PubMed Health⌕ Search

Biomedical subjects

V Bauer

Publications and source records attributed to V Bauer.

At least 37 records · Page 2Linked to original sources
PubMed1987

The effect of local anaesthetics on noncholinergic-nonadrenergic (NCNA) responses of the gut.

The newly synthesized carbamate local anaesthetics (heptacaine and BK-141) affected the NCNA responses of different segments of the guinea-pig small (jejunum, ileum) and large (colon, taenia coli) intestine in a similar manner to the classic local anaesthetics (procaine and trimecaine). The sensitivity of NCNA responses to the action of local anaesthetics was, in order: primary contraction greater than rebound contraction greater than primary relaxation. The action of the carbamate local anaesthetics resembled that of trimecaine more than that of procaine. The results presented suggest that different Ca2+ channels participate in primary and rebound contraction and that local anaesthetics affect the receptor-operated Ca2+ channels in lower concentrations than the voltage-dependent ones.

Action Potentials↗
PubMed1986

Effect of desensitization induced by adenosine 5'-triphosphate, substance P, bradykinin, serotonin, gamma-aminobutyric acid and endogenous noncholinergic-nonadrenergic transmitter in the guinea-pig ileum.

The cholinergic and noncholinergic-nonadrenergic (NCNA) excitatory and inhibitory responses of the guinea-pig ileum to transmural nerve stimulation (TNS) were studied. Unlike the contraction induced by histamine and acetylcholine the responses to TNS, ATP, substance P, bradykinin, 5-HT and GABA were not sustained. The contraction and its fading during TNS involved the activation of cholinergic, adrenergic and NCNA neurons. Substance P, 5-HT and ATP desensitization resulted in reduction of the excitatory NCNA response whereas that due to bradykinin attenuated both the excitatory and inhibitory NCNA responses. The desensitization against TNS and the potential transmitters studies was selective except in the case of ATP. The present results suggest that it is unlikely that ATP, bradykinin or GABA would be the NCNA transmitters in the guinea-pig ileum. The cross-desensitization between the excitatory NCNA transmitter on the one hand, and substance P (markedly expressed) and 5-HT (slightly expressed) on the other hand, give further evidence in favor of the possible transmitter role of substance P-like peptide in excitatory NCNA transmission and of the role of 5-HT in the activation of NCNA neurons.

Adenosine Triphosphate↗
PubMed1986

Localized thyroid plasmacytoma.

Two cases of localized thyroid plasmacytoma are described and the literature is reviewed. In most cases the tumors arise in thyroid glands with lymphocytic thyroiditis. Thyroidectomy with regional lymph node biopsy seems to be the initial treatment of choice. Postoperative irradiation appears to be indicated in cases with residual thyroid tissue remaining and in those with documented regional nodal involvement.

Aged↗
PubMed1986

Evidence that sensory neurons participate in the non-cholinergic, non-adrenergic contractile response of the guinea-pig ileum.

The possible role of non-cholinergic, non-adrenergic (NCNA) nerves in responses of the guinea-pig terminal ileum to transmural nerve stimulation (TNS) and that of sensory nerves in NCNA responses were investigated. The action of acetylcholine was almost abolished in the presence of histamine, whereas the contractions elicited by TNS were changed to frequency-dependent contraction followed by a secondary relaxation. Guanethidine did not alter the contractions or secondary relaxations. Atropine abolished the action of acetylcholine and transiently suppressed the responses to low (up to 2 Hz) and attenuated (by about 50%) those to high (4 to 20 Hz) frequency stimulation. The remaining complex NCNA response was the sum of the excitatory and inhibitory responses. During desensitization to capsaicin, and in its presence, the NCNA contractions were reduced, whereas the relaxations were not significantly enlarged. The present results suggest that besides the cholinergic innervation, the excitatory and inhibitory NCNA innervation also participates in the responses of the guinea-pig ileum to TNS even without suppression of cholinergic and adrenergic transmission, and that the sensory nerves are, at least to some extent, involved in the NCNA excitatory response.

Animals↗
PubMed1986

The non-adrenergic non-cholinergic innervation and transmission in the small intestine.

An attempt has been made to summarize the present knowledge on the non-adrenergic non-cholinergic (NANC) transmission in the small intestine. The paper presents old and recent findings as well as the author's own results on the basic characteristics of the NANC mechanical and membrane potential changes. Further the sensitivity of NANC transmission to different influences, such as elevation or reduction of the muscle tension and membrane potential level, drug actions, desensitization of receptors, etc. are elucidated. The nature of the putative NANC neuromediator/s (purines, peptides, etc.) in the small intestine is discussed.

