Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Autacoids”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 721 records · Page 40Linked to original sources
PubMed1978

Action of salicylate on failing heart lung preparations of guinea-pig perfused with red blood cells suspended in Tyrode-dextrane.

Heart lung preparations (HLP) of guinea-pig were perfused with homologous red blood cells suspended in 1.5 volumes of Tyrode containing 6% dextrane. Red blood cells were freshly obtained by centrifugation of heparinized blood and subsequent washing with saline. Reduced pulmonary expansion due to bronchoconstriction, increased pulmonary vascular resistance and heart failure rapidly occurred in these preparations. Addition of salicylate to the perfusing medium delayed and attenuated both the respiratory and the cardiac disturbances. A full protection against cardiopulmonary failure was obtained when salicylate was added to the heparinized blood used for red blood cells preparation and to the saline used for red blood cells washing. It is concluded that pulmonary microembolism, due to platelet aggregation, is the primary factor responsible for HLP failure. Bronchoconstriction and pulmonary vasoconstriction are aggravating factors secondary to microembolism. Salicylate appears to prevent the microembolism and the microembolism depending release of broncho- and vaso-constrictor autacoids.

Animals↗
PubMed1993

Contribution of bradykinin to the cardiovascular effects of ramipril.

From pharmacologic investigations and clinical studies it is known that angiotensin-converting enzyme (ACE) inhibitors exhibit additional local actions, which are not related to hemodynamic changes and which cannot be explained simply by interference with the renin-angiotensin system with subsequent inhibition of angiotensin II formation. Because ACE is identical to kininase II, which inactivates the nonapeptide bradykinin (BK), potentiation of BK might be responsible for these additional effects of ACE inhibitors. To prove the specificity of BK-mediated effects by ACE inhibition, we used the specific B2 kinin receptor antagonist HOE 140 in different models: endothelial cell cultures; atherosclerosis in high-cholesterol-fed rabbits; neointima formation with smooth cell proliferation and migration after endothelial denudation in rats; myocardial ischemia in rats, rabbits, and dogs; and left ventricular hypertrophy in rats. The beneficial effects of ramipril or BK given in non-blood pressure-lowering doses in these models were abolished by HOE 140 (icatibant). Ramipril exerts cardioprotective effects in different experimental models. The formation of the endothelial autacoids nitric oxide and prostacyclin, enhanced when BK degradation is inhibited by ACE inhibition, may contribute to the observed beneficial effects.

Amino Acid Sequence↗
PubMed1977

Drug-induced motility of sow (Sus scrofa) graafian follicles isolated during pre and post-ovulatory periods of the sex cycle.

The spontaneous as well as the drug-induced motility of sow graafian follicles during the early-preovulatory (E-preovulatory), late-preovulatory (L-preovulatory) and post-ovulatory stages of the sex cycle, were studied. Spontaneous motility was present only in 30.9% of the E-preovulatory and in 18.1% of the L-preovulatory, whereas none of the post-ovulatory follicles showed spontaneous contractions. All the quiescent preparations reacted, with a comparable enhancement of tension, to the addition of acetylcholine. On the other hand, norepinephrine (NE) elicited upon L-preovulatory and post-ovulatory follicles a significantly greater contractile response than over E-preovulatory preparations. The presence of MJ-1999 augmented clearly the positive influence of NE upon the contractile tension of E-preovulatory follicles, whereas cocaine, U-0521 or indomethacin failed to alter the reactivity towards NE in all the groups. The inotropic influence of prostaglandins were also explored over quiescent follicles. PGE1 diminished the basal tension of the three types of follicles, whereas PGF2-alpha produced the opposite effect. On the other hand, PGE2 enhanced the tonic tension of E and L-preovulatory preparations and reduced the basal tone of post-ovulatory follicles. The role of the spontaneous motility of smooth muscle fibers surrounding graafian follicles, as well as the effects of several autacoids and neurotransmitters prior and following ovulation are discussed in relation to their possible relevance for the ovulatory process.

Acetylcholine↗
PubMed1995

Augmentation of coronary responsiveness to serotonin at the site of X-ray-induced intimal thickening in miniature pigs.

