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Biomedical subjects

F Lembeck

Publications and source records attributed to F Lembeck.

At least 109 records · Page 6Linked to original sources
PubMed1983

Heat loss reaction to capsaicin through a peripheral site of action.

The intravenous injection of 15 micrograms capsaicin produced an increase in the temperature of tail skin and paw pad and a fall in the colon temperature in conscious rats. These reactions reflect increased heat dissipation. The increase in skin temperature induced by intravenous capsaicin was absent when the function of small diameter primary afferent neurones was impaired by treatment of the rats with capsaicin as neonates. Thus it appears that intravenous capsaicin triggered the thermoregulatory response predominantly by stimulation of peripheral heat receptors. By means of local application of capsaicin to the nerves of the hind leg and by their chronic denervation, by treatment with phenoxybenzamine and guanethidine, evidence was obtained that reflex withdrawal of sympathetic vasoconstrictor tone mediates the heat loss reaction intravenous capsaicin.

Animals↗
PubMed1983

Serum levels of dimenhydrinate. Determination by HPLC with UV detection after intake of dimenhydrinate in a coated chewing gum dragee.

HPLC with UV detection allowed to separate dimenhydrinate and three major metabolites (diphenyl-methoxy-ethylamine, diphenyl-methoxy-acetic acid, diphenyl-methoxy-N-methyl-amine) in human serum without extraction procedure. Detection limit was 25 ng per 500 microliter injected sample, the recovery ranged from 70 to 95%. Serum levels of dimenhydrinate were measured in healthy volunteers 15, 30, 60 and 120 min after intake of two commercially available preparations, one of them a dimenhydrinate tablet, the other one a dimenhydrinate containing coated chewing gum dragee (Travel-Gum dragee). The rise of the serum concentration of dimenhydrinate up to 30 min was smaller after intake of the coated chewing gum preparation than after swallowing the tablet. The serum concentrations at 1 or 2 h after the intake of either a tablet or the chewing gum were comparable. The variability of the serum concentrations was considerable with both preparations and seemed to be influenced more by individual factors than by previous food intake.

Administration, Oral↗
PubMed1982

Inhibition of neurogenic vasodilation and plasma extravasation by substance P antagonists, somatostatin and [D-Met2, Pro5]enkephalinamide.

The substance P (SP) analogues [D-Pro2, D-Phe7, D-Trp9]SP and [D-Pro2, D-Trp7,9]SP, which have been reported to be SP antagonists, inhibited the vasodilation and plasma extravasation induced by antidromic stimulation of the saphenous nerve or by i.a. infusion of SP. Somatostatin inhibited the vasodilatation and plasma extravasation induced by saphenous nerve stimulation, but had no effect on the vascular responses to i.a. infused SP. The opiate agonist [D-Met2, Pro5]enkephalinamide inhibited the vasodilation evoked by antidromic nerve stimulation in a naloxone reversible manner, but did not change the effect of i.a. infusion of SP. Calcitonin and caerulein had no effect on neurogenic vasodilatation. These results further support the concepts that neurogenic vasodilatation and plasma extravasation are mediated by SP, and that somatostatin and opiates inhibit the release of SP from peripheral sensory nerve endings.

Animals↗
PubMed1982

Evidence for the involvement of substance P in the atropine-resistant peristalsis of the guinea-pig ileum.

In the isolated, vascularly perfused guinea-pig ileum, peristalsis could be induced by raising the intraluminal pressure in the presence of atropine. Atropine-resistant peristalsis was greatly inhibited or abolished by the substance P antagonist (D-Pro2, D-Trp7.9)-substance P, substance P desensitization, hexamethonium and by the enkephalin analogue FK 33-824. It is concluded that substance P neurones of the intestine play an important role in the atropine-resistant peristalsis of the guinea-pig ileum.

Animals↗
PubMed1982

Distribution of capsaicin-sensitive nerve fibres containing immunoreactive substance P in cutaneous and visceral tissues of the rat.

Treatment of newborn rats with capsaicin causes a selective and permanent degeneration of unmyelinated sensory fibres, some of which contain immunoreactive substance P (ISP). Following treatment of newborn rats with capsaicin (50 mg/kg), the ISP content was decreased by 66-75% in various skin areas and in the oral and nasal mucosae as measured at the age of 3-4 months. There was no significant depletion of ISP in the mucosa of the tongue. The ISP content of trachea, lungs, myocardium, hepatic duct, ureter and urinary bladder, was decreased by 60-84%. The ISP concentrations in stellate and mesenteric ganglia were reduced by 54 and 81%, respectively. These results indicate a widespread innervation of cutaneous and visceral tissues by sensory nerve fibers containing ISP.