Adenine Nucleotides↗
PubMed1986

The effects of some carbamate local anaesthetics on the guinea-pig ileum.

The action of some carbamate local anaesthetics, pentacaine, BK-52 and heptacaine, was compared in the guinea-pig ileum with that of classic local anaesthetics, procaine and trimecaine. Contractions of the ileum were evoked by transmural stimulation, nicotine, acetylcholine, noradrenaline, histamine, K+ and Ba++. Although the evoked contractions were inhibited by all the local anaesthetics, there was a marked difference in their ability to influence the smooth muscle activation induced by different stimuli. The differences among the IC50 values were slight in the case of pentacaine, moderate in the case of trimecaine and BK-52 and large in the case of procaine and heptacaine. It is suggested that besides their effects on the unmyelinated autonomic nerves, the carbamate local anaesthetics studied can also affect the smooth muscle membrane, similarly to the classic agents. The mechanism of their direct effect is discussed.

Anesthetics, Local↗
PubMed1986

Carbamate-induced rhythmic activity in the guinea-pig ileum.

The action of newly synthesised basic esters of alkoxy-substituted derivatives of phenylcarbamic acid was compared with that of procaine and trimecaine in the guinea-pig small intestine. Some of the carbamate local anaesthetics, in concentrations high enough to markedly suppress cholinergic twitches, elicited regular rhythmic activity of the guinea-pig ileum. This effect of the carbamates was dependent on the position of the alkoxysubstituent and was independent of the basic group (pyrrolidine, piperidine or perhydroazepine) present. Only the ortho-substituted derivatives were active. It was also found that the rhythmic activity evoked was of myogenic origin, produced by rhythmic undulations of the sodium-pump activity, accompanied by a potential-dependent change in Ca2+ permeability. It is suggested that the mechanism by which carbamates reveal this endogenous rhythm in the guinea-pig ileum could be a selective block of noncholinergic, nonadrenergic innervation or the TEA-like activity of carbamates.

Anesthetics, Local↗
PubMed1986

The effect of carbamate local anaesthetics on vascular smooth muscle.

The effect of carbamate local anaesthetics (pentacaine and heptacaine) on contractile responses induced by transmural nerve stimulation, exogenous noradrenaline (NA) and KCl, as well as on noradrenaline-induced Ca2+ mobilization, were investigated in isolated rabbit blood vessels under isometric conditions. Pentacaine and heptacaine inhibited the neurogenic contractions and those elicited by exogenous NA and KCl. The neurogenic contractions were more sensitive to the local anaesthetics than those evoked by exogenous NA. The onset of inhibition was slow and developed gradually. This inhibition was concentration-dependent and continued for several hours in spite of repeated washings of the vessels. Pretreatment of the vascular preparations with pentacaine and heptacaine reduced NA- and Ca2+-induced contractions in Ca2+-free K+-depolarizing solution. The Ca2+-contracted vessels were also relaxed by the anaesthetics studied. It is suggested that carbamate local anaesthetics inhibit not only neuronal conductance but also Ca2+ entry into the vascular smooth muscle cells and NA-induced release of intracellular Ca2+.

Anesthetics, Local↗
PubMed1985

Effects of 3,4-diaminopyridine and tetraethylammonium on the pre- and post-junctional alpha-adrenoceptor mediated inhibitory actions of noradrenaline in the guinea-pig ileum.

The effects of potassium channel blockers, 3,4-diaminopyridine (DAP) and tetraethylammonium (TEA) were studied on the pre- and post-junctional alpha 2-adrenoceptor mediated effects of noradrenaline in the guinea-pig proximal ileum. Both DAP (4 to 500 mumol l-1) and TEA (0.3 to 3 mmol l-1) transiently increased the basal tension of the ileum. However, DAP also increased the amplitude of the smooth muscle twitches evoked by transmural nerve stimulation, whereas TEA marginally depressed them. Atropine (2 mumol l-1) antagonized the contractions induced by DAP but did not affect the similar effects of TEA. On the other hand, DAP restored the smooth muscle twitches depressed by atropine, while TEA did not. DAP, in a concentration-dependent manner, reduced or abolished the prejunctional inhibitory alpha 2-adrenoceptor mediated effect of noradrenaline, whereas TEA (up to 3 mmol l-1) was almost ineffective. The postjunctional inhibitory alpha 2-adrenoceptor mediated effect of noradrenaline was attenuated even at the smallest TEA concentration used (0.3 mmol l-1) and its postjunctional stimulatory alpha 1-adrenoceptor mediated effect was unmasked. However, DAP, was only marginally effective, even at the highest concentrations used (100 and 500 mumol l-1). From these results it would appear that in both the pre- and post-junctional inhibitory alpha 2-adrenoceptor mediated actions of noradrenaline in the guinea-pig ileum the primary step might be an increased potassium conductance. However, the potassium channels on the neuronal and the smooth muscle membrane have different sensitivities to DAP and TEA.

