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At least 289 records · Page 16Linked to original sources
PubMed1998

Ultrastructural correlates of the antidiuretic hormone-dependent and antidiuretic hormone-independent increase of osmotic water permeability in the frog urinary bladder epithelium.

Electron and confocal microscopy, using immunocytochemical methods, was employed to assess osmotic water permeability of the frog (Rana temporaria) urinary bladder during transcellular water transport, induced by antidiuretic hormone (ADH) or by wash-out of autacoids from serosal, ADH-free Ringer solution. The increase of osmotic water permeability of the urinary bladder was accompanied by relevant ultrastructural changes, the most remarkable being: (1) the appearance of aggregates of intramembranous particles in the apical membrane of granular cells, and the extent of the membrane area covered by the aggregates proportional to that of the water flow; (2) redistribution of actin filaments in the cytoplasm of granular cells; judging from the anti-actin label density, the number of actin filaments in the apical region of cytoplasm was reduced by 2.5-4 times compared with normal; (3) a decrease in the total electron density of the cytoplasm due to the increased water content of granular cells.

Actins↗
PubMedDate not supplied

Discovery of some of the biological effects of nitric oxide and its role in cell signaling.

The role of nitric oxide in cellular signaling in the past 22 years has become one of the most rapidly growing areas in biology with more than 20,000 publications to date. Nitric oxide is a gas and free radical with an unshared electron that can regulate an ever-growing list of biological processes. In many instances nitric oxide mediates its biological effects by activating guanylyl cyclase and increasing cyclic GMP synthesis from GTP. However, the list of effects of nitric oxide that are independent of cyclic GMP is also growing at a rapid rate. For example, nitric oxide can interact with transition metals such as iron, thiol groups, other free radicals, oxygen, superoxide anion, unsaturated fatty acids and other molecules. Some of these reactions result in the oxidation of nitric oxide to nitrite and nitrate to terminate its effect, while other reactions can lead to altered protein structure, function, and/or catalytic capacity. These diverse effects of nitric oxide that are either cyclic GMP dependent or independent can alter and regulate important physiological and biochemical events in cell regulation and function. Nitric oxide can function as an intracellular messenger, an autacoid, a paracrine substance, a neurotransmitter, or as a hormone that can be carried to distant sites for effects. Thus, it is a unique simple molecule with an array of signaling functions. However, as with any messenger molecule, there can be too little or too much of the substance and pathological events result. Some of the methods to regulate either nitric oxide formation, metabolism, or function have been in clinical use for more than a century as with the use of organic nitrates and nitroglycerin in angina pectoris that was initiated in the 1870's. Current and future research with nitric oxide and cyclic GMP will undoubtedly expand the clinicians' therapeutic armamentarium to manage a number of important diseases by perturbing nitric oxide and cyclic GMP formation and metabolism. Such promise and expectations have obviously fueled the interests in these signaling molecules for a growing list of potential therapeutic applications.

Animals↗
PubMed2002

Mechanisms of pressure natriuresis.

A central component of the feedback system for long-term control of arterial pressure is the pressure-natriuresis mechanism, whereby increases in renal perfusion pressure lead to decreases in sodium reabsorption and increases in sodium excretion. The specific intrarenal mechanism for the decrease in tubular reabsorption in response to increases in renal perfusion pressure appears to be related to increases in hemodynamic factors such as medullary blood flow and renal interstitial hydrostatic pressure (RIHP), and renal autocoids such as nitric oxide, prostaglandins, kinins, and angiotensin II. Increases in renal perfusion pressure are associated with significant increases in RIHP, nitric oxide, prostaglandin E2, and kinins, and decreases in angiotensin II. The mechanism whereby RIHP increases in the absence of discernible changes in whole kidney renal blood flow and peritubular capillary hydrostatic and/or oncotic pressures may be related to increases in renal medullary flow as a result of nitric oxide-induced reductions in renal medullary vascular resistance. Several lines of investigation support an important quantitative role for RIHP in mediating pressure natriuresis. Preventing RIHP from increasing in response to increases in renal perfusion pressure markedly attenuates pressure natriuresis. Furthermore, direct increases in RIHP, comparable to increases measured in response to increases in renal perfusion pressure, have been shown to significantly decrease tubular reabsorption of sodium in the proximal tubule and increase sodium excretion. The exact mechanism whereby RIHP influences tubular reabsorption is unknown, but may be related to alterations in tight junctional permeability to sodium in proximal tubules, redistribution of apical sodium transporters, and/or release of renal autacoids such as prostaglandin E2.

