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PubMed1991

Prostaglandins modulate hormonal effects on rabbit myometrial alpha 1-adrenergic responses.

Estrogen increases the alpha 1-adrenergic contractile sensitivity of the rabbit uterus. Since estrogen treatment increases prostaglandin (PG) production by the perfused rabbit uterus, and PGs contribute to the alpha 1-adrenergic contractile response, we postulated that estrogen's effects on PG production or response may play a role in the increased alpha 1-adrenergic sensitivity induced by estrogen. We studied the effects of the eicosanoid synthesis inhibitor meclofenamate (60 microM) on the response to epinephrine (10(-9)-10(-5) M) of uterine strips from ovariectomized, mature, and estrogen-treated rabbits in terms of both contractile response and PGE2 and PGF2 alpha production. We also measured the contractile response to PGE2 and PGF2 alpha (both 10(-10)-10(-5) M) and KCl (70 mM) of uterine strips from these groups. We found that in the ovariectomized rabbits, meclofenamate decreased PG production, but did not alter the alpha 1-adrenergic sensitivity. In the mature rabbit uterus, meclofenamate decreased both PGE2 and PGF2 alpha production and reduced the alpha 1-adrenergic sensitivity. In the estrogen-treated rabbit uterus, meclofenamate decreased PGF2 alpha, but not PGE2, production and did not alter the alpha 1-adrenergic sensitivity. Finally, meclofenamate reduced the contractile response to KCl in all three groups, and exposure to PGE2 increased the contractile response to KCl in both the mature and estrogen-treated rabbits. We conclude that PGs play a role in the increase in the alpha 1-adrenergic sensitivity of the uterus in mature rabbits, and that this may be the result of an estrogen-mediated alteration in the postreceptor effects of PGs.

Animals↗
PubMed1992

Effect of desmopressin acetate on hindlimb perfusion pressure in rats: what is the mechanism?

Desmopressin acetate (DDAVP) is a synthetic analogue of vasopressin used to promote hemostasis and reduce postoperative blood loss. Desmopressin acetate can cause hypotension in humans. Our study evaluated the hemodynamics of rapid administration of DDAVP into the isolated hindlimb in live rats and assessed this response after pretreatment with various antagonists. Thirty male Sprague-Dawley rats (350-450 g) were given intraperitoneal pentobarbital anesthesia (50 mg/kg). Perfusion was set at a rate that gave a control mean hindlimb perfusion pressure (HPP) of 100-120 mm Hg. Rats were assigned to five groups (N = 5, each group), with each rat serving as its own control. As a control, saline solution (in volumes equivalent to those used for the antagonists) was injected into the hindlimb preparation before the agonist injections. Each group received both the clinical preparation of DDAVP (i.e., with preservative) and a laboratory preparation of DDAVP in doses of 0.3-3 ng. Group 1 was tested before and after injection of saline solution control; group 2, before and after propranolol (0.5 mg/kg); group 3, before and after meclofenamate (1.5 mg/kg), a cyclooxygenase inhibitor; group 4, before and after nitroarginine (5 mg/kg) an inhibitor of nitric oxide synthesis; and group 5, before and after atropine sulfate (1 mg/kg). Chlorobutanol (25-75 micrograms), the preservative in the clinical preparation of DDAVP, was tested for changes in HPP in five rats similarly prepared. Systemic mean arterial pressure remained constant during the study. The HPP decreased with increasing doses of the clinical preparation of DDAVP, compared with saline solution controls, whereas no change occurred with the laboratory preparation of DDAVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1983

Comparison of piroxicam, meclofenamate, ibuprofen, aspirin, and prostacyclin efficacy in a chronic model of cerebral vasospasm.

