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PubMed1984

Meclofenamate and prostaglandin E2 affect breathing movements independently of glucose concentrations in fetal sheep.

Fetal breathing movements in sheep are stimulated by infusions of a prostaglandin synthetase inhibitor, meclofenamate; they are inhibited by prostaglandin E2. Recent studies suggest that these effects are mediated through changes in fetal plasma glucose concentrations. We infused into chronic fetal sheep preparations (1) glucose, (2) meclofenamate, and (3) prostaglandin E2, followed by prostaglandin E2 and glucose together. Infusions of glucose alone did not affect fetal breathing movements despite a significant twofold increase in glucose concentrations. During meclofenamate infusions, fetal breathing movements increased from 34.9% to 80.6% (p less than 0.005); glucose concentrations did not change. During prostaglandin E2 infusions, fetal breathing movements decreased from 36.5% to 4.1% (p less than 0.005) without any change in glucose concentrations; the addition of glucose did not alter the effects of prostaglandin E2 on fetal breathing movements. We conclude that fetal infusions of glucose in sheep do not affect fetal breathing movements and the effects on these breathing movements produced by meclofenamate and prostaglandin E2 are independent of the changes in plasma glucose concentrations.

Animals↗
PubMed1986

Effects of meclofenamate and acetaminophen on abdominal pain following tubal occlusion.

To test the hypothesis that the postoperative abdominal pain of tubal occlusion is mediated by prostaglandins, the effects of meclofenamate, a potent inhibitor of cyclooxygenase, on postoperative analgesia and incidence of abdominal pain were compared with those of acetaminophen, a weak inhibitor of prostaglandin activity. One hundred patients undergoing tubal occlusion under local anesthesia were studied. The patients were randomly divided into four equal groups: control; acetaminophen, 1300 mg; meclofenamate, 100 mg; meclofenamate, 200 mg. The fallopian tubes were occluded by electrocautery in 47 patients and by application of Falope rings in 53 patients. Both acetaminophen and meclofenamate provided substantial analgesia for 4 hours after the operation (p less than 0.05). Meclofenamate reduced the incidence of abdominal pain by one half (p less than 0.02), but acetaminophen did not. These results suggest that a portion of pain relief achieved by meclofenamate may be due to suppression of myosalpingian and/or myometrial contractions, a process mediated by prostaglandins.

Acetaminophen↗
PubMed1989

Blunted vasoreactivity in pregnant guinea pigs is not restored by meclofenamate.

Pregnant women show a reduced pressor responsiveness to angiotensin II, but the mechanism responsible in unclear. We sought to determine whether reduced pressor responsiveness was due to decreased vasoreactivity and the involvement of increased vasodilator prostaglandin production in decreases observed. We found that pregnancy decreased systemic vascular resistance and the systemic vascular resistance response to angiotensin II infusion but not to phenylephrine hydrochloride infusion in awake, unstressed guinea pigs. The decreased systemic vascular resistance response to angiotensin II in the pregnant animals was accompanied by a reduced pressor response. Contractility to phenylephrine hydrochloride and norepinephrine was reduced in aortic rings isolated from pregnant, compared with nonpregnant, guinea pigs. Treatment with meclofenamate, a prostaglandin synthesis inhibitor, did not restore vasoreactivity in either the pregnant animal or the isolated vessel to levels observed in the nonpregnant state. We concluded that pregnancy reduced systemic vascular resistance and vasoreactivity but that mechanisms other than increased vasodilator prostaglandin production were likely responsible.

Angiotensin II↗
PubMed1991

The effect of the inhibition of prostaglandin synthesis on renal blood flow in fetal sheep.