OBJECTIVE: X-irradiation is known to enhance atherosclerotic change. We tested whether coronary vasoconstrictor responses are augmented at the sites of X-ray-induced intimal thickening in Göttingen miniature pigs. METHODS: In 17 pigs, a major branch of the left coronary artery was denuded with a balloon catheter. In 10 pigs, the denuded portion of the left coronary artery was selectively irradiated with 15 Gy of X-rays twice at 3 and 4 months after denudation (group 1). The remaining 7 pigs were not irradiated (group 2). The effects of intracoronary administration of serotonin, histamine and phenylephrine on the coronary diameter were studied 3 (3M) and 5 months (5M) after denudation. After the angiographical study at 5M, the vessels were isolated and isometric tension was measured in an organ chamber. RESULTS: The percent reduction in coronary diameter evoked with 10 micrograms.kg-1 of serotonin increased from 39(s.e.m. 4)% before X-irradiation (3M) to 75(6)% after X-irradiation (5M) in group 1 (P < 0.01), while it did not differ in group 2 [39(6)% at 3M vs. 33(8)% at 5M[ [39(6)% at 3M vs. 33(8)% at 5M]. In group 1, serotonin-induced coronary constriction was frequently accompanied by ischemic ECG changes. Histamine (10 micrograms.kg-1)-induced vasoconstriction was also augmented but to a smaller degree [47(6)% at 3M vs. 62(4)% at 5M; P < 0.05] in group 1, while it remained unchanged in group 2[52(5)% at 3M vs. 44(7)% at 5M]. Phenylephrine did not cause detectable contraction in either group at 3M or 5M. Methysergide and ketanserin attenuated serotonin-induced hypercontraction in a dose-dependent fashion. In the in vitro studies, endothelium-dependent relaxation to serotonin was impaired at the denuded site with (group 1) and without (group 2) X-irradiation to a similar extent. Isometric tension of medial smooth muscle developed by serotonin was significantly greater at the denuded site with X-irradiation (group 1) than the control site and the denuded site without X-irradiation (group 2) (P < 0.05). Intimal thickening was significantly greater at the denuded sites with X-irradiation [group 1, 238(45) microns] than at the denuded sites without X-irradiation [group 2, 58(5) microns] (P < 0.05). CONCLUSIONS: These results indicate that X-irradiation augments the coronary vasoconstrictor responses to autacoids, predominantly to serotonin, and that this augmentation is accompanied by enhanced intimal thickening. Serotonin-induced hypercontraction after X-irradiation resulted mainly from the hyperreactivity of medial smooth muscle.

Animals↗
PubMedDate not supplied

Sensory nerves, nitric oxide and NANC vasodilatation.

Primary afferent neurons, originating from the dorsal root ganglia, provide a perivascular network of fibres around the arterial system throughout the body. When stimulated, these fibres cause a nonadrenergic noncholinergic (NANC) vasodilatation by release of calcitonin gene-related peptide (CGRP). This peptide is a potent vasodilator and, in this action, cooperates with nitric oxide (NO) in a tissue-specific manner. The hyperaemic effect of intravascularly injected rat CGRP-alpha in the rat gastric mucosa is reduced by blockade of the NO synthesis, which indicates that CGRP dilates the gastric microvascular bed via NO-dependent and -independent mechanisms. This is also true for endogenous CGRP, as the gastric mucosal hyperaemia, which is caused by gastric acid challenge and involves CGRP, is likewise blocked by inhibition of the NO synthesis. The CGRP/NO-mediated vasodilatation is an important element of a neural emergency system that strengthens the resistance of the gastric mucosa in the face of pending acid injury. In the rat skin, CGRP participates in neurogenic inflammatory processes but the cutaneous vasodilator action of exogenous CGRP and the CGRP-mediated vasodilatation, evoked by antidromic stimulation of afferent nerve fibres, do not depend on the formation of NO. This L-arginine-derived autacoid, however, plays a role in the release of CGRP from afferent nerve fibres in the skin since it contributes to the CGRP-mediated vasodilator responses to chemical irritation or immunological challenge via interleukin-1 beta. These data indicate that the type of interaction between CGRP and NO in causing a NANC vasodilatation varies with the vascular bed under study. Depending on the tissue, NO may facilitate the release of CGRP from afferent nerve fibres or be a secondary vasorelaxant messenger of the peptide.

Afferent Pathways↗
PubMed1995

Platelet-activating factor. Role in fetal lung development and relationship to normal and premature labor.