Animals↗
PubMed1982

Capsaicin applied to peripheral nerve inhibits axoplasmic transport of substance P and somatostatin.

Capsaicin was applied locally to the sciatic or saphenous nerve, and the effects on axoplasmic transport, neurogenic plasma extravasation, and thermal pain were studied. Capsaicin (10 mg/ml) led to a complete block of axoplasmic transport of immunoreactive substance P (I-SP) and somatostatin (I-SRIF) in rat sciatic nerve without affecting the transport of noradrenaline or acetylcholinesterase. Inhibition of I-SP transport was also found in sciatic nerves of guinea-pig, cat and rabbit. In contrast, one or two weeks after systemic capsaicin treatment (125 mg/kg s.c.), orthograde transport of I-SP was the same in control and capsaicin-treated rats. After local capsaicin application to the sciatic nerve, a decrease of I-SP was found not only in skin and sciatic nerve distal to the site of application, but also in dorsal root ganglia, dorsal roots and the dorsal half of the spinal cord segments L 4-5. This was accompanied by a loss of acid phosphatase activity in the substantia gelatinosa supplied by sciatic nerve afferents. Plasma extravasation by mustard oil was reduced in the skin of the hind paw with a time course identical to the I-SP depletion. The response to noxious heat (hot plate test) was, however, abolished earlier. These results indicate that capsaicin applied to a peripheral nerve inhibits axoplasmic transport in sensory but not in adrenergic or cholinergic neurons, which leads to long-term biochemical and functional changes of the entire sensory neuron. In addition, capsaicin appears to inhibit impulse propagation in certain populations of sensory neurons.

Acetylcholinesterase↗
PubMed1982

Effects of antibodies against nerve growth factor on the postnatal development of substance P-containing sensory neurons.

Administration of anti-nerve growth factor (NGF)-antibodies to newborn rats produces a marked but reversible reduction of the substance P content in dorsal root ganglia. This is in contrast to the effect of anti-NGF-antibodies on sympathetic ganglia, where they cause a destruction of the adrenergic neurons as is evident in the irreversible reduction of tyrosine hydroxylase activity.

Animals↗
PubMed1982

Analysis of the effects of intravenously injected capsaicin in the rat.

1. I.v. injection of 1 or 3 micrograms capsaicin led to a triphasic blood pressure response in Sprague-Dawley rats but, in contrast to Wistar rats, did not affect heart rate and respiration. The blood pressure response was a sequence of fall (A), return to normal levels or slight rise (B), and fall (C) in blood pressure. The blood pressure response to capsaicin remained unchanged after treatment with adrenoceptor or cholinoceptor antagonists. 2. The initial fall in blood pressure (A) was absent after bilateral vagotomy and in the pithed rat. The delayed fall in blood pressure (C) remained unchanged after vagotomy, but was absent after neonatal capsaicin pretreatment and in the pithed rat. Effect B was not diminished after vagotomy or despinalization: it was augmented in rats treated neonatally with capsaicin. 3. I.a. injection of capsaicin into the hind leg caused a reflex fall in blood pressure which was changed to a reflex rise in rats treated with capsaicin as neonates. 4. The initial and the delayed fall in blood pressure after i.v. injection of capsaicin seems to be reflex responses to stimulation of capsaicin-sensitive small diameter afferent fibres. The intermediate rise in blood pressure appears to result mainly from a direct short vasoconstriction by capsaicin.

Animals↗
PubMed1982

Visceral pain reflex after pretreatment with capsaicin and morphine.

1. Distension of the proximal jejunum by increasing the intraluminal pressure for short time periods causes a reflex response in blood pressure of anaesthetized rats which correlates with the magnitude of distension. The blood pressure response consists of a short initial rise followed by a marked decrease for the time of distension. 2. The absence of the depressor response in capsaicin desensitized rats indicates its mediation by C fibre afferents. These afferents are located within the periarterial mesenteric nerves. The depressor response was also elicited by stimulation of these nerves and abolished by local application of percain or capsaicin onto the mesenteric stalk. Vagal afferents were not involved in this depressor response as shown by bilateral vagotomy or by afferent vagus stimulation. 3. The depressor response is absent in spinal rats. Therefore, the location of the reflex centre is assumed to be supraspinal. Because it is augmented by naloxone and abolished by morphine in a naloxone reversible way it is regarded as a nociceptive reflex response. 4. The efferent side of the depressor response is unknown; cholinergic and alpha-adrenergic activation were excluded. 5. The initial pressor response to intestinal distension or to afferent periarterial mesenteric nerve stimulation persists in capsaicin desensitized rats excluding the involvement of C fibre afferents and in spinal rats indicating that the reflex centre is within the spinal cord. It is not diminished by morphine and therefore not a nociceptive response. Its inhibition by phentolamine suggests an alpha-adrenergic spinal response to intestinal distension. In control rats the pressor response is greatly overlapped by the much more pronounced depressor response.