Blood Pressure↗
PubMed1991

Drug-induced modification of vascular structure: effects of antihypertensive drugs.

It has long been realized that hypertension causes alterations in the peripheral vasculature, with the arterial wall becoming thicker and the lumen relatively smaller. This is particularly true in small resistance arteries, but larger vessels are also affected. The precise mechanisms remain to be determined, although it is highly likely that growth-promoting autacoids are involved as well as mechanical forces. Numerous studies of hypertension in animal models and a few in hypertensive humans have tried to establish the reversibility of these changes after successful lowering of blood pressure. Too few data are available to form firm conclusions, but thiazides and hydralazine-like vasodilators appear to have only a minimal effect on the vasculature. On the other hand, angiotensin-converting enzyme inhibitors are clearly effective, and alpha-blockers may be active. However, it is difficult to derive even tentative conclusions from the available information on calcium antagonists and beta-blockers. These results are discussed in the context of future therapeutic and investigative approaches.

Animals↗
PubMed1992

Nitrates in different vascular beds, nitrate tolerance, and interactions with endothelial function.

The favorable anti-ischemic effect of nitrates is based on the unique distribution pattern of vascular relaxation that they evoke in different vascular sections. Nitrovasodilators reduce cardiac preload and wall tension, and thus myocardial oxygen consumption. They increase precollateral coronary perfusion pressure, thereby augmenting oxygen delivery to ischemic sections, especially to the subendocardial layers. These vasodilator actions are caused by the nitric oxide (NO)-induced activation of soluble guanylyl cyclase, which augments vascular cyclic guanosine monophosphate (cGMP) levels to suppress intracellular Ca2+ concentrations. After some metabolic steps NO is finally cleaved from all nitrovasodilators and is probably identical with, or very closely related to, endothelium-derived relaxing factor (EDRF). A dinitrosyl-iron complex may serve under biologic conditions to stabilize the NO- radical, which has an extremely short half-life. NO derived from nitrovasodilators is used therapeutically to substitute for a deficient endothelium-mediated vascular control and autacoid production.

Animals↗
PubMed1985

Eicosanoids as bioregulators in clinical medicine.

Formation of eicosanoids in stimulated cells and tissues is a ubiquitous phenomenon, but the precise physiologic or pathophysiologic role of these autacoids has not yet been defined. In contrast, understanding of synthetic mechanisms, metabolism, and catabolism of eicosanoids seems to have surpassed understanding of their pharmacologic actions. Early clinical research involving eicosanoids focused on reactions of the cyclo-oxygenase pathway, which are inhibitable by nonsteroidal anti-inflammatory drugs. The lipoxygenase pathway, which appears to be an important component of the allergic and inflammatory response, represents a new area of clinical research.

Arachidonic Acids↗
PubMed1986

Prostaglandins and nonsteroidal anti-inflammatory drugs. Effects on renal hemodynamics.

Renal prostaglandins are important modulators of renal hemodynamic function. Their synthesis from arachidonic acid precursor is regulated by neurohumoral vasoactive substances as well as by intrarenal factors. Endogenous renal prostaglandins exert little influence on renal blood flow and glomerular filtration rate in the basal state. In contrast, inhibition of cyclooxygenase-dependent arachidonic acid metabolism with nonsteroidal anti-inflammatory drugs in states of decreased renal perfusion causes marked alterations in these variables. Thus, clinical states characterized by decreased intravascular volume (decreased effective blood volume) with decreased renal perfusion augment the activity of various neurohumoral vasoactive systems and result in an increased dependence of renal hemodynamics on endogenous renal prostaglandin synthesis, which is stimulated, in a compensatory manner, by these same systems. The development of newer drugs that undergo biotransformation in the kidney between active and inactive forms may permit a lesser degree of renal cyclooxygenase inhibition, with the possibility of a reduction in the adverse effects on renal blood flow and glomerular filtration rate. Appropriate clinical use of nonsteroidal anti-inflammatory drugs requires careful consideration of the potential deleterious consequences of prostaglandin synthesis inhibition. Prostaglandins are considered to be autacoids and, as such, they exert their physiologic actions close to or at the site of synthesis. Therefore, production of prostaglandins, thromboxanes, and, possibly, leukotrienes in the renal cortex by the constituent cells of the glomeruli and the arterioles would be anticipated to influence their hemodynamic functions, that is, glomerular filtration rate, renal blood flow, renal vascular resistance, and juxtaglomerular granular cell renin release.