In this overview on the role of PAF in reproductive biology, we have emphasized its relationship to fetal lung maturation and the initiation and maintenance of parturition. In addition, we have discussed the role of this autacoid in certain complications of premature delivery. It should be pointed out, however, that it is our view that other mediators and cytokines also play a role in these processes. In the past, many investigators have suggested a central role for one of these mediators that serves as the "trigger" of these biologic events. It is our view that these systems are regulated by a number of effectors, among which PAF may play an important role.

Cytokines↗
PubMed1995

Formation of 8-iso-prostaglandin F2 alpha by human platelets.

F2-isoprostanes are free radical catalyzed prostaglandin F2 isomers formed from arachidonic acid in an enzyme independent manner (1). Analogous families of other prostaglandin isomers have also been described. Detection of these compounds in vivo has been postulated to represent an approach to the quantitative assessment of free radical generation in humans (2). Additionally, the 8-iso analogues of PGF2 alpha and PGE2 have been shown to induce vasoconstriction, a response which is prevented by pharmacological antagonists of the thromboxane receptor (3). Consequently, it is conceivable that these particular isomers might exhibit an autacoidal function. We chose to explore the factors which regulate the biosynthesis of one of these compounds, 8-iso-PGF2 alpha, in vivo and by human platelets in vitro, to understand more clearly how the discovery of these compounds might be exploited to further our understanding of free radical catalyzed processes in vivo.

Adult↗
PubMed1994

The role of the hypothalamic-pituitary-adrenocortical system during inflammatory conditions.

Infections and injury are often accompanied by the production of large quantities of proinflammatory mediators such as cytokines and eicosanoids. These substances have been shown to efficiently activate the hypothalamic-pituitary-adrenocortical (HPA) system. The glucocorticoid hormones secreted from the adrenal cortex seem to be crucial for survival because they have an inhibitory influence on inflammatory processes, which, if uncontrolled, may become toxic for the host. Furthermore, these steroid hormones are known to support thermogenesis by inducing or repressing key enzymes of carbohydrate, lipid, and protein metabolism, and thus may also facilitate energy mobilization during fever, which usually accompanies infectious diseases. Finally, a number of studies suggest that glucocorticoids attenuate debilitating symptoms of inflammatory mediators, such as sleepiness, loss of appetite, and suppression of reproductive functions. One can assume that glucocorticoids exert similar behavioral effects during inflammatory conditions, which are seen in infectious diseases. Corticotropin-releasing hormone (CRH), the major hypothalamic component of the HPA system, is a putative mediator of the central effects of cytokines and autacoids because it inhibits growth, reproduction, and food intake. In contrast, CRH decreases sleep duration. Vasopressin, another hypothalamic peptide of the HPA system, counteracts fever and sickness behavior and is thought to support recovery from inflammatory diseases. Apparently, a well-balanced, concerted action of proinflammatory mediators, glucocorticoids, and hypothalamic peptide hormones provides not only an efficient principle for combating microorganisms and support of tissue repair but also for self-protection of the host during the stress of inflammation. Therefore, an impairment of the HPA system under inflammatory conditions often has severe pathological consequences, for example, in patients suffering from Addision's disease and arthritis.

Animals↗
PubMed1994

Modulation by adenosine of thromboxane A2 receptor-mediated constriction in the human umbilical artery.

The powerful vasoconstrictor autacoid thromboxane A2 (TxA2) has pathological roles in many diseases including pre-eclampsia or pregnancy induced hypertension (PIH). Adenosine and other purines are released by tissues during ischemia as occurs in the utero-placental circulation during PIH. These substances, particularly adenosine, may modulate TxA2 constrictor responses. We therefore characterized TxA2 receptors in the umbilical artery in vitro using the competitive antagonist GR32191. Also examined was the Ca2+ channels' involvement in adenosine-induced inhibition of TxA2 vasoconstriction. Results showed that TxA2 receptors on umbilical arteries are identical to those present in platelets, the placenta and umbilical vein. Adenosine was found to inhibit equally constriction involving either voltage or receptor operated Ca2+ channels.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1994

Control of nitric oxide and prostacyclin synthesis in endothelial cells.