Treatment with prostaglandin synthesis inhibitors has been associated with oligohydramnios in the fetus. The presumed mechanism is a reduction in fetal renal blood flow. We examined the effect of meclofenamate administration on renal blood flow in chronically catheterized fetal sheep during normoxia and during moderate and severe hypoxia. Ten fetal sheep were made hypoxic twice at least 4 days after surgery: once in the presence and once in the absence of meclofenamate infusion. Renal blood flow and combined ventricular output were measured with radioactive microspheres. Prostaglandin synthesis blockade with meclofenamate caused no significant change in blood pressure, combined ventricular output, renal blood flow, or renal vascular resistance in either the normoxic or hypoxic animals. These data challenge the contention that prostaglandin activity protects the renal vascular bed of the fetus from vasoconstriction during hypoxia and they also do not support the hypothesis that prostaglandin synthesis inhibition causes oligohydramnios through reduction of fetal renal blood flow.

Animals↗
PubMed1992

Endogenous modulation of the blunted adrenergic response in resistance-sized mesenteric arteries from the pregnant rat.

OBJECTIVE: We tested the hypothesis that during pregnancy the endothelium mediates the blunted response to adrenergic vasoconstriction. STUDY DESIGN: Mesenteric resistance arteries from late pregnant (n = 6) and age-matched virgin control (n = 6) Sprague-Dawley rats were studied in a myograph. RESULTS: Arteries from pregnant rats were 35% less sensitive to phenylephrine vasoconstriction than were those from nonpregnant rats (mean effective concentration that produced a 50% response 2.26 vs 1.48 mumol/L, pregnant vs nonpregnant, p < 0.01). Meclofenamate had no effect on the vasoconstrictor response in arteries from either group. Inhibition of endothelium-derived relaxing factor with N(o)-nitro-L-arginine methyl ester or endothelial cell removal had a similar twofold increase in phenylephrine sensitivity in arteries from both the pregnant and nonpregnant rats (mean effective concentration that produced a 50% response 2.26 vs 1.11 mumol/L for pregnant rats and 1.48 vs 0.72 mumol/L for nonpregnant rats, p < 0.01). However, methacholine relaxation response was potentiated in pregnant versus nonpregnant rats (mean effective concentration that produced a 50% response 0.030 vs 0.049 mumol/L, p < 0.01). CONCLUSION: Although the potential for endothelium-dependent relaxation is augmented in mesenteric arteries of the pregnant rat, the decreased sensitivity to phenylephrine during pregnancy is not modulated acutely by endothelium-derived relaxing factor or by prostaglandin products of the cyclooxygenase pathway.

Animals↗
PubMed1981

Release of endogenous catecholamines from slices of hypothalamus of rats.

The release of endogenous catecholamines from superfused slices of rat hypothalamus was studied under basal conditions and during release evoked by 40 mM K+. Catecholamines in superfusates, and in extracts of the tissue after stimulation, were isolated by column chromatography and quantitated by liquid chromatography with electrochemical detection. Norepinephrine (NE) was not consistently demonstrable in superfusate collected under basal conditions, but 40 mM K+ caused the release of from 2 to 4 ng/g of tissue per min. The addition of cocaine to the superfusate caused increases in basal and evoked release of NE. Epinephrine (E) could be measured in superfusates of slices from male but not female rats and then only when cocaine was added to the superfusate. Accordingly, the concentration of E in hypothalamus was greater in male rats than in female rats. Dopamine (DA) was not consistently measurable in the spontaneous overflow from slices either in the presence or absence of cocaine. K+-evoked release of DA could be demonstrated in slices from female rats. The addition of cocaine increased the evoked release of DA from slices from both sexes. Corticosterone, added to cocaine, had no effects on the efflux of any of the catecholamines. The experiments suggest that neuronal reuptake of all catecholamines is very efficient in the hypothalamus both under basal conditions and during evoked release.

Animals↗
PubMed1993

Evaluation for roles of brain prostaglandins in the catecholamine-induced vasopressin secretion in conscious rats.

