Les animaux médecins d'eux-mêmes ?

RésuméLe regard posé par l'homme sur l'animal est-il une contribution à l'archéologie du savoir médical ? Déjà Aristote, au ive siècle avant notre ère, faisait des observations pertinentes sur le chien "mangeant une certaine herbe". Il y a de nombreux exemples, plus modernes et bien documentés, d'animaux recherchant "ce qui est bon pour eux" (Huffman et son école). Mais cette expression court le risque d'être anthropomorphique. Il y a un langage secret des animaux qu'ont entrevu sans doute les auteurs des "contes initiatiques des bergers Peuls" mais que de plus récentes observations confirment. Il y a en effet toute une série de médiations (physiques, chimiques, ...) possibles entre l'animal et son environnement. A ces messages correspondent des récepteurs, des organes adaptés et on doit même évoquer la réalité et la variété d'échanges de signaux dans le règne animal et végétal."Un jour, il y a très longtemps - alors que les animaux et les hommes se comprenaient encore" (Amidou Hampâté Bâ,1999

Allelic and tissue variation of rat fumarate hydratase (E.C. 4.2.1.2.)

1. 1. The polymorphism (two alleles at a single autosomal locus) of rat fumarate hydratase is described. 2. It provides a confirmatory genetic evidence for the tetrameric structure of the enzyme. 3. It is shown that fumarase may exist into two electrophoretically different (tissue-specific) forms. © 1976.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Chronic Exposure of Pigs to Airborne Dust and Endotoxins in an Environmental Chamber: Technical Note

A new experimental setup was developed to expose pigs to dust and airborne endotoxins in an environmental chamber, at levels liable to be encountered in pig farm buildings. The following parameters were evaluated in a chamber containing two pigs of 10 kg body-weight: inhalable and respirable dust gravimetric concentrations were measured using area samplers and expressed as mg/m3. The respirable dust concentration was also measured using a "TM digital microP respirable dust-measuring instrument', which has been shown to give similar results to the gravimetric method. The endotoxin concentration was evaluated using the Limulus-assay and expressed as ng/m3 of air containing the inhalable or respirable dust or as ng/mg of inhalable and respirable dust. Feed flour dust was introduced into the chamber to obtain different concentrations of inhalable and respirable dust ranging from 3.62 to 76.66 mg/m3 and from 0.24 to 1.40 mg/m3, respectively. The endotoxin concentration was modulated by mixing the feed flour with Escherichia coli endotoxins before blowing it into the chamber. The endotoxin concentrations in the air containing inhalable or respirable dust ranged from 28.9 to 270.0 ng/m3 and from 2.22 to 36.38 ng/m3, respectively, depending on the amount of endotoxins added to the dust. Data were also obtained in a piggery. The experimental setup detailed in this paper could be used to study the significance of air contaminants in the development of pig respiratory diseases

Endogenous nitric oxide modulates acetylcholine-induced edema and vasoconstriction in isolated perfused rabbit lungs.

The modulatory role of endogenous nitric oxide (NO) on pulmonary edema induced by acetylcholine (ACh), capsaicin, substance P (SP) and 5-hydroxytryptamine (5-HT) was investigated by using an inhibitor of NO synthase, N-omega-nitro-L-arginine (L-NNA). The effects of endogenous NO on the hemodynamic response to ACh, 5-HT and SP were also investigated. The capillary filtration coefficient (Kf,c), the total pressure gradient (delta Pt) and its four components [arterial (delta Pa), pre- (delta Pa') and post-capillary (delta Pv'), and venous gradient (delta Pv)] were evaluated on isolated, ventilated, perfused rabbit lungs. ACh (10(-8) to 10(-4) M) and SP (10(-10) to 10(-6) M) induced a concentration-dependent increase in the Kf,c. Capsaicin (10(-4) M) and 5-HT (10(-4) M) also increased this parameter. L-NNA (10(-4) M) completely inhibited the effects of ACh and capsaicin on the Kf,c, without preventing the effects of SP and 5-HT. ACh induced a concentration-dependent vasoconstriction in the precapillary segment. Pretreatment with L-NNA enhanced this increase in delta Pa' but also increased delta Pv' and delta Pv. 5-HT increased delta Pt and delta Pa proportionally to the concentration. This effect was enhanced by L-NNA, which also increased delta Pa'. SP had no significant hemodynamic effect. Pretreatment with L-NNA did not modify the response to SP. Sodium nitroprusside (10(-5) M) induced a left shift of the concentration-response curve to ACh on the Kf,c, although it did not change the response to SP. Sodium nitroprusside also inhibited the hemodynamic effect of ACh. It was concluded that endogenous NO is involved in ACh-and capsaicin-induced edema via a prejunctional stimulatory effect on the C-fibers. Endogenous NO can also modulate ACh- and 5-HT-induced vasoconstriction by exerting a vasodilator action on the whole pulmonary vascular bed

