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PubMed1991

Response of rabbit ear artery to endothelin-1 during cooling.

1. The effects of cooling on the response of rabbit central ear artery to endothelin-1 and the role of the endothelium in these effects were studied in 2 mm long cylindrical arterial segments. 2. Concentration-response curves for endothelin-1 (10(-10)-3 x 10(-7) M) were recorded isometrically in arteries with and without endothelium at 37 degrees C and during cooling (24 degrees C). To analyze further the endothelial mechanisms of the response to endothelin-1 during cooling, the effects of this peptide in the presence of NG-nitro-L-arginine methyl ester (L-NAME) (10(-4) M) or meclofenamate (10(-5) M) were also determined. 3. In every condition tested, endothelin-1 produced a marked, concentration-dependent arterial contraction. Sensitivity of intact arteries to this peptide was consistently lower at 24 degrees C than at 37 degrees C. At 37 degrees C there were comparable responses of arteries with and without endothelium, but at 24 degrees C arteries without endothelium showed a higher sensitivity than intact arteries to endothelin-1. 4. L-NAME (10(-4) M) increased the maximal contraction at 37 degrees C, and both the sensitivity and maximal contraction at 24 degrees C of intact arteries to endothelin-1. Meclofenamate (10(-5) M) did not affect the arterial response to endothelin-1. 5. Sensitivity of arteries with and without endothelium to nitroprusside (10(-9)-10(-3) M) was significantly decreased during cooling, and endothelium removal did not affect the relaxation to this nitrovasodilator. 6. These results suggest that cooling decreases sensitivity of cutaneous arteries (ear artery) to endothelin-1 probably by increasing the availability of endothelial nitric oxide.

Animals↗
PubMed1993

Efficacy of meclofenamate sodium versus placebo in headache and craniofacial pain.

Twenty patients were enrolled in a double-blind, placebo-controlled crossover study of meclofenamate sodium in headache and craniofacial pain. There were four observation periods of 15 days each: Period 1 was a wash-out period. In period 2, subjects were randomly assigned to a 15-day regimen of taking two capsules a day of 100mg meclofenamate sodium (group 1) or placebo (group 2). In period 3, group 1 was switched to placebo and group 2 to meclofenamate sodium for the next 15 days. Lastly, the patients took no medication for a further 15 days (period 4). A thermographic record of the craniofacial and neck areas was taken at the end of periods 1 and 4. A record of the pressure threshold and tissue compliance at different sites of the craniofacial, neck and shoulder areas was taken at the end of each period. During the trial, number and duration of painful events were recorded daily by the patients, and the level of pain evaluated on a visual analog scale. Mean data were analyzed for significant difference by ANOVA and paired t-test. During the meclofenamate sodium period, there was a significant decrease of days with painful events compared to the wash-out period in group 1 and compared to the placebo period in group 2. In the majority of patients, the meclofenamate sodium period scored lowest or second-lowest after the follow-up period in mean pain intensity. Data for pressure threshold, although not significant, were indicative of a possible increase during and after intake of meclofenamate sodium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Efficacy of meclofenamate sodium (Meclomen) in the treatment of rapidly progressive periodontitis.

This 6-month, double-blind, controlled clinical trial determined the efficacy of the non-steroidal anti-inflammatory drug, meclofenamate sodium (Meclomen), as an adjunct to scaling and root planing in the treatment of rapidly progressive periodontitis (RPP). 22 subjects (7 male, 15 female) aged 36.5 +/- 7.88 years with RPP and disease-active sites as determined by pretreatment bone scan had standardized radiographs at baseline and 6 months, and clinical measurements at baseline, 3 and 6 months. Following full-mouth scaling and root planing, subjects were randomly assigned to either a placebo, 50 or 100 mg meclofenamate sodium bid group. Bone change over the 6-month period as assessed by subtraction radiography was the primary efficacy determinant. Specialized software was used to isolate the lesion from the subtraction image and to measure bone change along the root surface. ANOVA using the subject as the unit of analysis revealed a significant dose response (p < 0.001) with the placebo group having a mean bone loss of 0.42 +/- 0.06 mm and the low and high dose groups having mean bone gains of 0.07 +/- 0.05 and 0.20 +/- 0.07 mm, respectively. These findings indicate that meclofenamate sodium may be a useful adjunct in the treatment of rapidly progressive periodontitis.