To evaluate roles of prostaglandins (PGs) in vasopressin (AVP) secretion elicited by stimulating alpha-adrenergic and dopaminergic receptors in the periventricular region, we examined in conscious rats the effects of intracerebroventricular (i.c.v.) injections of a cyclooxygenase inhibitor meclofenamate on the plasma AVP responses to i.c.v. applications of angiotensin II (ANG II), phenylephrine and dopamine. I.c.v. injections of 58 pmol ANG II produced, 5 and 15 min later, augmentations of plasma AVP accompanied by elevations of arterial pressure and tendencies of reduction in heart rate. Similarly, the administrations of 0.53 mumol phenylephrine or dopamine enhanced plasma AVP 5 min later, without altering arterial pressure and heart rate significantly. Meclofenamate (0.31 mumol) applied i.c.v. 30 min prior to the administrations of ANG II remarkably inhibited the AVP and pressor responses to this peptide. However, the responses of plasma AVP, arterial pressure and heart rate to phenylephrine or dopamine were not affected by the i.c.v. administrations of 0.31 mumol meclofenamate. The injections of meclofenamate followed by the administrations of a vehicle for ANG II and the catecholamines were without effect on plasma AVP and the cardiovascular parameters. Plasma osmolality, sodium, potassium and chloride in all the groups mentioned above were not significantly changed during experiments. These results suggest that PGs generated in the periventricular region, despite their probable stimulatory roles in the ANG II-evoked AVP secretion, may not participate in the AVP-releasing mechanisms activated by dopaminergic and alpha-adrenergic receptors, supporting the view that PGs and the catecholamines may facilitate AVP release via separate pathways.

Angiotensin II↗
PubMed1976

The effects of prostaglandin E1 and sodium meclofenamate on blood pressure in renal hypertensive rats.

Conflicting evidence exists regarding the ability of PGE1 to normalize blood pressure in renal hypertensive rats. We performed experiments to determine the effect of PGE1 (15 mug/kg i.p. daily for 3 weeks) in renal hypertensive Wistars and found no significant change in systolic pressure. A higher dose (150 mug/kg i.p.) lowered pressure after 14 days of treatment, but not back to control levels. Further investigations are required to establish the mechanism whereby PGE1 evokes this fall. To test the hypothesis that endogenous prostaglandins have a hypotensive function in renal hypertension, experiments were performed using sodium meclofenamate to inhibit prostaglandin biosynthesis. In chronic hypertensive rats the drug had no significant effect, while in the acute phase of renal hypertension there was a dose-dependent inhibition of the pressure rise. The possibility is suggested that prostaglandins may initiate or sustain the acute phase of renal hypertension in rats.

Animals↗
PubMed1984

Yohimbine induces sympathetically mediated renin release in the conscious rat.

The preferential alpha 2-adrenergic antagonist yohimbine (4 mg/kg s.c.) caused a time-related increase in serum renin activity and heart rate in conscious Sprague-Dawley rats. Although mean arterial pressure was not decreased significantly over the 2-h period, heart rate was elevated significantly at 15 and 30 min post-injection. In contrast, serum renin activity remained elevated for up to 2 h with a 9-fold and 9.7-fold increase occurring at 30 and 60 min post-injection, respectively. Yohimbine (0.3, 1, 3 and 10 mg/kg s.c.) elicited a dose-related increase in serum renin activity and heart rate (30 min post-injection). The 1 mg/kg dose of yohimbine did not alter blood pressure whereas the 3 mg/kg dose caused a variable decrease in mean arterial pressure. The highest dose of yohimbine (10 mg/kg) significantly lowered blood pressure. The beta-adrenergic receptor antagonist propranolol (1.5 mg/kg s.c.), blocked the renin release and tachycardia caused by yohimbine (1 and 3 mg/kg s.c.), and the ganglionic blocking agent chlorisondamine partially inhibited the renin release elicited by 3 mg/kg (s.c.) of yohimbine. The prostaglandin synthetase inhibitors indomethacin (5 mg/kg s.c.) and meclofenamate (5 mg/kg s.c.) impaired the ability of yohimbine (3 mg/kg) to elevate SRA but did not alter the hemodynamic effects of yohimbine. Thus, the increase in renin release caused by yohimbine appears to be mediated by the sympathetic nervous system. Because the smaller doses of yohimbine increase renin release in the absence of a decrease in mean arterial pressure, it is unlikely that yohimbine stimulates renin release by baroreflex-mediated activation of the renal sympathetic nerves.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

The effect of aspirin, indomethacin and sodium meclofenamate on coronary artery ligation arrhythmias in anaesthetized rats.

