Effect of PAF on the Cardiovascular System

Feuerstein, Giora; Goldstein, Robert E.

doi:10.1007/978-1-4684-5284-6_19

Cited by 22 publications

(14 citation statements)

References 63 publications

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“…For example, administration ofexogenous PAF to laboratory animals leads to cardiac dysfunction (18)(19)(20)28). However, this agent alters vascular tone, activates the sympathetic nervous system, and stimulates most cells ofthe systemic circulation (3,7,8,27). Thus, it is difficult to delineate specific cardiac effects in such models.…”

Section: Discussionmentioning

confidence: 99%

“…This phospholipid is now known to have profound ef-fects on many tissues including muscle cells, vascular tissue, and neurons (3)(4)(5). PAF can be synthesized in and released from many tissues including kidney, lung, and heart, as well as from cells in the circulation in response to appropriate stimuli (3,(6)(7)(8). Biochemical investigation into the biosynthesis of PAF indicates that heart muscle could be exposed to this molecule in a physiological setting.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Molecular and cellular actions of platelet-activating factor in rat heart cells.

Massey¹,

Kohout²,

Gaa³

et al. 1991

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Molecular and cellular actions of platelet-activating factor in rat heart cells.

Massey¹,

Kohout²,

Gaa³

et al. 1991

J. Clin. Invest.

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“…However, after the high dose of zymosan, a simultaneous decrease of right ventricular systolic pressure is observed. This reduction would result either from a direct effect of PAF on cardiac muscles, as already described in some circumstances in vitro (Feuerstein, 1989), or from a decrease of cardiac filling due to haemoconcentration and transient accumulation of blood in vasodilated systemic vessels stimulated by PAF. Indeed, the reduction of right ventricular systolic pressure was inhibited by the PAF antagonist.…”

Section: Discussionmentioning

confidence: 79%

“…The systemic hypotension depends mainly on the release of PAF which induces systemic vasodilatation in rats (Feuerstein, 1989). However, after the high dose of zymosan, a simultaneous decrease of right ventricular systolic pressure is observed.…”

Section: Discussionmentioning

confidence: 99%

Dissociation between the effects of zymosan on the systemic and pulmonary vessels of the rat

Damas

Lagneaux

1991

British J Pharmacology

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1 Zymosan, an activator of the alternative complement pathway, (2 to 16mgkg-1) injected intravenously via the tail vein of anaesthetized rats, dose-dependently increased the vascular permeability of lung parenchyma, as measured by the accumulation of 1251-labelled albumin in lungs. 2 Pretreatment of the animals with cyclo-oxygenase inhibitors, indomethacin or ketoprofen (3 mg kg 1) or with the lipoxygenase and cyclo-oxygenase inhibitor, BW755C (40mgkg-') abolished the vascular permeability changes induced by zymosan (16mg kg-1). Neither, the PAF antagonist, WEB 2086 (10mg kg-1) nor the antagonists of mast cell amines, mepyramine and methysergide (3mg kg-) affected the plasma exudation in lungs. Zymosan did not induce any accumulation of labelled albumin in lungs of rats made leucopenic by rabbit anti-neutrophil serum. 3 Zymosan (16mgkg-1) increased the haematocrit. This increase was not modified by indomethacin but reduced by WEB 2086. 3 Intravenous injection of zymosan (3 and 8 mgkg ')in anaesthetized rats transiently increased right ventricular blood pressure and pulmonary arterial pressure, accelerated respiratory rate and decreased systemic blood pressure. 5 WEB 2086 largely reduced the systemic hypotension but did not affect the increase of pulmonary vascular resistance. Indomethacin inhibited the increase of blood pressure in the right ventricle and the modification of the respiratory rate. This drug did not inhibit but increased the systemic hypotension induced by zymosan. 6 Zymosan (16mg kg-) reduced serum complement haemolytic activity by 46%. 7 These data suggest that the pulmonary vascular changes induced by intravascular complement activation with zymosan in rats are mediated by neutrophils and prostanoids while the systemic vascular effects depend mainly on PAF.