Previous studies have suggested that certain prostanoids are mediators of the pathological features of subarachnoid hemorrhage (SAH) and that a reduced synthesis of prostacyclin in the vessel wall might also contribute to the cerebral vasospasm associated with this malady. The present study was performed, therefore, to ascertain whether known inhibitors of prostanoid synthesis would negate the changes that accompany the intracisternal administration of 4 ml of autogenous arterial blood to dogs and whether prostacyclin would lyse the vasospasm that is present 24 hours after this intrathecal blood. Nonsteroidal anti-inflammatory drugs (NSAIDs) were given intravenously to anesthetized dogs 30 minutes before and again 3 hours after the intracisternal injection of blood. The induced cerebral vasospasm was studied arteriographically for 1 hour after the intrathecal blood and again on the following day. Behavioral recovery of the animals was also evaluated on the day after the simulated hemorrhage. The results show that, as a group, NSAIDs significantly (P less than 0.001) reduced the occurrence of vasospasm and behavioral change associated with intrathecal blood. However, piroxicam was more efficacious than meclofenamate, ibuprofen, or aspirin in preventing both the vascular and the behavioral changes observed. This efficacy may be due to the long half-life of piroxicam and to known and unknown pharmacological differences among these compounds. On the other hand, prostacyclin infused via the vertebral artery failed to affect the vasospasm present 24 hours after intrathecal blood. The findings suggest that a suitable NSAID could provide clinical protection from the deleterious consequences of SAH.

Animals↗
PubMed2001

Nitric oxide buffers renal medullary vasoconstriction induced by prostaglandins synthesis blockade.

The aim of this study was to examine whether nitric oxide (NO) buffers the renal medullary vasoconstriction induced by a prostaglandins (PG) synthesis inhibitor. Daily blood pressure measurements were made with implanted catheters and changes in cortical blood flow (CBF) and medullary blood flow (MBF) were determined by implanted optical fibers and laser-Doppler flow measurement techniques in conscious rats. Sodium and water balance were also determined. Infusion of meclofenamate, a nonisozyme-specific cyclooxygenase (COX) inhibitor, at 5 microg/kg/min over 4 consecutive days (n=12 rats) elicited a transitory increase (p<0.05) in mean arterial pressure (MAP) and a transitory decrease (p<0.05) in MBF and sodium excretion without altering CBF. In contrast, the simultaneous infusion of meclofenamate and N(G)-nitro-L-arginine methyl ester (L-NAME, 0.8 microg/kg/min), a NO synthesis inhibitor, over 4 consecutive days (n=12) produced a continuous increase (p<0.01) in MAP and a continuous decrease (p<0.05) in MBF and sodium excretion without altering CBF. The results of this study suggest that the renal medullary vasoconstrictor effects and sodium retention induced by meclofenamate are enhanced by a subpressor dose of L-NAME, and that NO may buffer the renal medullary vasoconstriction induced by the blockade of PG synthesis in conscious rats.

Animals↗
PubMed1998

Possible participation of prostaglandins generated in the anteroventral third ventricular region in the hypovolemia-induced vasopressin secretion of conscious rats.

OBJECTIVE: The aim of this study was to investigate the roles of prostaglandins (PGs) in the anteroventral third ventricular region (AV 3V), a cerebral site for cardiovascular homeostasis, in hypovolemia-induced vasopressin (AVP) secretion. METHODS: We infused meclofenamate (78. 3 nmol in 1 microl), a PG synthesis inhibitor, or PGE2 (7.1 nmol in 0.5 microl) into the AV 3V of conscious rats, examining their effects on plasma AVP and other variables in the presence or absence of hemorrhages. The hemorrhages (about 14% of blood volume) were conducted successively by taking femoral arterial blood over a 30-s period at 10-min intervals. RESULTS: The first hemorrhage increased plasma AVP in blood samples obtained 10 min later, without affecting plasma angiotensin II (ANG II), arterial pressure and heart rate. The second hemorrhage after 10 min raised plasma AVP further and, remarkably, augmented plasma ANG II, and reduced arterial pressure. The AVP responses to both the first and second hemorrhages were attenuated by meclofenamate infusion into the AV 3V performed 35 min before the first hemorrhage. The meclofenamate infusion did not alter the response of ANG II, while that of arterial pressure was potentiated and heart rate was decreased after the second hemorrhage. These effects of meclofenamate on plasma AVP and the cardiovascular parameters were not found when the drug was infused into the nucleus accumbens, the region slightly distant from the AV 3V, or the lateral cerebral ventricle. In the normovolemic state, meclofenamate administered into the three brain regions did not affect any of the variables monitored. In contrast, application of PGE2 into the AV 3V enhanced plasma AVP, heart rate and arterial pressure after 5 and 15 min. Histological examination indicated that infusion sites of meclofenamate in the AV 3V were close to those of PGE2 in several cases and included areas such as the organum vasculosum of the lamina terminalis, periventricular hypothalamic nucleus, and the median and medial preoptic nuclei. CONCLUSION: These results suggest that PGs synthesized in and/or near the AV 3V may be involved in the regulation of AVP release and cardiovascular function in the hypovolemic state.

