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At least 37 records · Page 2Linked to original sources
PubMed1976

Release of creatine kinase by antigen, histamine, and catecholamines.

In mepyramine treated, ovalbumin sensitized anaesthetized guinea pigs protracted anaphylactic shock was produced by i.p. injection of antigen, and serum creatine kinase (CK) activities were determined 4, 6, or 17 hrs thereafter. Significant increases above nonsensitized controls were obtained. In nonanaesthetized guinea pigs shock course and serum CK increase were considerably accelerated. Histamine increased the serum CK only when given in high amounts (10 mg/kg) s.c., in the presence or absence of mepyramine. I.p. injection of histamine in mepyramine treated animals had no effect. Adrenaline (1 or 10 mg/kg) given as a s.c. depot in oil produced a significant increase of serum CK, as well as noradrenaline (0.1, 1, or 10 mg/kg). Dibenamine reduced the effect of adrenaline. In isolated perfused guinea pig hearts a significant CK liberation occurred already within the first hour after eliciting anaphylaxis. Nonanaphylactic hearts released CK too, but significant amounts were obtained only in the total 4 hrs after ovalbumin administration. Isolated anaphylactic hearts incubated in Tyrode solution liberated significantly more CK than did nonsensitized control hearts. The findings are discussed in view of a possible myocardial damage in anaphylaxis.

Anaphylaxis↗
PubMed1977

Nature of adrenoceptor sites in bovine teat muscles.

The motility of smooth muscles excised from the wall of bovine teats was studied "in vitro". These muscle preparations often show spontaneous rhythmic contractions. Administration of isoprenaline results in relaxation and decreased spontaneous motility, these effects being blocked by propranolol. Noradrenaline elicits contraction and stimulates rhythmical activity, these effects being inhibited by dibenamine. The effect of adrenaline is variable as it induces contraction or inhibition or biphasic responses. Dibenamine blocked contractions, whereas propranolol inhibited relaxations. It appears that alpha and beta adrenoceptors are present in teat muscles. Stimulation of the former elicits activation, whereas stimulation of the latter results in inhibition. These "in vitro" results are largely in agreement with "in vivo" responses described previously.

Animals↗
PubMed1986

Effects of diethylcarbamazine on the motility of Angiostrongylus cantonensis and Dirofilaria immitis.

Effects of piperazine derivatives, especially of diethylcarbamazine (DEC) on adult Angiostrongylus cantonensis and Dirofilaria immitis were examined. Piperazine (3 X 10(-5)-10(-4) M) paralyzed A. cantonensis and the action was antagonized by picrotoxin. 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP) (10(-5)-10(-4) M) caused contraction but little effect was produced by strychnine. An inhibitory effect on untreated preparations was caused by lower concentrations (3 X 10(-6)-10(-5) M) of diethylcarbamazine citrate (DEC) and also on the preparations contracted by eserine. A stimulatory effect was also seen when higher concentrations (10(-4)-3 X 10(-4) M) of this drug were applied to both preparations. The inhibitory action of DEC was antagonized by gabergic antagonists such as picrotoxin and bicuculline, but not by alpha-adrenergic antagonists like dibenamine and phentolamine. When the worm preparation was paralyzed by strychnine or hexylresorcinol (inhibitors of the release of acetylcholine in this worm), the stimulatory effect of DEC was blocked, but pyrantel (a nicotinic cholinergic agonist) contracted the paralyzed preparation. However, the effect of DEC on D. immitis (10(-7)-3 X 10(-4) M) was inhibitory, and this action was also antagonized by picrotoxin. These results suggest that the DEC inhibitory and stimulatory action is through the gabergic and cholinergic mechanisms in adult A. cantonensis and D. immitis.

Angiostrongylus↗
PubMed1992

In vitro effects of milbemycin oxime: mechanism of action against Angiostrongylus cantonensis and Dirofilaria immitis.