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“…The renal vasoconstrictor response to TRH, on the other band, is reduced to 50% in adrenal demedullated animals and the vasodilation in skeletal muscle almost totally inhibited by bretylium in these rats. As compared to the other known vasoactive substances such as epinephrine, norepinephrine, angiotensin, vasopressin or platelet activating factor ((11, 13,51], unpublished findings of our laboratory), the pattem ofthe changes in blood flow in skeletal muscle, mesenteric and renal vascular beds by TRH mostly resembled that induced by norepinephrine while all the other above mentioned agents induced totally different changes in blood flow as that produced by TRH. Furthermore, direct resolving of renal sympathetic nerve activity in anesthetized rats revealed a profound activation of nerve firing by TRH even at doses which did not affect the arterial pressure (Fig.…”

Section: The Role ~~R Thc Autonomie Nerl'lws Sy\·tcmmentioning

confidence: 81%

Cardiovascular pharmacology of thyrotropin releasing hormone

Sirén

1988

Peptides

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SIREN A.-L. Cardiovascu/ar pharmacology of thyrotropin releasing hormone. PEPTIDES 9: Suppt. l, [69][70][71][72][73] 1988.-Thyrot;opin releasing hormone (TRH) and its receptors are present in th~ car~iovascul~ nuclei ofthe brain as ~ell as in ~he intermediolateral cell column of spinal cord. Anatomical, neurophysiological, funchonal and pharmacological stud1es suggest that TRH is a neurotransmitter/neuromodulator in the centrat nervous system. Administration of TRH to experimental animals or human subjects induces pressor and tachycardic responses and increases plasma Ievels of catecholamines. These effects are likely tobe mediated by a central nervous system activation of the sympathoadrenomedullary system with no involvement of vasopressin or renin-angiotensm system. ln the conscious rat, the TR~-induced pressor response is accompanied by an increment in cardiac output and a distinct change in organ blood flow, a hmdquarter skeletal muscle vasodilation accompanied bv renal and mesenteric vasoconstriction. The rote ofTRH in hypertension has not been studied. However, the extremely potent pressor and vasoconstrictor properties of TRH makes this tripeptide a candidate for neurotransmitters/modulators involved in the development and/or maintenance ofhypertension. The role ofTRH in the therapy of shock is at present controversial. Though preliminary experimental work raised hopes and expectations for therapeutic usage of TRH in shock and trauma, the more recent studies have shown no effect or a detrimental effect for TRH in some experimental shock states. TRHBlood pressure Organ blood flow Sympathetic nerve activity THYROTROPIN releasing hormone (TRH, 1-pyroglutamyl-1-histidyl-1-prolinamide) was the first hypothalamic releasing factor to be isolated, chemically characterized and synthesized [43]. In addition to its neuroendocrine effects (TSH, prolactin, growth hormone release), this tripeptide has centrat nervous actions which are totally unrelated to its effect on the hypothalamopituitary axis (for review see [29,38]). The presence of TRH immunoreactivity and TRH receptors in brain areas related to the cardiorespiratory control, together with the extremely potent pressor and tachycardic actions of exogenously administered TRH suggest that this peptide might have a role in modulating the brain regulation of blood pressure and respiration. This review aims to summarize the sturlies on TRH in the centrat nervous system with special emphasis on the cardiovascular pharmacology of this peptide. TRH SYSTEM IN THE DRAINTRH immunoreactivity is unevenly distributed throughout the centrat nervous system (see [42,43]). Although the highest local concentrations are found in the hypothalamus (especially in the median eminence, periventricuJar arcuate, dorsomedial and ventromedial nuclei), more than 70% of the total CNS TRH is located in extrahypothalamic areas. Outside the hypothalamus high locallevels of TRH are found in the lateral nucleus of the septum in the limbic area and in the nucleus of the solitary tract (NTS) in the...

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Effect of PAF on the Cardiovascular System

Cited by 22 publications

References 63 publications

Molecular and cellular actions of platelet-activating factor in rat heart cells.

Molecular and cellular actions of platelet-activating factor in rat heart cells.

Dissociation between the effects of zymosan on the systemic and pulmonary vessels of the rat

Cardiovascular pharmacology of thyrotropin releasing hormone

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