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H Juan

Publications and source records attributed to H Juan.

At least 55 records · Page 3Linked to original sources
PubMed1982

[On the evidential value of diatoms in cases of death by drowning (author's transl)].

With the aid of experiments in animals we have again investigated the question as to the quantitative and qualitative immigration of diatoms into the greater circulation and thus into the bone marrow at the time of drowning. We have applied an experimental method which meets this complex topic. Thus, just before the animals (rabbits) were drowned, one of their hind legs was amputated, and the vessels of one of their kidneys were clamped to learn how many diatoms were present before the drowning. After the drowning, a qualitative and quantitative examination of the bone marrow of both hind legs and of both kidneys was carried out. In all cases, an increase in the number of diatoms could be recorded as compared to the initial number of diatoms present prior to the drowning. Based on the results of the experiments and the information gained in the examinations criteria are discussed which, when applied, allow positive diatom findings to indicate valuable diagnostic information about death by drowning. References is made to preservation of the death causing liquid in the stomach.

Animals↗
PubMed1982

Release of different prostaglandins from vascular tissue by different stimulators.

The prelabelling technique (incorporation of (1-14C)-arachidonic acid) was used to investigate the influence of bradykinin, the divalent cation ionophore A 23187, acetylcholine and phospholipase A2 (PLA2) on release and metabolism of arachidonic acid (AA) in peripheral vessels. Bradykinin stimulated the release of PGI2 and PGE2, both to the same extent. The main metabolite released by A 23187 was PGE2 which far exceeded the release of PGI2. PGD2 was released to the same degree as PGI2. Stimulation by acetylcholine released mainly PGI2. In contrast, the main metabolite of AA released by PLA2 was PGE2. Although the substances used were injected i.a. into the same tissue (isolated perfused rabbit ear) they produced a different pattern of PG release. The underlying reason may be different "microkinetics" of the substances due to a different lipophilia or different resistance to metabolizing enzymes. Thus, several cell types may have been reached which have different components of the various enzymes of the PG biosynthesis system.

Acetylcholine↗
PubMed1982

Nicotinic nociceptors on perivascular sensory nerve endings.

Intra-arterial injection of increasing doses of acetylcholine, nicotine, carbachol and pilocarpine into the pain reflex ear of the rabbit dose-dependently caused a reflex fall in mean arterial blood pressure. The order of potency of the algesic substances was: nicotine greater than acetylcholine much greater than carbachol much greater than pilocarpine, whereas the purely muscarinic agonist bethanechol was inactive up to 3 mg. Atropine at 1 microgram/ml did not influence the effect of acetylcholine. At 30 micrograms/ml it reduced the effect of acetylcholine but also that of bradykinin suggesting an unspecific action. Hexamethonium (1 microgram/ml) blocked the algesic effect of acetylcholine and nicotine without influencing that of bradykinin. Morphine, given systemically, blocked the algesic effect of acetylcholine and nicotine. Since nicotine showed the highest algesic potency (whereas bethanechol was inactive) and hexamethonium blocked the effect of acetylcholine and nicotine, the cholinergic "pain receptor" on sensory nerve endings is assumed to be of the nicotinic type.

Acetylcholine↗
PubMed1981

Dependence of histamine-evoked nociception on prostaglandin release.

Intraarterial injection of histamine into the isolated perfused rabbit ear causes a reflex fall in mean arterial blood pressure by stimulation of perivascular pain receptors. This effect is reduced by a low concentration of indomethacin (1 microgram/ml). The histamine H1-receptor antagonist mepyramine (10 micrograms/ml) reduced the effect of histamine. However, it also reduced the effect of acetylcholine. The histamine H2-receptor antagonist cimetidine (3-10 micrograms/ml) did not reduce the effect of histamine. Exogenously applied phospholipase A2 did not stimulate pain receptors on its own but enhanced the algesic effect of histamine, acetylcholine or bradykinin. This enhancement was abolished by indomethacin. Prostacyclin also enhanced the effect of histamine. The results suggest that histamine releases prostaglandins (E-type and prostacyclin) which in turn render the 'pain receptors' more sensitive to histamine. This effect may be of importance in inflammatory pain in that the effect of algogens (including histamine) is enhanced by an increased phospholipase A2-mediated synthesis of prostaglandins. Not only endogenously activated phospholipase A2 is able to split off prostaglandin precursors followed by subsequent generation of prostaglandins but also exogenously administered phospholipase A2 is able to induce the release of pain-enhancing prostaglandins.

Animals↗
PubMed1980

Histamine-induced release of arachidonic acid and of prostaglandins in the peripheral vascular bed: mode of action.