Animals↗
PubMed1975

Inhibition by aspirin and indomethacin of uterine hypertrophy induced by an IUD.

An IUD inserted into one uterine horn caused an increase in its weight when this was compared with that of the contralateral control horn in rats. Such an increase could be partly prevented by treating the animals with indomethacin and aspirin. It is suggested that the IUD-induced increase in weight is at least in part mediated by release of prostaglandins.

Animals↗
PubMed1997

Cyclooxygenase metabolites possibly produced by endothelial cells mediate the lung injury caused by mechanically stimulated leukocytes.

To determine whether mechanically stimulated leukocytes increase pulmonary vascular permeability and resistance and, if so, whether cyclooxygenase metabolites mediate the increase, we assessed the effects of stimulated and unstimulated leukocytes, and of a cyclooxygenase inhibitor on pulmonary vascular permeability and resistance in isolated perfused lungs from Sprague-Dawley rats. Leukocytes were stimulated by gentle agitation in a glass container for 10 seconds. After baseline measurements were made, stimulated or unstimulated leukocytes were added to the perfusate. The effects of the cyclooxygenase inhibitor, meclofenamate, on the pulmonary vascular filtration coefficient and pulmonary vascular resistance were measured. In the rats that received stimulated leukocytes, the pulmonary vascular filtration coefficient and the vascular resistance were about 2.5 times and 3.3 times higher, respectively, than those in the rats that received unstimulated leukocytes. These increases were completely and partly blocked by meclofenamate. Histological examination indicated that meclofenamate did not prevent the adhesion of leukocytes to the pulmonary vascular endothelium. These findings suggest that mechanically stimulated leukocytes increase pulmonary vascular permeability and that cyclooxygenase metabolites produced by endothelial cells may injure the cells.

Animals↗
PubMed1994

Endothelial-derived nitric oxide inhibits sodium transport by affecting apical membrane channels in cultured collecting duct cells.

Previously, it has been shown that the addition of bradykinin (Bk) to M-1 cortical collecting duct cells in the presence of endothelial cells decreased short-circuit current (Isc), a measure of net active transport. This effect is presumably due to the release of endothelium-derived nitric oxide (EDNO), because the decrease in Isc could be blocked with Nw-nitro-L-arginine. To show that the inhibition of Isc was due to EDNO rather than prostaglandins, the ability of a cyclooxygenase inhibitor to block the inhibition was examined. When Bk was added to cocultures in the presence of meclofenamate (10(-5) M), Isc decreased from 62 +/- 12 to 44.5 +/- 7 muA/cm2, not significantly different from that in the absence of meclofenamate. To determine if the effect was due to an alteration of sodium absorption, Bk (10(-9) M) was added to cocultures, resulting in a decrease in Na flux from 28 +/- 3.1 to 20 +/- 2.2 nEq/min (P < 0.05), with Isc decreasing from 25 +/- 2.4 to 20 +/- 3.6 nEq/min (P < 0.05). To examine if the inhibition was due to blockade at the apical membrane sodium channel or the basolateral Na+/K+ ATPase, the cation-selective ionophore nystatin was used. Nystatin reversed the effect of EDNO on Isc. The effects of EDNO on Na+/K+ ATPase were also measured directly. Under maximum rate conditions, the Na+/K+ ATPase activity of control and Bk-treated cocultures was 5.2 +/- 0.3 and 6.8 +/- 1.0 nmol/min per square centimeter, respectively (not significantly different).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Water and protein permeability is regulated by the glomerular epithelial slit diaphragm.