Adolescent↗
PubMed1982

Central cardiovascular and thermal effects of prostaglandin E2 in rats.

Prostaglandin E2 (PGE2) increased the blood pressure, heart rate and body temperature, when administered at the doses of 0.001-10 micrograms into the lateral cerebral ventricle (i.c.v.) of the urethane-anesthetised rat. The highest dose of 10 micrograms/rat induced a strong initial hypotensive effect. Intravenously (i.v.), PGE2 at the doses of 0.01-10 micrograms/rat caused a biphasic blood pressure response with dose-related initial decreases followed by slight increases in blood pressure. The heart rate and body temperature were slightly increased by i.v. administrations of PGE2. The highest i.v. dose of 10 micrograms/rat initially decreased also the heart rate. Central pretreatment with indomethacin (1 mg/rat i.c.v.) partly antagonised all of the recorded central effects of PGE2, while sodium meclofenamate (1 mg/rat i.c.v.) abolished the hypertensive response to i.c.v. administered PGE2 but failed to significantly affect the PGE2-induced rises of heart rate and body temperature. The results support the previous suggestions that PGE2 may participate in the central cardiovascular and thermoregulatory control. The results also suggest that indomethacin and sodium meclofenamate antagonize the effects of exogenous prostaglandins. Since sodium meclofenamate, unlike indomethacin, affected preferentially the hypertensive response to centrally administered PGE2, there may be differences in the sites and/or modes of action between these drugs.

Animals↗
PubMed1999

Vasodilator responses to the endomorphin peptides, but not nociceptin/OFQ, are mediated by nitric oxide release.

The endomorphin peptides, endogenous ligands for the mu-opioid receptor, and nociceptin (orphanin FQ; OFQ), an endogenous ligand for the ORL1 receptor, have substantial vasodilator activity in the rat. The roles of nitric oxide, vasodilator prostaglandins, and the opening of K+ATP channels in mediating vasodilator responses to these novel agonists were investigated in the hindquarters vascular bed of the rat. Under constant-flow conditions, injections of the mu-selective agonists, endomorphin 1 and 2, PL017 ([N-MePhe3, D-Pro4]-morphiceptin), and DAMGO, and the ORL1 receptor agonist, nociceptin/OFQ, produced dose-dependent decreases in hindquarters perfusion pressure. Vasodilator responses to endomorphin 1, PL017, and DAMGO were attenuated by the nitric oxide synthase inhibitor L-NAME at a time when vasodilator responses to nociceptin/OFQ were not altered. Responses to endomorphin 1 and 2, PL017, DAMGO, and nociceptin/OFQ were not altered by the cyclooxygenase inhibitor sodium meclofenamate or the K+ATP channel blocker U-37883A. The results of these studies indicate that responses to endomorphin 1 and 2, PL017, and DAMGO are mediated in large part by the release of nitric oxide, while responses to nociceptin/OFQ are mediated by an L-NAME-insensitive mechanism. Moreover, these results demonstrate that responses to these peptides are not mediated by the release of vasodilator prostaglandins or K+ATP channel opening in the hindquarters vascular bed.

Adamantane↗
PubMed1983

Methods for the treatment of twin pregnancy in the mare.

Within a group of 130 mares which, in the event, carried twin pregnancies, 29 (22.3 per cent) produced their twins following diagnosis of a single palpable follicle at service and a single pregnancy 42 days later. The whole group of 130 twin-pregnant mares gave birth to only 17 live foals (13 per cent). Breeding results for the following season were available for 102 of these mares, when 38 (37 per cent) produced live foals. Thus over the two seasons an average 23 per cent of this group produced live foals. In a second group, comprising 70 mares, twin pregnancy had been diagnosed in all of them by rectal palpation. Five methods of treatment were then applied to five subgroups of mares and 20 (28 per cent) of the 70 mares produced live foals that season. Breeding results for the following season were available for 53 of these mares; 33 (61 per cent) then produced live foals. Thus over the two seasons an average 46 per cent of the treated group produced live foals. The administration of a prostaglandin analogue at less than 35 days of gestation was outstandingly successful as a method of treatment.