Animals↗
PubMed1986

Eicosanoids in experimental and human renal disease.

The renal prostaglandins and thromboxanes are powerful autacoids with potential effects on renal hemodynamics, salt and water metabolism, and the immune system. The possibility of adverse effects on renal function in certain patients with renal disease due to cyclooxygenase inhibition with nonsteroidal anti-inflammatory drugs has long been appreciated. Experimental evidence indicates that renal prostaglandin and thromboxane production is increased in several models of renal disease and that similar decrements in renal function occur with cyclooxygenase inhibition and may be due to inhibition of vasodilator prostaglandins. Additionally, several investigators have shown that administration of prostaglandins may be therapeutic in some forms of renal disease, particularly immunologically mediated diseases. Dietary modification to affect prostaglandin production has also been promising in certain experimental models. In contrast to vasodilator prostaglandins, thromboxane is a potent vasoconstrictor and would be expected to have adverse effects on renal function. Despite demonstration of elevated glomerular thromboxane, studies using inhibitors of thromboxane synthesis in immunologically mediated glomerular disease have been disappointing. There is some evidence, however, that these drugs may be of benefit in ureteric obstruction and renal transplant rejection.

Acute Kidney Injury↗
PubMed1989

Alpha 2-adrenoceptors and endothelium-derived relaxing factor.

The endothelium can release potent vasodilator substances, in particular prostacyclin and endothelium-derived relaxing factor. The triggers for the release of endothelium-derived relaxing factor include increases in levels of shear stress, neurotransmitters, autacoids, platelet products, and hormones. The endothelium-dependent response to catecholamines involves stimulation of alpha 2-adrenoceptors on the endothelial cells. Indeed, in a number of blood vessels, selective alpha 2-adrenergic agonists cause endothelium-dependent relaxations. These are seen most typically in blood vessels with long-term exposure to high flows and high partial pressures of oxygen. In addition to the release of endothelium-derived relaxing factor, alpha 2-adrenergic agonists can stimulate postjunctional (postsynaptic) alpha 2-adrenoceptors on vascular smooth muscles. These receptors, which are more abundant in hypertensive blood vessels, activate the contractile process. However, the alpha 2-adrenergic vasoconstrictors act as partial agonists (with a limited receptor reserve) and hence their vasoconstrictor response is very sensitive to functional antagonists such as endothelium-derived relaxing factor. Thus, the presence of endothelial cells can blunt the vasoconstrictor response to these substances not only because of an augmented release of endothelium-derived relaxing factor but also because the vasoconstriction that they induce is particularly susceptible to the inhibitory effect of the factor.

Animals↗
PubMed1983

An assessment of the participatory role of prostaglandins and serotonin in the pathophysiology of endotoxic shock.

The well-documented acute cardiodynamic changes in canine endotoxemia were significantly altered by pretreatment with either a newly synthesized serotonin receptor antagonist (ketanserin) or with a prostaglandin synthetase inhibitor (indomethacin). Ketanserin, but not indomethacin, significantly attenuated the endotoxin-induced pulmonary hypertension and vasoconstriction but had no effect on the typical systemic hemodynamic changes. In sharp contrast, indomethacin significantly attenuated systemic hypotension and enhanced peripheral vascular resistance. Neither drug influenced the typical acute fall in cardiac output or the capillary permeability edema; neither drug attenuated the metabolic acidosis of endotoxemia. These results imply that, although serotonin and the prostaglandins each participate in a unique manner in the pathophysiology of experimentally induced endotoxic shock, neither autacoid appeared singularly responsible for the hemodynamic and metabolic alterations consistently observed.

Animals↗
PubMed1990

Detection of platelet-activating factor in amniotic fluid of complicated pregnancies.