Endothelial cells produce a variety of factors involved in the control of vascular tone, platelet activation and cell growth, the most important being nitric oxide (NO) and prostacyclin (PGI2). Although continuously produced in small amounts, synthesis and release of these autacoids are enhanced by mechanical (e.g. fluid shear stress) and humoral stimuli (e.g. acetylcholine, bradykinin, histamine). By counteracting neuro- and myogenic vasoconstriction, the continuous release of NO and PGI2 from the vascular endothelium represents a sensitive and highly effective local system for the maintenance of an adequate blood flow to the organs. This overview resumes current knowledge concerning the intracellular pathways which link endothelial cell activation by receptor-dependent and -independent stimuli to the formation of NO and PGI2.

Animals↗
PubMed1993

Acadesine improves surgical myocardial protection with blood cardioplegia in ischemically injured canine hearts.

BACKGROUND: Adenosine is a cardioprotective autacoid that exerts receptor-mediated protection from ischemia/reperfusion injury. In ischemically injured hearts, avoidance of ischemia/reperfusion injury with hypothermic chemical cardioplegia may be incomplete, and consequently, postischemic left ventricular (LV) function may be severely depressed and chamber stiffness increased. This study tested the hypothesis that the adenosine-regulating agent acadesine improves myocardial protection with hypothermic blood cardioplegia (BCP), resulting in better postischemic LV function and diastolic characteristics in hearts injured by 45 minutes of normothermic global ischemia. METHODS AND RESULTS: Eighteen anesthetized (350 micrograms fentanyl citrate, 5 mg diazepam) dogs on total vented bypass were randomized to receive vehicle (n = 5), low-dose acadesine (LDA, 0.125 mg.kg-1.min-1, n = 6) or high-dose acadesine (HDA, 0.5 mg.kg-1.min-1, n = 7) continuously infused 30 minutes before global ischemia and discontinued 10 minutes after aortic cross-clamp removal. Hearts were protected with cold (4 degrees C) multidose (every 20 minutes) potassium BCP, which contained saline vehicle, 1 mg/L acadesine (LDA), or 4 mg/L acadesine (HDA) for a total of 1 hour of cardioplegic arrest. Postischemic LV function, assessed by the slope of the end-systolic pressure-volume (impedance catheter) relation, was depressed by 34 +/- 7% of baseline (5.6 +/- 1.0 versus 2.7 +/- 0.7 mm Hg/mL, P < .05) in vehicle. With LDA, there was variable improvement in postischemic function (5.1 +/- 1.3 versus 3.6 +/- 0.6 mm Hg/mL, P = .26 versus baseline). In contrast, there was complete postischemic functional recovery with HDA (5.9 +/- 0.6 versus 5.2 +/- 0.8 mm Hg/mL, P = .54). Postischemic chamber stiffness was preserved in both LDA and HDA. CONCLUSIONS: We conclude that the higher dose of acadesine improves myocardial protection when used as a pretreatment and BCP adjuvant, resulting in better postischemic LV systolic function and diastolic characteristics.

Aminoimidazole Carboxamide↗
PubMed1993

Presence of platelet-activating factor-acetylhydrolase in milk.

Human milk contains numerous factors such as immunoglobulins, lactoferrin, lysozyme, macrophages, etc., which serve an immunoprotective role. Platelet-activating factor (PAF) is one of the most proinflammatory agents thus far described. PAF is metabolized to the biologically inactive lysoPAF by the enzyme PAF-acetylhydrolase (PAF-AH). In the present study we have demonstrated that PAF-AH activity is present in human milk. The activity was associated with aqueous phase and was not stimulated by the addition of bile salts or Ca2+. The activity of PAF-AH in human milk was not affected by the addition of propranolol or NaCl. PAF, and 1-acyl-2-acetyl-glycerophosphocholine were the only substrates cleaved by the enzyme. Based on these properties it is concluded that the milk PAF-AH is not the lipoprotein or bile salt-stimulated lipase known to be present in milk. Inhibitor studies revealed that the enzyme in human milk was the plasma type PAF-AH. The activity of PAF-AH was stable at pH 4.0 at 37 degrees C and the activity varied in milk samples obtained from various species. The enzyme was secreted by milk macrophages. The presence of PAF-AH in human milk may explain, in part, the beneficial effects of breast feeding in the prevention of necrotizing enterocolitis by inactivating the potent proinflammatory autacoid, PAF.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1993

PAF molecular heterogeneity: pathobiological implications.