Abortion, Induced↗
PubMed1986

The activity of non-steroidal anti-inflammatory drugs in the rat mesenteric vasculature.

Rat isolated, perfused mesenteric blood vessels have been used to determine whether non-steroidal anti-inflammatory drugs (NSAIDs) display selectivity for inhibition of vasoconstrictor responses to noradrenaline compared with those to calcium. The rank order of potency of the NSAIDs for inhibition of responses to noradrenaline was: meclofenamate greater than flufenamate = diclofenac greater than indomethacin greater than fenbufen greater than phenylbutazone greater than ibuprofen greater than ketoprofen greater than naproxen greater than paracetamol (included as an inhibitor of cyclo-oxygenase). All NSAIDs show selectivity for noradrenaline (mean selectivity molar ratio = 0.19; s.e.m. 0.15-0.23) but there was a positive correlation (r = 0.98, P less than 0.001) between inhibition of responses to noradrenaline and those to calcium. The depressant effect of meclofenamate and of fenbufen, the most potent and most selective in the series, respectively, on responses to noradrenaline, was completely reversed to control values by prostaglandin E2. The results support previous findings that inhibition of cyclo-oxygenase in rat mesenteric blood vessels leads to a loss of response to noradrenaline. Comparison of the present data for inhibition of responses to noradrenaline in the mesentery with published data indicates that the mesentery bears a greater similarity to other in-vitro rather than in-vivo models for screening NSAIDs.

Animals↗
PubMed1977

The effect of prostaglandin synthesis inhibitors on renal blood flow distribution in conscious rabbits.

1. We have studied the effects of two prostaglandin synthesis inhibitors on renal cortical blood flow distribution in conscious rabbits. 2. Renal blood flow distribution was estimated by means of radioactive microspheres injected into chronically implanted left atrial cannulae. Cardiac output was measured by a thermodilution technique. 3. Measurements were made in groups of animals treated with either indomethacin, meclofenamate or control injections of phosphate buffer. 4. A method of microtome slicing of the renal cortex was developed to standardize measurements. Microtome sections were grouped into inner, middle and outer zones. After both indomethacin and meclofenamate there was a reduction in total renal blood flow with a redistribution of flow from inner to outer cortex. 5. Estimated renal vascular resistance rose in all three cortical zones. 6. The data support the hypothesis that renal prostaglandin synthesis is necessary for maintaining flow to the deep cortex. It is suggested that renal prostaglandins may also influence flow in more superficial zones. 7. Estimated total systemic vascular resistance was increased both with meclofenamate and indomethacin, suggesting an inhibiting effect of prostaglandins on arteriolar tone throughout a major part of the systemic circulartion.

Animals↗
PubMed1979

The effects of renal denervation and meclofenamate on renal blood flow regulation in conscious rabbits.

1. The effect on renal blood flow regulation of unilateral renal denervation followed by administration of a prostaglandin synthesis inhibitor has been studied in nine conscious rabbits.2. Renal blood flow distribution was estimated using radioactive microspheres injected via a pre-implanted left ventricular cannula. Cardiac output was estimated by thermodilution. Measurements were made before and after intravenous injection of Meclofenamate, Parke Davis Ltd (4 mg/kg).3. Renal denervation caused a fall in renal cortical catecholamine concentration of approximately 50% by 48 hr.4. Resting renal blood flow did not differ significantly between denervated and innervated kidneys.5. Meclofenamate caused a significant rise in arterial pressure from a mean of 59 to 70 mmHg. In innervated kidneys, Meclofenamate caused a fall in renal blood flow from 8.1 +/- 0.6 (mean +/- S.E. of mean) to 6.5 +/- 0.4 ml./min.g kidney weight while in denervated kidneys it caused a fall from 8.9 +/- 0.7 to 6.25 +/- 0.3 ml./min.g. After Meclofenamate flow was redistributed away from the inner cortex in the innervated kidney and paradoxically towards the inner cortex in the denervated one.6. It was concluded that in conscious animals, resting sympathetic tone has little effect on renal blood flow. The exaggerated reduction in flow in the outer cortex of the denervated kidney following Meclofenamate may indicate denervation hypersensitivity to circulating catecholamines unmasked by reduced synthesis of vasodilator prostaglandins. Alternatively, renal sympathetic nerves may normally prime prostaglandin synthesis in the outer cortex.