Role of Neuropeptides in Acetylcholine-Induced Edema in Isolated and Perfused Rabbit Lungs

Changes in pulmonary endothelial permeability and in microvascular hemodynamics in response to cumulative concentrations of acetylcholine (ACh) (10(-8) M to 10(-5) M) were investigated in isolated, perfused rabbit lungs. The total pressure gradient was partitioned into four components: arterial, pre- and postcapillary and venous. The capillary filtration coefficient (Kf, c) also was evaluated. ACh caused a significant increase in arterial and precapillary pressures at concentrations higher than 3 x 10(-6) M. The total pressure gradient and precapillary were significantly increased whereas arterial, postcapillary and venous pressure gradient remained unchanged. In papaverine (3 x 10(-4) M)-pretreated lungs, the vasoconstriction was abolished and a concentration-dependent increase in Kf,c was recorded from 10(-8) to 10(-5) M ACh. This reaction was accompanied by pulmonary edema. Atropine, indomethacin, aspirin, ketanserin, clonidine, morphine and (+/-)-CP 96-345, an antagonist of neurokinin NK1 receptors, completely prevented the effects of ACh on Kf,c. In contrast, cromolyn sodium and SR48968, a neurokinin NK2 antagonist, did not inhibit the response to ACh. Terfenadine together with cimetidine had a partially inhibitory effect. Changes in the Kf, c similar to those observed with ACh were induced by capsaicin (10(-4) M) by exogenous substance P (10(-7) M) and by 5-hydroxytryptamine (5-HT) (10(-4) M). The effects of SP were inhibited by aspirin, (+/-)-CP 96,345 and ketanserin, but not by atropine and antihistaminics. 5-HT effects were prevented by aspirin and not by (+/-)-CP 96,345. It was concluded that ACh-induced pulmonary edema was due to an increase in the capillary filtration coefficient.(ABSTRACT TRUNCATED AT 250 WORDS

Toxicité des herbicides chez les animaux domestiques

peer reviewe

Le récepteur NMDA : base moléculaire du mécanisme d’action de la kétamine

peer reviewe

Multiple muscarinic receptor subtypes mediating pulmonary oedema in the rabbit.

The effects of various muscarinic antagonists on acetylcholine (ACh)-induced pulmonary oedema were studied in isolated perfused rabbit lungs. ACh induced a dose-dependent increase in the capillary filtration coefficient (Kf,c). This effect has been previously related to the activation of the capsaicin-sensitive nerve fibres and the release of substance P. Atropine, pirenzepine (M1-selective antagonist) and 4-DAMP (M3-selective antagonist) altered this response, producing a dose-dependent shift to the right of the ACh concentration-Kf,c response curve. By contrast, the M2-selective antagonist AFDX-116 shifted the ACh concentration-response curve to the left. Atropine, pirenzepine and 4-DAMP also significantly reduced the capsaicin-induced increase in the Kf,c, while AFDX-116 enhanced it. We conclude that multiple muscarinic receptor subtypes are present in the rabbit lung, located on the C-fibres, and are involved in the ACh-induced pulmonary oedema. M1 and M3 receptors seem to stimulate the release of neuropeptides from C-fibres, whereas M2 receptors have an inhibitory effect on these fibers