The neuropharmacological mechanisms underlying the action of milbemycin oxime on the motility of Angiostrongylus cantonensis and Dirofilaria immitis were examined in vitro. In A. cantonensis, milbemycin oxime caused inhibitory effects at low concentrations of > or = 10(-9) g/ml, and paralysis was elicited at 10(-8) - 10(-6) g/ml. The paralysis was antagonized by picrotoxin and bicuculline but not by dibenamine. In addition, stimulatory effects were observed when the antibiotic was used at higher concentrations of 3-5 x 10(-6) g/ml, and the action was antagonized by strychnine. Both effects were also observed in the preparation contracted by eserine or pyrantel. When D. immitis was treated with milbemycin oxime at concentrations of 10(-7) and 3-5 x 10(-6) g/ml, only slight inhibitory and stimulatory effects, respectively, were observed. These effects were partially antagonized by picrotoxin and strychnine, respectively. These results suggest that the inhibitory and stimulatory actions of milbemycin oxime are caused through gabergic and cholinergic mechanisms in A. cantonensis and D. immitis.

Angiostrongylus↗
PubMed1975

[Kidney in heart failure (author's transl)].

The adaptability of the kidney in heart-failure is restricted. This is due to a sympathetically mediated renal vasoconstriction, forming part of a sympathetically induced general rearrangement of haemodynamics. This is reflected in a rise of the total peripheral vascular resistance and of the right auricular pressure and can be normalized to a large extent by sympathetic gamma-blockade. The renal vasoconstriction reduces the glomerular filtration rate and, thus, the tubular sodium load. Simultaneously, possibly by the same sympathetic stimulus, more renin is liberated from the juxtaglomerular apparatus. This increases the production of angiotensin and in turn, raises the production of aldosterone. By the combined effect of the reduced glomerular sodium load and aldosterone-mediated increase in tubular reabsorption of sodium, sodium and water will be retained in the body. During the night-rest the load on the circulatory system diminishes. In the early stages of heart-failure this emergency circulatory reaction, therefore, subsides and the rise of the renal fraction of the cardiac output leads to the excretion of the retained fluid and is the basis of nocturia.

Blood Proteins↗
PubMed1985

Carrageenin-induced thrombosis in rats and mice: a model for testing antithrombotic substances?

Among different carrageenins, kappa-carrageenans were found to be thrombogenic, whereas lambda-carrageenins were inactive in this respect, although the latter substances exerted a stronger edemogenic activity. Kappa-carrageenin (Sigma) was the most potent thrombogen. As the consequence of thrombosis tail infarction became visible some minutes after i.v. administration, but it was delayed for about 3 hours after the i.p. route and for about 6 hours after subplantar injection. Infarction frequency as well as extent of infarction was inhibited by heparin, cyproheptadine, phentolamine and dibenamine. Other substances like aspirin and dipyridamole showed no or only weak effects. Advantages of the carrageenin-induced thrombosis model in rats and mice are: (i) simple induction in small laboratory animals, (ii) easy observation and quantification all the time without killing the animals, and (iii) possible external testing of antithrombotic agents by applying substances on the tail.

Animals↗
PubMed1983

Membrane transport in vascular smooth muscle and its relation to normal and altered excitation during hypertension.

Evidence is presented for the operation of Cl-Cl exchange diffusional transport system in rat aortic smooth muscle. The efflux of 36Cl associated with this mechanism is doubled in rats made hypertensive with aldosterone-salt treatment. The residual efflux of Cl is similarly elevated in the hypertensives. This finding supports the hypothesis that increased membrane permeability to Cl is associated with aldosterone hypertension. The agonist-induced increases in aortic effluxes of 42K exhibit a 10-fold reduction in the ED50 to norepinephrine in aldosterone hypertensive rats. The possible contributors to this supersensitivity were studied by means of a pharmacologic analysis of the action of competitive (phentolamine) and non-competitive (dibenamine) antagonism of norepinephrine induced increases in 42K efflux. The dissociation constant for phentolamine, KB= 1 x 10-8M, was relatively unaltered in the hypertensive group, as was the dissociation constant for norepinephrine, KA= 3.4 - 5.8 x 10-7M. A substantial increase in receptor number and/or transduction efficiency (3-12 fold) was derived from the analysis. It is tentatively concluded that supersensitivity to norepinephrine during aldosterone hypertension may be more closely related to changes in receptor number and/or efficiency than in receptor affinity.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