The glomerular barriers to water and macromolecular movement were examined 2 and 24 h after the administration of a monoclonal antibody (mAb) specific to an antigen located on the epithelial slit diaphragm and the external aspect of the glomerular basement membrane. By micropuncture techniques 2 h after mAb administration, single-nephron GFR (SNGFR) and plasma flow were unchanged but the glomerular capillary hydrostatic pressure gradient and glomerular capillary hydrostatic pressure were increased and the glomerular ultrafiltration coefficient (LpA) decreased to values that were 50% of the normal control. There was no increase in urinary protein excretion at 2 h. However, at 24 h after mAb, nephron plasma flow (SNPF) and SNGFR increased and the glomerular ultrafiltration coefficient returned to values indistinguishable from the normal control. At 24 h, there was a marked increase in protein excretion. The administration of meclofenamate decreased values for SNGFR and SNPF to normal. Immunoglobulin G was exclusively bound to glomerular capillary walls in a linear or continuous fashion at 2 h, but in a discontinuous, granular pattern at 24 h. These studies suggest that after mAb, important limiting glomerular barriers for hydraulic conductivity and protein excretion reside on the epithelial aspect of the glomerular capillary basement membrane, specifically at the level of the slit diaphragm. Studies also suggest that alterations in glomerular capillary hydraulic conductivity can be effectively separated from increases in macromolecular permeability.

Animals↗
PubMed1992

Effects of sodium meclofenamate on postoperative pain following periodontal surgery.

The analgesic activity of single doses of meclofenamate (100 mg) was compared to aspirin (500 mg) and to placebo on 99 outpatients with moderate to severe pain following periodontal surgery under double-blind conditions. Pain intensity differences scores (PID) at the first, second, and third hour after the ingestion of the first capsule of each medication were used to determine the analgesic efficacy of the studied drugs. Kruskal Wallis test followed by the Mann-Whitney rank sum test were used in the statistical analysis of results. Meclofenamate was statistically superior to placebo and superior to aspirin in the second hour of evaluation, while aspirin was not superior to placebo during the 3-hour period of pain evaluation. It is concluded that meclofenamate is a non-steroidal antiinflammatory drug with interesting analgesic properties which can be used as directed as an alternative to aspirin or acetaminophen for the control of postoperative pain following periodontal surgery.

Adult↗
PubMed1987

Prostaglandin mediation of hemodynamic responses to pulmonary microembolism in rabbits: effects of ibuprofen and meclofenamate.

The effect of the cyclooxygenase inhibitors ibuprofen and meclofenamate were studied to assess the role of prostaglandin release in mediating the hemodynamic response to acute pulmonary microembolism in awake rabbits. In Group I (n = 10), a control group receiving only saline infusion, there was no change in pulmonary artery pressure, thermodilution cardiac output, or pulmonary vascular resistance. Group II (n = 12) received sequential intravenous doses of polyacrylamide microspheres averaging 34 mu in diameter, and demonstrated a progressive decrease in cardiac output and stroke volume and increases in pulmonary artery pressure and pulmonary vascular resistance. Pretreatment with either ibuprofen (Group III; n = 10) or meclofenamate (Group IV; n = 9) resulted in no change in resting hemodynamics and only minimally altered the effect of microembolism on pulmonary artery pressure. However, both ibuprofen and meclofenamate abolished the microembolism-induced decrease in cardiac output and stroke volume and blunted the increases in pulmonary artery pressure and pulmonary vascular resistance. The hemodynamic consequences of pulmonary microembolism in awake rabbits, particularly the decrease in cardiac output, are partly mediated by prostaglandin release, which alters pulmonary vascular tone and/or myocardial function.