The existence and potential (patho)physiologic significance of PAF molecular heterogeneity can no longer be summarily dismissed or ignored. While significant advances in the chemistry of PAF have been made, the (patho)physiologic behaviors of most of the PAF molecular species of biologic origin await further study. This is because to date, investigators have studied the biologic activities of what was previously thought to be PAF, i.e., only 16:0- and 18:0-AGEPC. In view of the evidence presented in this review, a comprehensive investigation of the possible biologic relevance and significance of PAF molecular heterogeneity is warranted. Hopefully, such studies will be designed to elucidate the extent to which the various molecular species of PAF differ in their intrinsic in vitro and in vivo (patho)physiologic behaviors (agonistic, synergistic, and possibly antagonistic) and modes of action. Once this additional information has been derived, the pathobiologic relevance of this class of phospholipid autacoid may be better understood.

Animals↗
PubMed1993

[Analysis of platelet-activating factor and its effect on the lung].

One of the lipid mediators, platelet-activating factor (PAF), is reported to be involved in a variety of biological phenomena including not only harmful reactions such as allergy or inflammation, but also physiological phenomena like nerve cell differentiation, sperm mobilization, ovulation, implantation, parturition etc. We reviewed the methods of detecting PAF in biological fluids and the effects of PAF on fetal lung maturation and pulmonary diseases. Fetal lung has a capacity to produce PAF and this autacoid is involved in glycogen breakdown to furnish both glycerol backbone, such as dihydroxyacetone phosphate and glycerol-3-phosphate, and the fatty acids utilized to synthesize pulmonary surfactant. PAF also enhances secretion of pulmonary surfactant. However, PAF causes eosinophil recruitment to the lung, activation of eosinophil and neutrophil, bronchoconstriction, and lung edema, and increases bronchial hyperreactivity. All are characteristics of the pathophysiology of bronchial asthma. We examined PAF acetylhydrolase activity in plasma from patients with bronchial asthma, and found the activity was significantly lower in severe cases than that in mild or moderate cases. Ketotifen had no effect on this enzymatic activity. Evaluating PAF acetylhydrolase activity may help determine the severity of bronchial asthma. PAF is also involved in chronic lung disorders of newborns, such as bronchopulmonary dysplasia. We treated a 3-month-old child with frequent pulmonary problems who was made a diagnosis of bronchopulmonary dysplasia during neonatal period. After administration of Ketotifen for one and a half months, his clinical symptoms improved dramatically.

Animals↗
PubMed1996

Human mononuclear cells express 12-LX: coordinated mRNA regulation with 5-LX and FLAP genes.

Lipoxygenases (LXs) catalyze formation of leukotrienes and hydroxy-eicosatetraenoic acids (HETEs), proinflammatory, and spasmogenic autacoids that are critical for host defense systems. We studied the expression and regulation of LX genes (12-LX, 5-LX, and 15-LX) and the 5-lipoxygenase activating protein (FLAP) in human mononuclear cells (MNC) and granulocytes using a quantitative reverse transcription polymerase chain reaction (RT-PCR) technique. We show that 12-LX mRNA is constitutively expressed in resting platelet-free MNC. 12-LX gene expression was upregulated by activation with lipopolysaccharide (LPS). The formation of 12-HETE was inducible with ionophore in MNC, as assessed by high-performance liquid chromatography (HPLC) and gas chromatography, and increased after LPS pretreatment. In addition to 12-LX, resting MNC expressed the genes for 5-LX and FLAP constitutively. Quantitative time course analyses of 12-LX, 5-LX, and FLAP gene expression suggested coregulation of 12-LX and FLAP mRNAs, and reciprocal regulation of 5-LX and FLAP mRNAs. During cell stimulation with LPS 5-LX mRNA levels remained unchanged, whereas FLAP gene expression increased. No 15-LX mRNA expression or 15-HETE formation was detectable in unstimulated and activated MNC. In contrast to MNC, quantitative RT-PCR mRNA analysis showed intermittent intraindividual expression of the 5-LX and FLAP genes in resting granulocytes. mRNAs for 12-LX and 15-LX were not expressed. On stimulation of granulocytes ex vivo, mRNA expression of 5-LX and FLAP was upregulated. Stimulation by LPS differed from that by ionophore A23187. Neither LPS nor ionophore induced gene expression of 12-LX or 15-LX in granulocytes. Our data indicate that resting human MNC and granulocytes express LX and FLAP genes in a cell-specific manner. Cell activation induces coordinated upregulation of 12-LX and FLAP genes in MNC, and 5-LX and FLAP genes in granulocytes, respectively. The constitutive expression of 12-LX mRNA, its upregulation on cell activation, and the formation of 12-HETE clearly indicate the presence of a functional 12-LX in human MNC.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1996