The ether phospholipid PAF (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine) was originally described as a potent bioactive lipid associated with inflammatory responses. More recently, we have suggested a functional role for PAF in fetal lung maturation and the initiation of parturition. Previously, PAF was detected in the amniotic fluid of women at term during labor. A significant proportion of this PAF was associated with a lamellar body-enriched fraction. In addition, the PAF concentration was elevated in fetal rabbit lung during the latter stages of gestation and in human fetal lung in organ culture. It was therefore concluded that the PAF present in amniotic fluid during labor was, in part, of fetal lung origin. In the reported study, amniotic fluid samples were obtained from a group of patients with uncomplicated pregnancies at term "not in labor" and "in labor" and a group with complicated pregnancies. We found an eightfold greater concentration of PAF in amniotic fluid obtained from the "term, in labor" samples compared with that of the "term, not in labor" samples (40 vs. 312 fmol/ml). A twentyfold elevation in PAF (838 fmol/ml) was evident in the amniotic fluid of patients incurring "preterm labor" with an average gestational age of 32 weeks compared with the "term, not in labor" group. PAF concentrations also were elevated to 756 fmol/ml amniotic fluid in a group of patients with an average gestational age of 31.5 weeks who had premature rupture of membranes. We have previously suggested that a second autacoid, PAF, in addition to eicosanoids, may function in the initiation of parturition at term in uncomplicated pregnancies. On the basis of our findings of a severalfold increase in the PAF concentration in amniotic fluid from complicated pregnancies, it is suggested that this potent activator of myometrial contraction, together with the eicosanoids, may be a contributing factor associated with premature labor.

Amniotic Fluid↗
PubMed1991

Anticardiolipin antibody-positive serum enhances endothelial cell platelet-activating factor production.

Circulating antiphospholipids have been linked to recurrent pregnancy loss by a mechanism involving placental and decidual thrombosis. We hypothesized that platelet-activating factor, an autacoid synthesized by vascular endothelium, might mediate this phenomenon through its ability to promote platelet aggregation and fibrin deposition. Alternatively, antiphospholipid antibodies might exert a procoagulant effect by inhibiting the synthesis of prostacyclin. To evaluate these theories, endothelial cells (harvested from human umbilical veins) were grown to confluence and incubated for 48 hours with 20% concentrations of anticardiolipin antibody-positive and -negative human sera as well as fetal bovine serum. After incubation culture wells were stimulated with 10 mumol/ml calcium ionophore A23187 (an agonist of platelet-activating factor and prostacyclin synthesis). Intracellular platelet-activating factor was measured by tritiated acetate incorporation, phospholipid extraction, thin-layer chromatography, and scintillation spectrophotometry. Enhanced platelet-activating factor synthesis was identified in cultures incubated with anticardiolipin antibody-positive serum (25,544 +/- 2604 disintegrations per minute, mean +/- SD) when compared with anticardiolipin antibody-negative serum (18,600 +/- 3316 dpm) or fetal bovine serum (19,014 +/- 4233 dpm; analysis of variance, p = 0.033). In similar experiments, prostacyclin synthesis was determined by measuring its primary metabolite, 6-keto-prostaglandin F1 alpha, in culture supernatants. No differences between anticardiolipin antibody-positive and control cultures were observed (analysis of variance, p = 0.90). We conclude that in this endothelial cell model, anticardiolipin antibody-positive serum enhances ionophore-mediated platelet-activating factor synthesis but has no apparent effect on the production of prostacyclin. These findings suggest a potential role for platelet-activating factor in anticardiolipin antibody-mediated vascular thrombosis.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Release of vasoactive substances during cardiopulmonary bypass.

Cardiopulmonary bypass is associated with bleeding and thrombotic complications, massive fluid shifts, and cellular and hormonal defense reactions that are collectively termed "the whole body inflammatory response." A host of vasoactive substances are produced, released or altered during cardiopulmonary bypass. These hormones, autacoids, and cytokines react with specific receptor proteins distributed throughout the body, and mediate the vascular smooth muscle and endothelial cell contractions that are responsible for much of the morbidity associated with open heart operations. This essay briefly reviews the actions, sources, and perturbations of the approximately 25 vasoactive substances known or believed to be altered by cardiopulmonary bypass, and provides an introductory reference list.

Cardiopulmonary Bypass↗
PubMed1994

Adenosine in blood cardioplegia prevents postischemic dysfunction in ischemically injured hearts.

