and occurred most often in sun-exposed areas. Other reactions to nonsteroidal anti-inflammatory drugs not previously recognized include serum sickness, exfoliative erythroderma, and photosensitivity associated with sulindac; toxic epidermal necrolysis was reported with tolmetin, zomepirac sodium, and piroxicam. Fixed drug eruptions were noted with ibuprofen and naproxen, and photosensitivity was reported with sulindac and indomethacin. These findings illustrate the usefulness of a specialty-based system for spontaneous reporting of new and serious adverse reactions to drugs.

Aged↗
PubMed1984

Chronic propranolol treatment decreases pulmonary artery pressure in conscious dogs.

Daily administration of propranolol to 9 chronically instrumented, trained dogs for 2 weeks caused significant (p less than 0.05) decreases in heart rate (70 +/- 8 to 57 +/- 6 beats/min), cardiac output (3.6 +/- 0.3 to 2.9 +/- 0.2 liters/min), pulmonary arterial pressure (15.7 +/- 0.5 to 10.0 +/- 0.5 mm Hg) and total pulmonary vascular resistance (4.6 +/- 0.6 to 3.3 +/- 0.4 units). Nadolol, a structurally dissimilar beta-adrenergic receptor antagonist, caused a similar decrease in total pulmonary resistance. Acute meclofenamate administration did not return to normal pulmonary arterial pressure and resistance in the dogs chronically treated with beta-adrenergic receptor blockers. We therefore conclude that chronic beta-adrenergic receptor blockade lowered pulmonary arterial pressure and resistance by a mechanism independent of cyclooxygenase. In addition, chronic beta-adrenergic receptor blockade did not affect the potential for hypoxic vasoconstriction.

Animals↗
PubMed1984

Radiation induced brain edema in primates, studied with sequential brain cat scanning and histopathology. Protective effect of sodium meclofenamate. A preliminary report.

Four Cynomologous monkeys (Mecaca fascicularis) received 2000 Rad whole brain irradiation. One remained untreated and exhibited loss of hair, facial edema, brain edema and hydrocephalus. There was loss of alertness and motor activity. One was scheduled to be treated with phenobarbital, but died in 24 hours after irradiation. One animal received 2 mg/kg dexamethasone I.M. daily. It died two weeks after irradiation apparently due to treatment related infection. One animal received 20 mg/kg sodium meclofenamate (Meclomen) orally daily. This animal showed no brain edema and only minimal hydrocephalus, delayed and incomplete hair loss and no facial edema. Further studies of this treatment appear to be justified.

Animals↗
PubMed1983

Biphasic blood pressure response to angiotensin II in the conscious rabbit: relation to prostaglandins.

The injection of a large bolus of angiotensin II causes a biphasic blood pressure response in the conscious rabbit. To investigate contribution of prostaglandins (PGs) to the depressor phase of the blood pressure response, we studied the blood pressure effect of i.v. bolus injections of angiotensin II before and after the administration of an inhibitor of cyclooxygenase, indomethacin or sodium meclofenamate (10 mg kg-1), and in relation to associated changes in the plasma concentration of immunoreactive PGs. In conscious rabbits, angiotensin II (0.05-5.00 microgram kg-1) produced a dose-related pressor response which at both 1.5 and 5.0 micrograms kg-1 was followed by lowering of blood pressure to below the preinjection level. Neither indomethacin nor meclofenamate affected the maximal rise in pressure produced by angiotensin II, but both cyclooxygenase inhibitors augmented the duration of the pressor phase and abolished the depressor phase of the hemodynamic response to angiotensin II at 1.5 to 5.0 micrograms kg-1. After administration of angiotensin II, 5 micrograms kg-1, the plasma concentration of 6-keto-PGF1 alpha increased (P less than .01) from 218 +/- 21 pg/ml by 221 and 235% during the pressor and the depressor phases of the blood pressure response, respectively. Increments in plasma 6-keto-PGF1 alpha correlated inversely with the duration of the pressor phase and directly with the maximal lowering of blood pressure during the depressor phase. Plasma levels of PGE2 and PGF2 alpha also were increased by the peptide but the increments were not correlated with any aspect of the blood pressure response. These data suggest that a mechanism involving PGs both curtails the pressor phase and mediates the depressor phase of the hemodynamic response to pharmacological doses of angiotensin II in the conscious rabbit.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Dissociation of effects of xanthine analogs on renal prostaglandins and renal excretory function in the awake rat.