4-Aminopyridine↗
PubMed1982

Non-cholinergic, non-adrenergic responses to nerve stimulation of different regions of the guinea-pig small intestine.

Non-cholinergic, non-adrenergic responses to nerve stimulation recorded from smooth muscles of the guinea-pig duodenum, jejunum, proximal and terminal ileum were investigated in an attempt to characterize these responses. In the presence of atropine (1-2 mumol X l-1) and guanethidine (10 mumol X l-1) coaxial stimulation induced in all regions of the guinea-pig small intestine an initial relaxation (primary relaxation) upon which contraction (primary contraction) appeared, followed by rebound contraction. Noradrenaline decreased the cholinergic smooth muscle twitches, predominantly at low stimulation frequencies, and had a similar effect on the non-cholinergic, non-adrenergic primary relaxation, primary and rebound contractions. ATP decreased the smooth muscle twitches; however, this agent had only a transient influence on the non-cholinergic, non-adrenergic responses of muscle (tension and membrane potential) to single stimuli. With higher stimulus frequencies ATP increased the primary relaxation and decreased the contraction phases. ATP also inhibited the post-tetanic inhibition induced by non-cholinergic, non-adrenergic nerve stimulation. In most of the muscle cells of the guinea-pig proximal and terminal ileum the non-cholinergic, non-adrenergic nerve stimulation generated i.j.p.s., while about 15-20% of the cells responded with e.j.p.s. During long-lasting stimulation (10s) the i.j.p.s were sometimes "interrupted" by action potentials or by a gradual depolarization of the membrane. The i.j.p.s were followed by a marked rebound depolarization accompanying the action potentials. Those cells which generated i.j.p.s in response to field stimulation, were depolarized by ATP, while those cells, which generated e.j.p.s, were hyperpolarized by ATP. A reduction in the concentration of extracellular sodium chloride decreased both the primary and rebound contractions; the primary contraction was, however, more sensitive than was the rebound contraction. Theophylline increased the primary and rebound contractions with no marked influence on the primary relaxation, lowered the action potential threshold, increased the rebound depolarization and did not markedly influence the i.j.p.s. Quinidine enhanced the primary relaxation and inhibited the primary contraction in a concentration-dependent manner. Inhibition of the rebound contraction by quinidine was slight (less than 50%). The present results demonstrate that primary relaxation, primary and rebound contractions are associated with i.j.p.s and e.j.p.s, and rebound depolarization with action potentials, respectively; they are typical responses of various regions of the guinea-pig small intestine to activation of inhibitory and excitatory non-cholinergic, non-adrenergic nerves. The P1 and P2 receptors, proposed by Burnstock (1975), probably do not mediate the non-cholinergic, nonadrenergic postsynaptic responses of the guinea-pig small intestine...

Adenosine Triphosphate↗
PubMed1982

Role of Ca2+ in non-cholinergic, non-adrenergic responses to nerve stimulation of the guinea-pig small intestine.

The effects of calcium channel blockers (D-600, verapamil), sodium nitroprusside, papaverine, indomethacin, local anaesthetics and blockade of sodium pump activity on the non-cholinergic, non-adrenergic transmission in the guinea-pig duodenum, jejunum, proximal and terminal ileum were analysed in the presence of atropine and guanethidine. A decrease of the extracellular Ca2+ concentration inhibited the primary and rebound contractions but only in Ca2+ -free solution was the primary relaxation diminished. D-600, verapamil, sodium nitroprusside and papaverine inhibited both the primary and rebound contractions to the same degree and their effects on the primary relaxation were less pronounced than on the contractions. Indomethacin dissolved in alkaline solution did not depress the non-cholinergic, non-adrenergic responses in any region of the small intestine, whereas indomethacin dissolved in ethanol antagonized both the primary and rebound contractions in the muscles. Local anaesthetics (procaine, trimecaine) in low concentrations inhibited only the primary contraction. Higher concentrations also inhibited both the rebound contraction and primary relaxation. Procaine in low concentrations did not markedly affect the non-cholinergic, non-adrenergic i.j.p.s and e.j.p.s, but did block the action potentials induced by e.j.p.s. Our findings indicate that the primary relaxation, and primary and rebound contractions are probably induced by different mechanisms and are not mediated by ATP. We confirmed that prostaglandins did not participate in the generation of the rebound contraction.

