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Biomedical subjects

H Juan

Publications and source records attributed to H Juan.

68 records · Page 4Linked to original sources
PubMed1977

Inhibition of the algesic effect of bradykinin and acetylcholine by mepacrine.

1. The isolated perfused rabbit ear connected to the body by its nerve only was used to investigate the influence of mepacrine on the algesic effect of bradykinin and acetylcholine. For comparison, quinidine was included in this investigation. 2. Infusion of mepacrine or quindine (2-10 microgram/ml) into the rabbit ear reduces the algesic effect of bradykinin as well as of acetylcholine in proportion to the dose. 3. Infusion of postglandin E1 (10 ng/ml) in addition to mepacrine or quinidine restores theinhibited algesic effect of bradykinin more than that of acetylcholine. 4. Mepacrine and quinidine (10 microgram/ml) reduce the brief vasoconstriction elicited by bradykinin in the rabbit ear. 5. The results suggest that mepacrine or quinidine reduce the algesic effect of bradykinin primarily by inhibiting the release of E-type prostaglandins which sensitize pain receptors and secondarily by an unspecific antagonism (local-anaesthetic action). The effect of acetylcholine, however, appears to be reduced mainly by an unspecific antagonism.

Acetylcholine↗
PubMed1977

The function of prostaglandins in transmucosal water movement and blood flow in the rat jejunum.

1. Jejunal loops of anaesthetized rats were perfused with isotonic buffer containing PGE1, PGF2alpha or indomethacin. Intestinal blood flow, absorption and secretion of tritiated water were measured. 2. PGE1 at the low concentration of 0.1 microgram ml-1 did not influence intestinal blood flow but increased secretion and decreased absorption of tritiated water. In higher concentrations (0.5 and 6.5 microgram ml-1), blood flow, secretion and absorption were enhanced. 3. PGF2alpha, even in the high concentration of 50 microgram ml-1, did not influence intestinal blood flow but enhanced secretion and decreased absorption of tritiated water. 4. Indomethacin (1 microgram ml-1) decreased intestinal blood flow and secretion but enhanced absorption of tritiated water. 5. The effects of indomethacin on blood flow can be prevented and those on secretion can be even reversed by an additional infusion of PGE1 (0.5 microgram ml-1). 6. PGs appear to play a physiological role in the regulation of intestinal blood flow and transmucosal water movement, since inhibition of endogenous PG synthesis by indomethacin results in effects opposite to those of intraluminally applied PGE1. The results obtained with the low concentration of PGE1 (0.1 microgram ml-1) and with PGF2alpha (50 microgram ml-1) strongly indicate that intestinal water movement can be changed independently of intestinal blood flow.

Animals↗
PubMed1977

Prostaglandin F2alpha reduces the algesic effect of bradykinin by antagonizing the pain enhancing action of endogenously released prostaglandin E.

1 The isolated perfused ear of the rabbit connected to the body only by its nerve, was used to investigate the influence of prostaglandin F2alpha on the algesic effect of bradykinin and acetylcholine. 2 Bradykinin and acetylcholine, following intra-arterial injection into the isolated perfused ear elicited a dose-related reflex fall in blood pressure due to stimulation of paravascular pain receptors (= algesic effect). 3 Infusion of prostaglandin F2alpha (0.1 to 1 ng/ml) into the rabbit ear reduced the algesic effect of bradykinin but not that of acetylcholine. 4 The onset of the reflex fall in blood pressure by bradykinin but not that by acetylcholine was delayed by infusion of prostaglandin F2alpha into the ear. 5 Infusion of prostaglandin E1 into the rabbit ear led to an enhancement of the algesic effect of bradykinin and acetylcholine. Enhancement of both effects was abolished by infusion of prostaglandin F2alpha. 6 During inhibition of the endogenous synthesis of prostaglandins (mainly E-type) by indomethacin, a low concentration of prostaglandin F2alpha no longer reduced the algesic effect of bradykinin. However, a high concentration of F2alpha continued to enhance the effect of bradykinin and acetylcholine. 7 Prostaglandin F2alpha influenced neither the brief reduction in venous outflow produced by bradykinin nor the brief increase in venous outflow caused by acetylcholine. 8 The results suggest that prostaglandin F2alpha does not directly reduce the effect of bradykinin but inhibits the enhancement of its algesic effect produced by prostaglandin E that is released endogenously by bradykinin. That the algesic effect of acetylcholine is not reduced by prostaglandin F2alpha is in keeping with its releasing very little endogenous prostaglandin E.

Acetylcholine↗
PubMed1976

Release of prostaglandins by bradykinin as an intrinsic mechanism of its algesic effect.