In awake, male rats, oral theophylline (TH) or enprofylline (EN; 3-propyl xanthine), 10 to 50 mg/kg b.wt., similarly increased urinary prostaglandin (PG)E2 excretion, by 2- to 3-fold; urinary PGF2 alpha excretion was increased to a lesser extent (50%), while excretion of a PGI2 metabolite, 6-keto-PGF1 alpha, was not altered. In rat renal high-speed supernatant, neither TH nor EN inhibited activity of 15-hydroxyprostaglandin dehydrogenase, an intrarenal PG catabolizing enzyme, suggesting that the increased urinary PG excretion was due to increased synthesis. TH, at all doses that increased urinary PGE2 excretion, also caused dose-related 2-to 4-fold increases in urine volume and urinary excretion of sodium and potassium. In contrast, at low doses EN increased urinary PGE2 excretion without altering urine volume or electrolyte excretion; at the highest dose tested, EN produced a modest diuresis and natriuresis. Pretreatment of rats with indomethacin or meclofenamate (10 mg/kg b.wt., p.o.), chemically dissimilar PG synthesis inhibitors, prevented effects of TH and EN on urinary PG excretion, and also blocked their diuretic and natriuretic effects. Thus, increased renal PGs may be permissive and requisite for the diuretic and natriuretic effects of xanthines, but not sufficient to cause those effects. Enprofylline has been reported (Persson et al., Life Sci. 30: 2181, 1982) to be more active than theophylline as a phosphodiesterase inhibitor, but inactive as an adenosine antagonist, suggesting that the latter action is not required for xanthine stimulation of urinary PG excretion but may be a factor in the diuretic and natriuretic effects.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Differential response of the pulmonary circulation to prostaglandins E2 and F2 alpha in the presence of unilateral alveolar hypoxia.

Pulmonary hemodynamic responses to several prostaglandins (PGs) are augmented by hypoxia. To test whether responses to vasoconstrictor PGs would be enhanced in hypoxic areas of the lung, resulting in redistribution of blood flow to well-oxygenated areas, the effects of PGE2 and PGF2 alpha were evaluated in anesthetized dogs with divided ventilation, one lung being ventilated with 100% N2 and the other with 100% O2. Thermal dilution techniques coupled with electromagnetic flow measurements permitted estimates of blood flow to each lung. After indomethacin (5 mg/kg i.v.), PGE2 at 0.01, 0.025 and 0.10 micrograms/kg/min i.v. produced significant increases in flow to the O2-ventilated lung at each dose. In addition, PGE2 increased total pulmonary blood flow, but only at the two larger doses. Concomitantly, systemic arterial PO2 increased from 104 +/- 21 to 138 +/- 26 mm Hg (P less than .001). Identical results were obtained when meclofenamate (5 mg/kg i.v.) was used to block PG synthesis. PGF2 alpha increased total pulmonary blood flow (P less than .01) only at the largest dose (0.10 micrograms/kg/min), but did not redistribute flow or increase PO2. Atrial pacing increased total pulmonary blood flow (P less than .001) and flow to both O2 (P less than .001)- and N2 (P less than .05)-ventilated lungs with no change in PO2. We conclude that PGE2 redistributes pulmonary blood flow to well-oxygenated alveoli through mechanisms not related solely to its vasoconstrictor properties or to its capacity to increase cardiac output.

Animals↗
PubMed1984

Prostaglandin-vasopressin interactions on the renal handling of calcium and magnesium.

The role of prostaglandins in the regulation of sodium and water excretion has been widely studied, but little is known about the influence of prostaglandins (PGs) on the tubular handling of calcium, magnesium or phosphorus. Recent observations have suggested that PGE2 and vasopressin may interact and influence reabsorption of calcium and phosphorus in the cortical collecting duct. The present study investigated the effect of meclofenamate (2 mg/kg), and inhibitor of PG synthesis, on the excretion of calcium, magnesium and phosphorus. Experiments were performed in antidiuretic and water diuretic rats to examine potential PG-vasopressin interactions on the reabsorption of these ions by renal tubules. In antidiuretic rats given meclofenamate, urine osmolality increased whereas urine flow and the fractional excretion of water, urea, sodium, calcium and magnesium decreased by 30 to 50%. In water diuretic animals, urine osmolality and urea excretion were unaltered after meclofenamate administration. Fractional excretion of sodium, water, calcium and magnesium declined approximately 50% in water diuretic rats given meclofenamate. Urinary excretion of PGE2 was not significantly different in water diuretic and antidiuretic rats averaging 262 +/- 78 vs. 167 +/- 35 pg/min, respectively. Meclofenamate significantly reduced urinary excretion of PGE2 in both groups. The results indicate that renal PGs modulate renal tubular reabsorption of calcium and magnesium, as well as sodium and water.

Absorption↗
PubMed1984

Effect of sodium meclofenamate on radiation-induced esophagitis and cystitis.

Stumptailed monkeys (Macaca arctoides) received 2000 rad irradiation to the upper half of the esophagus and to the bladder by a 6-MEV linear accelerator. Endoscopy and biopsy was obtained from these organs weekly for 3 weeks. At the end of this period, the animals were autopsied and histopathologic examination undertaken. Sodium meclofenamate in doses of 5-20 mg/kg/day p.os was found effective in reducing or preventing radiation induced esophagitis and cystitis.

Animals↗
PubMed1980

Effects of meclofenamate on the renal actions of mannitol infusion in conscious rabbits. Evidence for osmotic control of renal prostaglandin synthesis?

Experiments in conscious rabbits were designed to determine whether the effects of mannitol on renal blood flow and sodium and water excretion depend on increased renal prostaglandin synthesis. Compared to controls mannitol caused: a) increased glomerular filtration rate, naturesis, and water diuresis, that were unaffected by meclofenamate, b) increased outer cortical flow, that was prevented by meclofenamate, and c) decreased inner cortical flow, that was accentuated by meclofenamate. Thus the diuretic effect of mannitol occurred independently of increases in renal blood flow or prostaglandin synthesis. Changes in renal blood flow distribution with mannitol may be due to altered renal prostaglandin synthesis secondary to changes in tissue osmolarity.

Animals↗