Adenosine Triphosphate↗
PubMed1982

Distribution and types of adrenoceptors in the guinea-pig ileum: the action of alpha- and beta-adrenoceptor blocking agents.

1 Transmurally stimulated segments of the guinea-pig ileum have been used to analyse the different adrenoceptors in the terminal (0 to 3 cm) and the proximal (> 50 cm from the ileocaecal valve) ileum.2 The prejunctional adrenoceptors (located on the final, cholinergic, motor nerve terminals) and postjunctional adrenoceptors (located on the smooth muscle membrane) have been characterized according to their sensitivity to alpha- and beta-agonists and antagonists.3 Phentolamine, phenoxybenzamine and yohimbine, in concentrations of 0.1 muM, transiently enhanced (up to 10%) the twitch response. At higher concentrations all the alpha- and beta-antagonists studied depressed the neurogenic twitches and relaxed the smooth muscle.4 The twitch-inhibitory effects of adrenoceptor agonists (noradrenaline, adrenaline and ephedrine) were not antagonized by phenoxybenzamine (0.1, 0.5 and 1 muM), carbidine (0.5, 1 and 5 muM) and propranolol (0.5, 1 and 5 muM); however, they were depressed by phentolamine (0.1, 0.5, 1.25 and 5 muM) and yohimbine (0.25, 0.5 and 5 muM).5 The smooth muscle contractions induced by noradrenaline and adrenaline in the terminal ileum and by phenylephrine in both the terminal and proximal ileum were antagonized by phenoxybenzamine, carbidine and phentolamine but were not influenced by yohimbine and propranolol.6 The smooth muscle relaxations of the proximal ileum induced by noradrenaline, adrenaline and ephedrine were inhibited by yohimbine, phentolamine, carbidine and phenoxybenzamine, and the isoprenaline-induced relaxation was antagonized by propranolol.7 All the agonists studied, except phenylephrine, elicited relaxations of the acetylcholine-induced sustained contraction of both proximal and terminal ileum. The relaxation induced by isoprenaline was antagonized by propranolol, and the effects of noradrenaline and ephedrine by yohimbine.8 It is concluded that in the guinea-pig ileum there are postsynaptic beta-adrenoceptors and at least two types of alpha-adrenoceptors: alpha(1)-excitatory postjunctional adrenoceptors activated by phenylephrine, noradrenaline and adrenaline and antagonized by phenoxybenzamine, carbidine and phentolamine; alpha(2)-inhibitory prejunctional adrenoceptors activated by ephedrine, noradrenaline and adrenaline and inhibited by yohimbine and phentolamine. The inhibitory postjunctional alpha-adrenoceptors are more close to the alpha(2)-adrenoceptors, since they were stimulated predominantly by ephedrine and noradrenaline and inhibited by yohimbine.9 It has been shown that all alpha-adrenoceptor subtypes are to be found at every distance (0 to 70 cm) from the ileocaecal valve and that they can be activated in the resting or in the acetylcholine-contracted states.

Adrenergic alpha-Agonists↗
PubMed1982

Evidence for non-cholinergic, non-adrenergic transmission in the guinea-pig ileum.