The intravenous administration of either aspirin, (in doses of 1 and 3 mg/kg) sodium meclofenamate (1 and 3 mg/kg) or indomethacin (1 and 3 mg/kg) markedly reduced ventricular arrhythmias (VT and VF) induced by coronary artery ligation in anaesthetised rats. Their effect were very pronounced on ventricular ectopic activity occurring between the sixteenth and thirtieth min. These effects suggest the desirability of combining the non steroidal anti-inflammatory drugs with beta-adrenergic blockers in the treatment of ventricular arrhythmias following acute myocardial infarction.

Animals↗
PubMed1988

The effect of inhibition of both diacylglycerol metabolism and phospholipase A2 activity on superoxide generation by human neutrophils.

A 'cocktail' consisting of an inhibitor of diacylglycerol kinase (R59022, 10 microM), an inhibitor of diacylglycerol lipase (RHC80267, 10 microM), and an inhibitor of phospholipase A2 (either 100 microM indomethacin, or 100 microM sodium meclofenamate) markedly enhanced superoxide production by human neutrophils stimulated with post-receptor stimuli, fluoride and gamma-hexachlorocyclohexane. On the other hand, the response to the C3b/Fc receptor stimulus, opsonized zymosan, was marginally decreased whilst that to the Fc receptor stimulus, aggregated IgG, was virtually unaffected. Since the inhibitors used are deemed to inhibit the main routes of arachidonate production, these results call into question the role of arachidonate in the transduction of O2- generation by post-receptor stimuli, but support a role for arachidonate in receptor-mediated transduction.

Cyclohexanones↗
PubMed1990

Cardiorenal actions of endothelin, Part II: Effects of cyclooxygenase inhibitors.

The effects of cyclooxygenase inhibitors (meclofenamate and indomethacin) on endothelin-induced changes in renal function were evaluated in pentobarbital anesthetized female rats. Two groups (n = 5/group) of rats were evaluated: one group received a continuous intravenous infusion of meclofenamate (0.03 mg kg-1 min-1) and the second group received a bolus injection of indomethacin (5 mg/kg). Following surgery, rats were allowed 60 min to stabilize and 3 X 20 min control clearances collected. Endothelin-1 (100 eta kg-1 min-1) was then added into the infusate for 30 min. Neither meclofenamate nor indomethacin caused significant changes on endothelin-induced systemic vasoconstriction; blood pressure increased from 107 +/- 3 to 136 +/- 2 mmHg (p less than 0.01) with endothelin alone, from 103 +/- 6 to 135 +/- 6 mmHg (p less than 0.01) with endothelin plus meclofenamate, and from 105 +/- 6 to 131 +/- 10 mmHg (p less than 0.01) with endothelin plus indomethacin. Similarly, endothelin-induced decreases in glomerular filtration rate (GFR) were not affected by either meclofenamate or indomethacin; GFR decreased from 2.7 +/- 0.2 to 0.8 +/- 0.3 ml/min (p less than 0.01) with endothelin alone, from 2.3 +/- 0.5 to 0.7 +/- 0.4 ml/min (p less than 0.01) with endothelin plus meclofenamate, and from 2.6 +/- 0.4 to 0.6 +/- 0.4 ml/min (p less than 0.01) with endothelin plus indomethacin. Baseline excretion rates of sodium, potassium and urine volume were also not affected by the inhibitors of cyclooxygenase. These data demonstrate that, under the conditions of the current study, endothelin-induced changes in renal and cardiovascular function are not affected by inhibiting prostaglandin production.