Morphological and functional changes of coronary vasculature caused by transcellular biosynthesis of sulfidopeptide leukotrienes in isolated heart of rabbit.

Morphological and functional modifications occurring in Langendorff rabbit heart preparations perfused with purified human leukocytes (PMNL), as an organ model of sulfidopeptide-leukotrienes (sLT) transcellular biosynthesis, were studied. Coronary perfusion pressure (CPP), monitored as an index of coronary vasospasm, increased by 295% after challenge with the Ca(2+)-ionophore A-23187 (0.5 micromol/L) for 30', accompanied by a significant formation of sLT. Increase in CPP was prevented by PMNL pretreatment with the 5-lipoxygenase inhibitor MK-886 (1 micromol/L) or by heart pretreatment with LTD4-receptor antagonist SKF 104353, indicating a pivotal role of PMNL-derived 5-lipoxygenase (5-LO) products in the observed functional modifications. Similar effects were obtained using granulocyte macrophage-colony stimulating factor-primed PMNL challenged with the tripeptide n-formyl-methionyl-leucyl-phenylalanine. Scanning electron microscopy (SEM) of coronary arteries showed craters on the vessel luminal surface, PMNL adhering to endothelial cells (EC), increased number of microvilli on EC, presence of nonviable, desquamating, fusiform EC. SEM and transmission electron microscopy of myocardial microvessels, showed presence of perivascular and intermuscle edema, presence of activated PMNL and decreased number of patent microvessels. These morphological alterations were significantly blunted by MK-886 or SKF 104353. These data provide evidence of close interaction between PMNL and myocardial EC, resulting in enhanced sLT formation via transcellular biosynthesis, originating from transfer of PMNL-derived LTA4 to EC. These potent proinflammatory autacoids are responsible for coronary vasospasm and the morphological alternations observed.

Animals↗
PubMed1996

[Pharmacology of nitrates and other NO donors].

The identification of nitric oxide (NO) as an endothelium derived relaxing factor (EDRF) has allowed a thorough investigation of the effects of organic nitrate esters as well as other nitrogen containing vasodilators such as nitrites, nitrosothioles, sydnonimines and nitroprusside. These substances can release NO or mediators derived from it, and have thus received annotation as NO donors. The pharmacokinetic characteristics of NO donors as well as the reactions which might mediate their bioactivation shall be reviewed. For organic nitrates this is of particular interest, since clinical tolerance arises because mechanisms involved in their bioactivation become exhausted. In contrast however, both the molsidomine metabolite SIN-1 as well as nitroprusside are considered to act as direct NO donors since their biological activity is not limited by the mode of their bioactivation. The principles of NO¿s actions as well as the related biological activities of NO donors will be covered in this article. The vascular selectivity and dose dependency of the haemodynamic nitrate effects shall also be described as well as the potential interactions of nitrates with endothelium, thrombocytes and leukocytes. The significance of specific tolerance to nitrates and the loss of responsiveness due to neurohormonal counter-regulation, which has also been observed with molsidomine, shall be discussed. Newly acquired knowledge therefore justifies consideration of NO donors as therapeutic substitutes for the protective autacoid NO, which is the basis for further pharmacological and clinical development of NO donors.

Angina Pectoris↗
PubMedDate not supplied

[Antihistaminics].

The antihistamines are drugs who compete for the histamine receptor H-1, blocking the liberation of autacoid mediators, that is the reason for their action in allergic diseases. It's important to know the pharmacodynamics and pharmacokinetics of these drugs in order to choose the best one for the patient, looking for the ones who have less side effects and work better. We show a summary of the principal antihistamines, their actions and side effects.

Eicosanoids↗