Animals↗
PubMed1999

Modulation of vasomotion in resistance arteries of JCR:LA-cp rats: a model of insulin resistance.

Obesity and insulin resistance are strongly associated with an increased risk of vascular disease. Vasomotion is the cyclic variation in the diameter of arteries and is a general feature of the vasculature that may have important physiological consequences. We tested the hypothesis that obesity - insulin resistance is associated with abnormal vasomotion by comparing obese, insulin-resistant JCR:LA-cp rats, known to develop vasculopathy, atherosclerosis, and ischemic lesions of the heart, with lean insulin-sensitive animals from the same strain. Vasomotion was assessed using isolated mesenteric arteries on a myograph system after preconstriction to 50% of maximal constriction with norepinephrine. The amplitude of vasomotion was enhanced by the presence of meclofenamate, a prostaglandin H synthase inhibitor, and was diminished by N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor. Removal of the endothelium essentially abolished vasomotion, and meclofenamate had no effect on de-endothelialized arteries. Frequency was not altered by either L-NAME or meclofenamate. Although pharmacological inhibition of nitric oxide and eicosanoid production clearly altered vasomotion, there was no difference in the amplitude or frequency of vasomotion in arteries from obese rats compared with lean rats. These results indicate that the endothelium plays a central role in modulating vasomotion, involving both enhancing and inhibiting effects, and that vasomotion is similar between obese, insulin-resistant and lean, insulin-sensitive rats.

Animals↗
PubMed2006

Angiotensin-(1-7) potentiates responses to bradykinin but does not change responses to angiotensin I.

Angiotensin-(1-7) (Ang-(1-7)), a bioactive peptide in the renin-angiotensin system, has counterregulatory actions to angiotensin II (Ang II). However, the mechanism by which Ang-(1-7) enhances vasodepressor responses to bradykinin (BK) is not well understood. In the present study, the effects of Ang-(1-7) on responses to BK, BK analogs, angiotensin I (Ang I), and Ang II were investigated in the anesthetized rat. The infusion of Ang-(1-7) (55 pmol/min i.v.) enhanced decreases in systemic arterial pressure in response to i.v. injections of BK and the BK analogs [Hyp3, Tyr(Me)8]-bradykinin (HT-BK) and [Phe8psi (CH2-NH) Arg9]-bradykinin (PA-BK) without altering pressor responses to Ang I or II, or depressor responses to acetylcholine and sodium nitroprusside. The angiotensin-converting enzyme (ACE) inhibitor enalaprilat enhanced responses to BK and the BK analog HT-BK without altering responses to PA-BK and inhibited responses to Ang I. The potentiating effects of Ang-(1-7) and enalaprilat on responses to BK were not attenuated by the Ang-(1-7) receptor antagonist A-779. Ang-(1-7)- and ACE inhibitor-potentiated responses to BK were attenuated by the BK B2 receptor antagonist Hoe 140. The cyclooxygenase inhibitor sodium meclofenamate had no significant effect on responses to BK or Ang-(1-7)-potentiated BK responses. These results suggest that Ang-(1-7) potentiates responses to BK by a selective B2 receptor mechanism that is independent of an effect on Ang-(1-7) receptors, ACE, or cyclooxygenase product formation. These data suggest that ACE inhibitor-potentiated responses to BK are not mediated by an A-779-sensitive mechanism and are consistent with the hypothesis that enalaprilat-induced BK potentiation is due to decreased BK inactivation.

Angiotensin I↗
PubMed1977

A pharmacological study of SRS-A on the bovine cutaneous vasculature.