Animals↗
PubMed1994

L-NAME modulates responses to adrenomedullin in the hindquarters vascular bed of the rat.

Responses to synthetic human adrenomedullin (ADM), a novel hypotensive peptide recently discovered in human pheochromocytoma cells, and calcitonin gene-related peptide (CGRP), a structurally related peptide, were investigated in the hindquarters vascular bed of the rat. Under conditions of controlled hindquarters blood flow, intraarterial injections of ADM (0.01-0.3 nmol) and of CGRP (0.03-0.3 nmol) caused dose-related decreases in hindquarters perfusion pressure and decreases in systemic arterial pressure. Following administration of the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME), hindquarters vasodilator and systemic depressor responses to ADM were significantly decreased, whereas L-NAME did not significantly decrease the vasodilator response to CGRP in either the hindquarters or systemic vascular beds. Following administration of the cyclooxygenase inhibitor, meclofenamate, vasodilator responses to ADM and to CGRP were not significantly decreased. When the relative vasodilator activity of the two peptides was compared on a nmol basis, responses to ADM were similar to responses with CGRP in the hindquarters vascular bed, whereas ADM was 30-100 fold less potent than CGRP in decreasing systemic arterial pressure. The present data demonstrate that ADM has significant vasodilator activity in the hindquarters vascular bed of the rat, that hindquarters vasodilator and systemic vasodepressor responses to ADM, but not to CGRP, are dependent upon the release of nitric oxide from the endothelium.

Adrenomedullin↗
PubMed1985

Control of pain with meclofenamate sodium following removal of an impacted molar.

The analgesic effectiveness of meclofenamate sodium (Meclomen) at two dose levels, 200 mg and 100 mg, was compared with the effectiveness of a placebo and aspirin, 600 mg, in a double-blind study of 174 adult outpatients who had undergone removal of impacted third molars. When compared with the placebo, meclofenamate sodium at either dose level produced a significantly greater reduction in pain intensity, greater pain relief, fewer withdrawals for inefficacy, greater percentage of patients who considered their medication effective, and greater percentage of patients considered by the investigator to have received drug-attributable benefits. In comparison with aspirin, 600 mg, meclofenamate sodium at either 200 mg or 100 mg produced significantly greater reduction in pain intensity and greater pain relief. The other measures of efficacy showed no significant differences between the two drugs. Side effects were minimal in all treatment groups. Meclofenamate sodium appears to be a safe and effective analgesic for the control of pain.

Adolescent↗
PubMed1993

Single dose and multidose analgesic study of ibuprofen and meclofenamate sodium after third molar surgery.

The purpose of this study was to compare the analgesic efficacy and safety of meclofenamate sodium with ibuprofen after dental impaction surgery. This study was double-blind and used a unique methodology. Patients (N = 254) were first randomized into the single dose phase of the study that included placebo, meclofenamate 50 mg, meclofenamate 100 mg, ibuprofen 200 mg, and ibuprofen 400 mg, followed by a 7-day multidose phase in which patients in the placebo group were rerandomized into one of the active treatment cells. In the single dose phase, all active treatments were significantly more efficacious than placebo for every summary analgesic measure. A positive dose-response was seen for both active drugs with meclofenamate 100 mg and ibuprofen 400 mg exhibiting the greatest efficacy for pain relief, pain reduction, time to remedication, and overall evaluation. Side effects were reported by 26 patients. They were evenly distributed among treatment groups with headache and drowsiness being the most common. During the multidose phase, there were only small differences in efficacy measures among active treatment groups. However, meclofenamate produced a higher incidence of stomach cramps and diarrhea than did ibuprofen (8.8% and 7.2% versus 0.8% and 0.8%). This study indicates that higher doses of nonsteroidal anti-inflammatory drugs are most effective immediately after surgery and that lower doses of these drugs can be used after the first postoperative day. The side effect profile of nonsteroidal anti-inflammatory analgesics is best observed with the use of a multidose study design.

Abdominal Pain↗