Adenosine (ADO) is an endogenous cardioprotective autacoid that exerts receptor-mediated cardioprotection from ischemic-reperfusion injury. This study tested the hypothesis that blood cardioplegia (BCP) supplemented with ADO reduces postischemic left ventricular dysfunction in ischemically injured hearts. Twenty-one anesthetized dogs on total bypass were subjected to 30 minutes of normothermic global ischemia. Cold (4 degrees C) potassium BCP was then delivered every 20 minutes for 60 minutes of cardioplegic arrest. In 7 dogs, unsupplemented BCP was used; in 7 dogs, BCP was supplemented with 400 mumol/L ADO; and, in 7 dogs, ADO receptors were blocked with 8-p-sulfophenyltheophylline (30 mg/kg) given with 400 mumol/L ADO in BCP. Preischemic and postischemic left ventricular systolic function was assessed by the slope and volume axis intercept of the end-systolic pressure-volume (impedance catheter) relationship (ESPVR). In unsupplemented BCP, the postischemic slope of the ESPVR was significantly depressed by 42% versus the preischemic value (from 6.8 +/- 1.2 mm Hg/mL to 3.9 +/- 0.4 mm Hg/mL; p < 0.05 versus the preischemic value). In contrast, BCP supplemented with ADO was found to restore the postischemic ESPVR slope to preischemic levels (7.7 +/- 1.0 mm Hg/mL versus 7.4 +/- 1.2 mm Hg/mL, respectively). This cardioprotection was reversed by 8-p-sulfophenyltheophylline (9.9 +/- 1.5 mm Hg/mL versus 4.5 +/- 0.7 mm Hg/mL; p < 0.05 versus the preischemic value). Postischemic plasma creatinine kinase activity was elevated equally in all groups over the baseline values. We conclude that ADO in BCP attenuates postcardioplegia dysfunction in severely injured hearts through the operation of receptor-mediated mechanisms.

Adenosine↗
PubMed1985

Binding of prostaglandin E1 to human erythrocyte membrane.

Prostaglandin E1 is known to alter the structural and functional characteristics of red blood cells, yet, little is understood about the membrane receptors mediating this process. We therefore studied the binding of tritium-labeled prostaglandin E1 to the intact human erythrocyte membrane and demonstrated that the interaction is highly specific, rapid, saturable and reversible. Scatchard analysis of prostaglandin E1 binding to the membrane preparations showed the presence of two independent classes of prostaglandin E1 binding sites which differed in their affinity for the autacoid. The high-affinity class had Kd = 3.6 X 10(-9) M and the low-affinity class had Kd = 5.6 X 10(-5) M. The optimum pH for the binding of [3H]prostaglandin E1 to the erythrocyte membrane was found to be around 7.5 and maximum specific binding occurred at a concentration of 5 mM Mg2+ in the incubation mixture. [3H]Prostaglandin E1 bound to the membrane preparation could not be displaced by GTP or by its stable derivative Gpp[NH]p. However, prostaglandin E1 bound to the erythrocyte membrane preparation could be rapidly displaced by cyclic AMP. The IC50 (concentration of the nucleotide displacing 50% bound [3H]prostaglandin E1 from the membrane) was 75 nM. Other adenine nucleotides or cyclic GMP could not substitute for cyclic AMP. Unlike the right-side-out erythrocyte membrane, the inside-out membrane preparations do not bind [3H]prostaglandin E1. Treatment of right-side-out erythrocyte membrane preparation with neuraminidase markedly decreases the binding of prostaglandin E1. Incubation of the erythrocyte membrane preparation with trypsin resulted in total loss of the binding activity. These results indicate that the prostaglandin E1 binding sites located on the cell surface and sialic acid residues are required for prostaglandin E1 binding to the human erythrocytes. These results also indicated that the binding sites are glycoprotein in nature.

Adenylyl Cyclases↗
PubMed1988

Selective hydrolysis of ether-containing glycerophospholipids by phospholipase A2 in rabbit lung.