1. Injection or infusion of histamine intraarterially into the isolated perfused rabbit ear dose-dependently stimulated the release of prostaglandins (PGs) as measured by radioimmunoassay (PGE), bovine coronary artery strips (PGI2) and by the prelabeling technic with [1-14C]-arachidonic acid (PGI2, PGE2, PGF2 alpha, PGD2). 2. PG release was abolished by indometacin (1-3 microgram/ml) and reduced by the phospholipase A2 inhibitor quinacrine (10 microgram/ml) as well as by perfusing with calcium-free, 1 mM EGTA containing solution. 3. The histamine H2-receptor antagonists burimamide (5 microgram/ml) and cimetidine (2 microgram/ml) did not influence histamine-induced PG release. The H1-receptor antagonist mepyramine (0.1-1 microgram/ml) abolished histamine-induced mepyramine (0.1-1 microgram/ml) abolished histamine-induced PG release. 4. In the presence, but not in the absence, of bovine serum albumin there was a basal release of high amounts of arachidonic acid. Histamine tended to increase the released amount of radioactive arachidonic acid. In contrast to indometacin which only blocked PG release, mepyramine significantly reduced the histamine-stimulated release of arachidonic acid, too. 5. The results show that in the peripheral vascular bed, histamine, via H1-receptors, activates a phospholipase A2 mainly by increasing a transfer of extracellular calcium into the cell. Activation of a phospholipase A2 results in the release of arachidonic acid possibly from a rather small endogenous pool which specifically provides substrate for the PG synthetase system.

Animals↗
PubMed1979

Effect of ricinoleic acid and other laxatives on net water flux and prostaglandin E release by the rat colon.

Ricinoleic acid, oleic acid, dioctyl sodium sulphosuccinate, deoxycholic acid, sennoside A + B and mannitol reduced or reversed water flux from lumen to blood in rat colon in situ. Stearinic acid was without any effect. Ricinoleic acid, oleic acid, dioctyl sodium sulphosuccinate, deoxycholic acid and sennoside A + B stimulated release of PGE-like material into the colonic lumen whereas the osmotic laxative mannitol and stearinic acid did not. Inhibition of PGE biosynthesis by pretreatment of the rats with indomethacin significantly reduced (but did not abolish) the effect of ricinoleic, oleic and deoxycholic acids on net water flux and PGE release. Indomethacin reduced the effect of dioctyl sodium sulphosuccinate and of sennoside A + B on PGE release but not their effect on the net water flux. The effect of mannitol was not influenced by indomethacin. The amount of PGE release in experiments with ricinoleic acid, oleic acid, stearinic acid and dioctyl sodium sulphosuccinate (with and without indomethacin) showed a good correlation (r = 0.99) with the change in net water flux. Deoxycholic acid, sennoside A + B and mannitol did not show this correlation. It is assumed that the action of non-osmotic laxatives is partially mediated by PGE, although other mechanisms also seem to be involved in their mode of action.

Animals↗
PubMed1978

Is the effect of diphenolic laxatives mediated via release of prostaglandin E?

The diphenolic laxatives, bisacodyl and phenolphthalein, and the osmotic laxative mannitol increase intestinal fluid volume in the rat colon in situ. The diphenolic laxatives stimulate the biosynthesis of prostaglandin E (PGE) whereas mannitol does not. Inhibition of PG-biosynthesis by pretreatment with indomethacin only reduces the effect of the diphenolic laxatives. It is suggested that diphenolic laxatives increase intestinal fluid volume via stimulation of PGE biosynthesis in the colon.

Animals↗
PubMed1978

PGE-release, blood flow and transmucosal water movement after mechanical stimulation of the rat jejunal mucosa.

1. The influence of weak mechanical stimulation of the jejunal mucosa in vivo on PGE-release, on intestinal blood flow and transmucosal water movement was studied in rats. 2. Mechanical stimulation of the mucosa increased PGE-release into the venous outflow and into the gut lumen. This increase is followed by an increase in intestinal blood flow and transmucosal movement of tritiated water in both directions. 3. Pretreatment of the rat with indomethacin reduced the effect of mechanical stimulation on PGE-release. Indomethacin further reduced the increase in blood flow and in secretion of tritiated water. Absorption of tritiated water was not changed in these experiments. 4. Pretreatment of the rat with atropine (1 mg/kg, i.p.) or perfusion of the gut with methysergide (10 microgram/ml) did not influence the increase in intestinal blood flow after mechanical stimulation. 5. It is suggested that enhanced intestinal blood flow and transmucosal movement of tritiated water after mechanical stimulation are mainly provoked by a preceding release of PGE. 6. It is further supposed that such a mechanism may be physiologically involved in regulation of intestinal blood flow and transmucosal water movement during food intake.

Animals↗