Animals↗
PubMed1986

Serum 13-14-diOH-15-keto-prostaglandin F2 alpha and airway response to meclofenamate and metaproterenol in relation to the menstrual cycle.

In order to evaluate whether adverse reactions to a nonsteroidal antiinflammatory agent (NSAIA) were related to variations in prostaglandin levels during the menstrual cycle, we measured 13-14-diOH-15-keto-prostaglandin F2 alpha in serum and the effect on airways of a single dose of 100 mg oral meclofenamate and 1.5 mg inhaled metaproterenol during the early (follicular phase) and late (luteal phase) menstrual cycle. Among 24 women with premenstrual asthma (PMA), four women with regular asthma (REA), and four healthy women, the 13-14-diOH-15-keto-PGF2 alpha averaged 140.9 +/- 68.4 pg/0.1 ml during the follicular phase but only 14.4 +/- 2.2 pg/0.1 ml during the luteal phase (p less than 0.0001). Acute asthma reactions to the meclofenamate occurred during the follicular phase in six women with PMA but were never observed during the luteal phase (p = 0.016). These reactions occurred preferentially in patients on corticosteroids (p = 0.004). Conversely, one patient with PMA had 18% improvement in FEV1 with meclofenamate during the luteal phase. A placebo-controlled, double-blind evaluation of the healthy women and the women with REA revealed a trend toward improvement in FEV1 during the luteal phase (0.15 less than p less than 0.10) but no change during the follicular phase. The effect of metaproterenol did not vary with the menstrual cycle, and there was no interaction between the effects of meclofenamate and those of metaproterenol. It appears that meclofenamate causes adverse effects on pulmonary function in asthmatic women primarily during the follicular phase of the menstrual cycle. This effect is associated with corticosteroid treatment and may be related to monthly variation in serum 13-14-diOH-15-keto-PGF2 alpha.

Adult↗
PubMed1983

Effect of cyclooxygenase inhibitors on PGE2-sensitive human lymphocyte receptors.

A short preincubation of human T and B lymphocyte populations with exogenous Prostaglandin E2 (PGE2) markedly depresses the expression of surface receptors binding the Fc portion of IgG, sheep and mouse erythrocytes (FcR-IgG, Ea and ME receptors respectively). Using two cyclooxygenase inhibitors (indomethacin and meclofenamate) it is shown that endogenous PGE2 does not modify the activity of these lymphocyte surface receptors. The lymphocyte sensitivity to exogenous PGE2, which is released under various physiologic and pathologic stimuli, may represent present another method to subdivide human lymphocytes in distinct subsets.

Cyclooxygenase Inhibitors↗
PubMedDate not supplied

The effects of salt and meclofenamate administration on the hypertension of spontaneously hypertensive rats.

The effects of prolonged (3 mos) high sodium intake and meclofenamate were studied in 2 groups of male SHR. Group 1 (6 rats) received 1% NaCl in tap water and Group 2 (8 rats) received 1% NaCl in tap water plus 50 microgram of meclofenamate per ml of drinking fluid. Renal metabolic and hemodynamic studies in the unanesthetized unrestrained state, showed that the meclofenamate treated rats had higher arterial pressures (p less than .005), left ventricular weight (p less than .05) and renal vascular resistance (p less than .005); lower glomerular filtration rate (p less than .005) than the control rats. The hematocrit and right ventricular weight were similar in the two groups of rats. This study has demonstrated that the combination of high sodium intake and meclofenamate have a greater damaging effect on the arterial pressure and renal function of SHR than salt alone.

Animals↗