The role of phospholipase A2 (PLA2) in the simultaneous generation of lyso-platelet-activating factor and arachidonic acid was investigated by examining the calcium dependency and substrate specificity of PLA2 activities in rabbit lung microsomes. Alkylarachidonoylglycerophosphocholine (alkylarachidonoyl-GPC) was preferentially hydrolyzed as compared to acylarachidonoyl-GPC, and both arachidonate-containing substrates were cleaved to a greater extent as compared to alkyl- and acyl-substrates with oleate at the sn-2 position. Hydrolysis of alkylacyl-GPC substrates was not dependent on calcium in the presence of EGTA (1 mM); however, addition of calcium (2 mM) increased hydrolysis of acylarachidonoyl-GPC 2-fold and hydrolysis of acyloleoyl-GPC 10-fold. Substitution of an alkenyl group in the sn-1 position further enhanced calcium-independent PLA2 hydrolysis, and another substitution of arachidonic acid at the sn-2 position of the plasmalogen substrates substantially increased hydrolysis as compared to hydrolysis of substrates containing oleic acid. Hydrolysis of the choline plasmalogen was 3-fold greater than hydrolysis of the ethanolamine plasmalogen containing arachidonate. Preferential calcium-independent hydrolysis of alkylacyl-GPC substrates was observed in several tissues, including adult and fetal rabbit lung and adult rabbit kidney and human amnion. PLA2 substrate specificity may account for the preferential hydrolysis of arachidonoyl-containing alkyl-GPC in several cell types and explain the simultaneous generation of the precursors of two potent autacoids, platelet-activating factor and eicosanoids.

Aging↗
PubMed1992

Heterogeneity of arachidonate and paf-acether precursor pools in mast cells.

In mammalian cells, arachidonate release and paf-acether formation are frequently associated. The alkyl-acyl-GPC has been proposed as an important source for released arachidonic acid and arachidonate-containing alkylacyl-GPC species as unique precursor for paf-acether. However, the specificity of precursor pools either concerning arachidonic acid or paf-acether is still a matter of controversy. We studied the relationship between the precursor pools for both autacoids in antigenically-stimulated cultured mast cells. We took advantage of the particular arachidonate turnover rate in each phospholipid to investigate the role of alkyl-arachidonyl-GPC in the supply of arachidonic acid by using newly and previously [14C]arachidonate-labeled cells. The specific activity of the released arachidonate was reduced 2-fold following overnight cell incubation, whereas labeling in alkyl-arachidonoyl-GPC was only slightly modified and never corresponded to that of released arachidonate when newly or previously labeled cells were triggered with the antigen. These results are not in favor of a major role for alkyl-arachidonoyl-GPC in supplying arachidonate. In contrast, by using previously labeled cells, we demonstrated that all arachidonate-containing phospholipids were involved in the release of arachidonic acid. The pattern of alkyl chains in alkyl-arachidonoyl-GPC, as well as in total alkylacyl-GPC, is unique since it consists mainly of 18:1 (more than 55%), whereas the 16:0 represents only about 30% of total alkyl chains. Therefore, we analyzed paf-acether molecular composition in order to compare it to the alkyl composition of the precursor pools. The content in 18:1 species of paf-acether, as measured by bioassay (aggregation of rabbit platelets), was always lower than that of 16:0 species and then did not correspond to the alkyl composition of the precursor. These data suggest that the enzymes involved in paf synthesis might be specific for 16:0 alkyl chains of precursor pool.

Acetyltransferases↗
PubMed1995

Molecular heterogeneity of PAF in normal human mixed saliva: quantitative mass spectral analysis after direct derivatization of PAF with pentafluorobenzoic anhydride.

Platelet-activating factor (PAF), a family of phospholipid autacoids with potent pro-inflammatory activities, is present in saliva. The current study has quantitated various species of PAF isolated from normal human mixed saliva. Choline-containing, sn-2 acetylated phospholipids with sn-1 ether- or ester-linked fatty alcohol/acid moieties (alkyl-PAF or acyl-PAF, respectively) were evaluated after direct derivatization with pentafluorobenzoic (PFB) anhydride. Individual species of PFB-derivatized PAF were separated by gas chromatography prior to mass spectral analysis; quantitative estimates of six different species of PAF in saliva were made by comparison to corresponding authentic, synthetic PAF standards. In each saliva sample, all six species of PAF were readily detected by this facile procedure. The predominant PAF was 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine or 16:0-alkyl-PAF (0.75 +/- 0.09 pmol/ml saliva; mean +/- S.E.; n = 5) which represented only 30.4 +/- 1.5% of the total PAF. Substantial amounts of 18:1- and 18:0-alkyl-PAF and 16:0-acyl-PAF were also identified (0.52 +/- 0.07, 0.35 +/- 0.06, and 0.35 +/- 0.02 pmol/ml saliva, respectively). In summary, mass spectrometric analysis of PAF after direct derivatization with PFB anhydride has revealed that at least six different species of PAF are present in normal human mixed saliva. This structural diversity may represent an important aspect of homeostasis in the healthy oral cavity.

Anhydrides↗