Anesthetics, Local↗
PubMed1982

A study of the concentrations of substance P and neurotensin in the gastrointestinal tract of various mammals.

Immunoreactive substance P and neurotensin in extracts of the digestive tract of man, cat, guinea-pig, pig, rabbit, and rat were measured by radioimmunoassay using antisera directed against the C-terminal portions of the two peptides. In all species except the cat, the concentrations of substance P were highest in the small intestine, intermediate in the large intestine and lowest in the stomach and oesophagus: the digestive tract of the cat displayed a rather even distribution of substance P. As observed in the ileum of guinea-pig, rabbit, and rat, the external muscle layer including the myenteric plexus contained 2-5 times higher concentrations of substance P than the whole ileal wall, whereas the substance P concentrations in the mucosa were only about one sixth of those in the whole wall. High performance liquid chromatography of extracts of human, feline and rabbit ileum showed that all the immunoreactive substance P eluted at the positions of substance P and substance P sulfoxide. The distribution of immunoreactive neurotensin along the digestive system of all six species was very similar. The highest concentrations of neurotensin were measured in the distal part of the small intestine, whereas the large intestine, stomach and oesophagus contained only low concentrations of neurotensin relative to the concentrations in the ileum. As examined in the ileum of guinea-pig, rabbit, and rat, the mucosa exhibited 2.5-4 times higher concentrations of neurotensin than the whole ileal wall, while the concentrations of neutrotensin in the external muscle layer including the myenteric plexus were only 4-20% of those in the whole wall. High performance liquid chromatography of the immunoreactive neurotensin extracted from the cat ileum yielded a single peak corresponding to neurotensin while the immunoreactive neurotensin extracted from the ileum of man and rabbit was eluted in two peaks, 55 and 72% of the recovered immunoreactivity, respectively, corresponding to neurotensin. These findings are in line with the proposed roles of substance P in the neural, and neurotensin in the endocrine, control and maintenance of gastrointestinal motility.

Animals↗
PubMed1982

Evidence that the contractile response of the guinea-pig ileum to capsaicin is due to release of substance P.

1. The possible roles of substance P and opioids in the contractile response of the isolated guinea-pig ileum to the sensory stimulant drug capsaicin were investigated, and the contractions were found to be inhibited by about 60% in preparations desensitized to substance P. 2. Contractions evoked by stimulation of the mesenteric nerves in the presence of the adrenergic blocking drug guanethidine were inhibited by about 75% after the ileum had been rendered insensitive to substance P. 3. Atropine partially inhibited the effect of capsaicin. The atropine-resistant component of the contractile response to capsaicin was inhibited by more than 85% in preparations desensitized to substance P and almost abolished by the substance P antagonist, (D-Pro2,D-Trp7,9)-substance P. 4. The opioid peptide (D-Met2, Pro5)-enkephalinamide inhibited, whereas the opiate antagonist naloxone enhanced the atropine-resistant contractions in response to capsaicin. 5. The results indicate that the contractile response of the guinea-pig ileum to capsaicin and mesenteric nerve stimulation is mediated by release of substance P, presumably from sensory nerve endings in the gut. Substance P appears to act on the smooth muscle both directly and indirectly via cholinergic neurones. It is proposed that opioids modulate the non-cholinergic response to capsaicin by inhibiting the release of substance P.

Animals↗
PubMed1981

Histamine in tissue: determination by high-performance liquid chromatography after condensation with o-phthaldialdehyde.

Histamine was determined by reversed-phase high-performance liquid chromatography in perchloric acid extracts after condensation with o-phthaldialdehyde. Fluorescence was monitored at 360 nm excitation and 450 nm emission wavelengths after elution with mixtures of 0.1 N acetic acid containing 0.1% pentanesulfonic acid and acetonitrile. The detection limit was 0.9 pmol of histamine. The histamine content was determined in rat whole brain, medulla oblongata, dorsal and ventral spinal cord, dorsal and ventral skin of the hind paw, stomach, ileum, rectum, lung and a hind-quarter perfusate, and compared to published data. The advantages of the described method over other methods are (A) rapid analysis in an automated system, (B) no selective extraction procedure is necessary, and (C) interfering substances are easily separated from the histamine fluorophore.

Animals↗