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Biomedical subjects

F Lembeck

Publications and source records attributed to F Lembeck.

At least 163 records · Page 9Linked to original sources
PubMed1978

The intestine as source of immunoreactive substance P in plasma of the cat.

1. Substance P (SP) was measured in acid acetone extracted plasma of cats using a sensitive radioimmunoassay. The immunoreactive material was submitted to ion exchange chromatography and at least 90% of immunoreactivity co-chromatographed with synthetic SP. 2. The level of immunoreactive SP (I-SP) in extracted plasma of the cat was 69.3 +/- 9.8 fmol/ml with values ranging from 2.5 to 165 fmol/ml. Evisceration of the cats caused a decrease of I-SP levels from 70.8 +/- 30.8 fmol/ml to 20.8 +/- 9.9 15 min and to 26.8 +/- 19.7 fmol/ml 60 min after the operation. 3. Ligation of intestinal blood vessels led to a fall in I-SP levels from 58.7 +/- 11.5 to 25.9 +/- 4.1 fmol/ml within 15 min. 4. No difference between I-SP values in portal (71.8 +/- 11.2 fmol/ml) and peripheral plasma (68.3 +/- 12.1 fmol/ml) was found under the conditions in which these experiments were performed. 5. It is concluded that a major part of circulating immunoreactive SP originates from the intestine.

Animals↗
PubMed1977

[Plasmapheresis in the elimination of toxic substances with marked plasma protein-binding properties (author's transl)].

Plasmapheresis is a method used to eliminate toxic substances with high plasma protein-binding properties. Poisoning by strongly plasma protein-binding substances cannot be treated by haemodialysis or peritoneal dialysis. Hence, an attempt was made to hasten the elimination of phenylbutazone, a suitable model substance (plasma protein binding affinity 98%), by plasmapheresis. Some of the experiments were performed with oxygen under high pressure (OHP). A singly plasmapheresis of the total blood volume or triple plasmapheresis of half of the blood volume, performed at 20 min intervals accelerated the elimination of phenylbutazone significantly and all animals survived. A single plasmapheresis of the threefold blood volume had the greatest effect in lowering the concentration of phenylbutazone in the blood, but only one of three animals survived. OHP had no influence on the half-life of phenylbutazone and did not increase the survival rate.

Animals↗
PubMed1977

[Interactions between oxygen under high pressure and drugs (author's transl)].

A. The clinical applications of oxygen under high pressure (OHP) are limited by oxygen toxicity. Hence, an investigation was carried out in mice on the influence of drugs on the lethal effect of OHP. 1. The lethal effect of OHP is diminished by phenobarbitone, propranolol, clonidine, succinate and tris buffer. 2. The lethal effect of OHP is enhanced by methamphetamine, acetazolamide and guanethidine. 3. The lethal effect of OHP is enhanced by reserpine two hours after administration, but diminished 12 hours after administration. B. The clinical usage of OHP is often necessarily connected with drug therapy. Hence, alteration in drug effects under OHP were investigated in mice and rats. 1. The convulsion threshold of pentetrazol is reduced under OHP by 26%. 2. The duration of the hypnotic effect of hexobarbitone is reduced under OHP by 27%. 3. The analgesic effect of morphine is unchanged by OHP. Practical aspects with regard to the use of drugs during clinical use of OHP are discussed.

Acetazolamide↗
PubMed1977

Lack of algesic effect of substance P on paravascular pain receptors.

1. Substance P (synthetic or extracted for intestine or central nervous system) is devoid of an algesic effect on paravascular pain receptors. 2. The algesic effect of a AP-containing acetone HCl-extract from spinal cord is explained by its high content of potassium ions. 3. SP-containing preparations which include an ammonium sulphate precipitation in the extraction procedure are algesic due to content of this salt. 4. SP-containing extract from intestine were found to be contaminated with a bradykinin-like peptide of high algesic potency. 5. These findings are discussed with regard to the restricted value of earlier results about central actions of SP-containing tissue extracts and with regard to the role of SP as a possible neurotransmitter.

Animals↗
PubMed1977

Substance P in rat brain synaptosomes.

1. Rat brain synaptosomes were incubated under different conditions to study the release of substance P (SP). 2. Potassium ions and electrical field stimulation induced a loss of SP from synaptosomes. The release of SP by potassium in high concentrations (23.8 mM) was shown to be calcium dependent. 3. Substance P was retained in synaptosomes during incubation in 0.32 M sucrose at +4 degrees C up to 120 min. During incubation at 30 degrees C the SP content fell initially (30 min) but was gradually restored (120 min). 4. If these pre-incubated synaptosomes were reincubated for 45 min at 30 degrees C in potassium free Krebs-Ringer-phosphate buffer a further rise in their SP content occurred which was taken as indication that SP is being synthesized in synaptosomes. 5. The newly synthesized SP is presumably stored by binding to phosphatidyl serine until a sudden release is initiated by depolarization.

Animals↗
PubMed1977

Convulsions induced by hyperbaric oxygen: inhibition by phenobarbital, diazepam and baclofen.

1. The anticonvulsive potencies of diazepam, phenobarbital and baclofen against convulsions induced by oxygen under high pressure (OHP), by isoniazid and by strychnine were investigated in mice and rats. 2. The anticonvulsive potency of diazepam was much higher than that of phenobarbital and baclofen against all three types of convulsions. 3. The selective activity of diazepam against isoniazid induced convulsions in rats (dose ratio ED50 phenobarbital/ED50 diazepam: 400) could not be confirmed in mice (dose ratio ED50 phenobarbital/ED50 diazepam: 20-40), where diazepam was equipotent against all three types of convulsions. 4. Baclofen which does not inhibit strychnine induced convulsions was equipotent in inhibiting convulsions evoked by isoniazid and OHP in mice. 5. The results are in agreement with the postulated GABA-inhibitory mechanism of OHP induced convulsions, whereas they make a glycine inhibitory mechanism very unlikely. Although the results do not allow further conclusions about the mode of action of diazepam, a clinical trial of diazepam in OHP-induced convulsions should be considered.

Aminobutyrates↗
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

The molecular weights of plasma and intestinal kallikreins in rats.

1. The molecular weights of kallikreins of rat intestine and rat plasma have been estimated using gel filtration. 2. Extracts of pooled tissue from rat jejunum, ileum, caecum and colon activated by autolytic processes gave a single peak of kallikrein activity with a molecular weights of 33000. 3. Acid-activated rat plasma gave two peaks of kallikrein activity with molecular weight of 125000 and 61500. 4. Rat intestinal tissue contains a kinin forming enzyme having a molecular weight similar to those of glandular kallikreins and different from those of the rat plasma kallikreins.

Animals↗
PubMed1976

Methylxanthines and intestinal drug absorption.

1. Jejunal loops of anaesthetized rats were filled with buffered isotonic solutions of tritiated water (HTO), urea, antipyrine and salicylic acid at pH 6-8. The venous outflow and the appearence rate of the substances in the intestinal venous blood were determined. Blood pressure was kept constant by adjustable supply of blood from donor rats throughout the experiment. 2. The absorption of urea, antipyrine and salicylic acid was, in concentrations from 0.001 to 1.0 mg/ml found to be directly proportional to the intraluminal concentration. 3. Theophylline and caffeine (2 mg/ml), when injected into the lumen, increased the blood flow to 188% and 166% of controls. 4. The theophylline induced increase in blood flow caused an enhancement in the absorption of antipyrine to 153%, HTO and urea to 135% and salicylic acid 123% of controls. 5. Caffeine influenced the absorption of HTO and salicylic acid similar to theophylline.

Animals↗
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↗