1. The release of PGs from the isolated perfused rabbit ear was measured by means of a radioimmunoassay. 2. Bradykinin in dose dependent amounts released mainly PGE (presumably PGE1) and in much smaller amounts also PGF. 3. Bradykinin released similar amounts of PGE in innervated and chronically denervated ears. 4. Indomethacin completely prevented the PGE release by bradykinin. 5. ACh showed a much lower efficacy than bradykinin in releasing PGE and PGF. Synthetic substance P was devoid of any PGE releasing action. 6. It is concluded that bradykinin increases its own algesic action by a concomitant rapid stimulation of the PGE synthesis, thus providing a mechanism for the facilitation of its own algesic action.

Acetylcholine↗
PubMed1976

Release of prostaglandins from the isolated perfused rabbit ear by bradykinin and acetylcholine.

(1) The isolated rabbit ear was perfused via its artery and the venous outflow superfused a PGE-sensitive rat stomach strip or a PGF-sensitive rat colon. (2) Injection of bradykinin intra-arterially into the ear produced a larger contraction of the rat stomach strip than the application of the same dose of bradykinin directly to the superfused muscle. (3) This difference is explained as a release of PGE-like material by bradykinin since indomethacin (infused i.a. into the ear) reduced the effect of the i.a. applied bradykinin. (4) PGF-like material could not be detected in the venous effluent. (5) ACh released only minimal amounts of PGE-like substance. (6) CONCLUSION: The amount of PGE-like material released by bradykinin is large enough to sensitize the paravascular pain receptors in the rabbit ear for the attack of bradykinin. Therefore, inhibition of PG-synthesis (i.e. by indomethacin) or inhibition of the sensitizing action of E-type PGs (i.e. by polyphloretin phosphate) reduces the pain producing effect of bradykinin. Since ACh releases only minimal amounts of E-type PGs, its effect is reduced only to a minimal extent by indomethacin or polyphloretin phosphate.

Acetylcholine↗
PubMed1976

Polyphloretin phosphate reduces the algesic action of bradykinin by interfering with E-type prostaglandins.

(1) The method of the isolated perfused rabbit ear connected to the body by its nerve only was used to investigate the influence of the prostaglandin-antagonist polyphloretin phosphate (PPP) on the algesic effect of bradykinin (B) and acetylcholine (ACh). (2) Intra-arterial injections of B and ACh into the ear elicit a reflex fall in systemic blood pressure of the anaesthetized animal. PPP reduces this effects of B in proportion to the dose. The effect of ACh is reduced only to a small extent and only under higher concentrations of PPP than those necessary for inhibiting the effect of B. (3) Prostaglandin E1 (PGE1), when infused i.a. into the ear, enhances the effect of B and ACh by a sensitizing action on the perivascular pain receptors. PPP reduces or totally abolishes the PGE1-induced enhancement of the effect of B and ACh. (4) It is concluded that PPP reduces the effect of B mainly by inhibiting directly the pain enhancing action of the endogenously released PGs of the E-type. The effect of ACh is reduced only in the high concentration of PPP to a small extent probably by inhibiting the ACh-action rather than the sensitizing action of the only minimal released amounts of PGs. The PG-antagonizing action of PPP is further proven by the fact that during an additional infusion of PGE1 the enhanced effects of both B as well as ACh are reduced or abolished by PPP.

Acetylcholine↗
PubMed1975

Inhibition of the action of bradykinin and acetylcholine on paravascular pain receptors by tetrodotoxin and procaine.

Intra-arterial injection of the algogens bradykinin and acetylcholine into the isolated perfused rabbit ear connected to the body by its nerve only elicit a dose-dependent reflex fall in blood pressure. Procaine and tetrodotoxin were used to investigate whether bradykinin and acetylcholine exerted their algesic effect via different types of nerve fibers. Procaine reduced the effect of bradykinin and acetylcholine to a very similar degree. Tetrodotoxin reduced the effect of bradykinin slightly more than that of acetylcholine. It is assumed that on the whole bradykinin and acetylcholine act via the same nerve fibers but bradykinin seems to have some more affinity to fibers with a fewer number of sodium channels than acetylcholine.

Acetylcholine↗
PubMed1975

Are there therapeutic indications of intravenous injection of calcium gluconate?

1. The action of i.v. injection of calcium gluconate on a) the release of catecholamines from the adrenals of cats and dogs, b) the adrenergic responses of circulation, nictitating membrane and spleen in cats, and c) the cardiac and circulatory response in dogs has been investigated. 2. Ca2+-effects mediated by release of catecholamines dominate in the cat, as do direct cardiac stimulating actions in the dog. 3. Ca2+-effects of therapeutic significance, if existent at all, could be assumed only with regard to an anti-anaphylactic effect of the catecholamines released by i.v. injected Ca2+.

Animals↗