Bovine slow-reacting substance of anaphylaxis (SRS-A) is capable of producing dose-dependent vascular permeability changes in the skin of calves. The wheals are well-defined indurations, similar to wheals induced by histamine but different from those induced by prostaglandin (PG) E2. Three proposed SRS-A receptor blockers (i.e., FPL 55712, PR-D-92-EA, and sodium meclofenamate) were studied with respect to their antagonism of wheals induced by SRS-A, histamine, and PGE2. PR-D-92-EA and FPL 55712 antagonized SRS-A, and also histamine and PGE2 at high concentrations. Meclofenamate was ineffective against SRS-A but antagonized histamine and PGE2 at higher concentrations. The significance of these results, especially with respect to passive cutaneous anaphylaxis, is discussed.

Animals↗
PubMed1983

Effects of phenoxybenzamine, metoprolol, captopril, and meclofenamate on cardiovascular function in deoxycorticosterone acetate hypertensive Yucatan miniature swine.

Eight adult Yucatan miniature swine were implanted with deoxycorticosterone acetate (DOCA) impregnated silicone strips (100 mg X kg-1). After 16 weeks of DOCA treatment mean arterial pressure (MAP) increased to 183 +/- 4 mmHg (1 mmHg = 133.322 Pa). In four normal animals arterial pressure was 126 +/- 8 mmHg. The increase in MAP in the DOCA animals was due to an elevated total peripheral resistance (TPR) with cardiac output remaining normal. In tests with conscious animals, phenoxybenzamine (1 mg X kg-1) significantly decreased arterial pressure via a selective decrease in TPR. Neither meclofenamate, metoprolol, nor captopril affected MAP in these DOCA hypertensive animals. Dose--response curves to exogenous norepinephrine and angiotensin II revealed that the DOCA animals had an increased pressor sensitivity to both of these agents. These data suggest that in the DOCA hypertensive Yucatan swine an increase in alpha adrenergic activity and (or) an increase in smooth muscle responsiveness to circulating catecholamines is responsible for the increase in blood pressure as a result of an increase in total peripheral resistance.

Animals↗
PubMed1985

Hormonal control of gap junctions in the myometrium.

Myometrial tissues from immature, ovariectomized mature, and pregnant rats were examined by thin-section or freeze-fracture electron microscopy for the presence of gap junctions following treatment with steroid hormones and inhibitors of prostaglandin synthesis. Gap junctions were present in the myometrium of immature rats after repeated injections of estradiol or diethylstilbestrol (500 micrograms/day). The frequency of gap junctions in immature rats after estradiol treatment was similar to that found during delivery. Concomitant administration of indomethacin or meclofenamate with estradiol (50 and 500 micrograms/day) for 3 or 4 days enhanced the effect of estradiol on gap junctions. Progesterone depressed the response of 500 micrograms/day estradiol and both 50 and 500 micrograms/day doses of estradiol when administered together with the inhibitors of prostaglandin synthesis. Gap junctions were also present in the myometria of ovariectomized mature rats after treatment with estradiol by itself or together with indomethacin, and these effects were suppressed by concomitant progesterone administration. These results indicate that the steroid hormones and prostaglandins may interact to modulate the presence of gap junctions in the myometrium.

Animals↗
PubMed1999

Vascular wall dysfunction in JCR:LA-cp rats: effects of age and insulin resistance.

We tested the hypothesis that aging and insulin resistance interact to increase vascular dysfunction by comparing the function of isolated mesenteric resistance arteries in obese, insulin-resistant JCR:LA-cp rats and lean, insulin-sensitive rats of the same strain at 3, 6, 9, and 12 mo of age. The peak constrictor responses to norepinephrine, phenylephrine, and high potassium were elevated in arteries from obese rats. Responses to these agents increased with age in both obese and lean rats. An eicosanoid constrictor contributed substantially to vasoconstriction in the arteries from both lean and obese animals. Inhibition of nitric oxide synthase increased the vasoconstrictor response to norepinephrine in both obese and lean rats. This effect increased with age in lean rats only. Vascular relaxation in response to acetylcholine and sodium nitroprusside was impaired in the obese rats and did not alter with age. The results suggest that obese JCR:LA-cp rats have enhanced maximal constriction, which originates in the arterial smooth muscle and increases with age. There is evidence that the ability of the arteries to compensate for the enhanced contractility is impaired in obese rats, particularly with advanced age.

Acetylcholine↗