To elucidate further the innervation of the longitudinal and circular muscle cells of the guinea-pig ileum, junction potentials elicited by field stimulation were recorded from both muscle layers in the presence and absence of atropine (1-2 muM) with guanethidine (10 muM) at 36 degrees C.1. In longitudinal muscle cells, a single stimulus elicited an atropine-sensitive transient depolarization (cholinergic e.j.p.), whereas in circular muscle cells, a transient hyperpolarization (non-cholinergic non-adrenergic i.j.p.) was elicited. With stimulation of nerves in the presence of atropine and guanethidine, responses of circular muscle cells to nerve stimulation were preserved while the longitudinal muscle cells generated depolarization (non-ch., non-adr. e.j.p.), hyperpolarization (non-ch., non-adr. i.j.p.) or both depolarization and subsequent hyperpolarization. These potential changes ceased with application of TTX or excess Mg(2+).2. The latency for junction potentials recorded from longitudinal muscles after field stimulation was in the following order; non-ch., non-adr. e.j.p. < cholinergic e.j.p. < non-ch., non-adr. i.j.p. The cholinergic e.j.p.s had a lower, and non-ch., non-adr. i.j.p.s a higher threshold.3. At low frequencies of stimulation (below 1 Hz) amplitudes of successively generated cholinergic e.j.p.s and non-ch., non-adr. i.j.p.s were gradually reduced, but at higher frequencies (2-20 Hz) of stimulation they were summated. The amplitudes of non-ch., non-adr. e.j.p.s were, however, not affected at low frequencies of stimulation (up to 0.5 Hz) and were summated at higher frequencies (over 1 Hz) of stimulation.4. Reversal potentials for non-ch., non-adr. e.j.p.s and i.j.p.s estimated from the amplitude of junction potentials and membrane potential were -27 and -80 mV, respectively. The reversal potential for non-ch., non-adr. e.j.p.s was higher (more negative) than that for cholinergic e.j.p.s5. Generation of i.j.p.s in longitudinal muscle cells elicited by repetitive stimulation was followed by a rebound depolarization on which was superimposed a burst of spikes. During repetitive stimulation, the amplitude of hyperpolarization was gradually reduced but the rebound depolarization and spike discharge were enhanced. Thus, while the rebound depolarization was related to the amplitude of the preceding hyperpolarization it was more related to the duration of the stimulation.6. Therefore longitudinal muscles of the guinea-pig ileum show evidence of having in addition to cholinergic and adrenergic innervation, both excitatory and inhibitory non-ch., non-adr. innervation. In the longitudinal muscle layer of the ileum, the non-ch., non-adr. excitatory fibres are more densely distributed in the terminal rather than in the proximal region, while in the case of non-ch., non-adr. inhibitory fibres, the distribution is reversed. Circular muscle cells are, however, homogenously innervated by non-ch., non-adr. inhibitory nerves.

Adrenergic Fibers↗
PubMed1982

The nature of non-cholinergic, non-adrenergic transmission in longitudinal and circular muscles of the guinea-pig ileum.

1. The nature of the non-cholinergic, non-adrenergic (non-ch., non-adr.) excitatory and inhibitory transmission in the longitudinal and circular muscle layers of the guinea-pig ileum was investigated, and the effects of various agents on the junction potentials were observed using the micro-electrode method.2. In longitudinal muscle cells, ATP (3 x 10(-5)-10(-4) M) and adenosine (10(-5)-10(-4) M) depolarized the membrane, decreased the input resistance, increased the spike activity and abolished the generation of cholinergic excitatory junction potentials (e.j.p.s).3. In the presence of atropine (10(-6) M) with guanethidine (10(-5) M), field stimulation evoked three different types of the response (non-ch., non-adr. e.j.p.s, i.j.p.s (inhibitory junction potentials) or both) from cells of the longitudinal muscle layers, and only one type of the response (non-ch., non-adr. i.j.p.s) from cells of the circular muscle layer. In the following experiments atropine and guanethidine were present in the bathing fluid for at least 20 min.4. In some longitudinal muscle cells (non-ch., non-adr. i.j.p. type), ATP (5 x 10(-6)-10(-3) M) and adenosine (10(-5)-3 x 10(-5) M) depolarized the membrane, while in other cells (non-ch., non-adr. e.j.p. type), ATP (10(-5)-10(-4) M) and adenosine (10(-5)-3 x 10(-5) M) hyperpolarized the membrane and further increases in the concentration of ATP (10(-3) M) resulted in a depolarization of the membrane.5. Apamin (10(-7)-3 x 10(-6) M) inhibited the generation of non-ch., non-adr. i.j.p.s in both longitudinal and circular muscle cells, while this agent had no effect on the non-ch., non-adr. e.j.p.s. As a consequence, in some cells of the longitudinal muscle layer (non-ch., non-adr. e.j.p. and i.j.p. type) the amplitude of e.j.p.s was enhanced in the presence of apamin. TEA (5 x 10(-3)-1.5 x 10(-2) M) suppressed the after-hyperpolarization of the spike and i.j.p.s recorded from both muscle layers, whereas the duration and amplitudes of cholinergic and non-ch., non-adr. e.j.p.s were enhanced.6. Vasoactive intestinal polypeptide (VIP; 10(-8)-10(-7) M) had no effect on the membrane potential and junction potentials of longitudinal and circular muscle layers.7. Substance P (SP; 10(-8)-10(-7) M) depolarized the membrane of cells of the longitudinal layer (non-ch., non-adr. e.j.p. type), while this agent had no effect on cells of longitudinal (non-ch., non-adr. i.j.p. type) and circular muscle layers. SP suppressed the generation of non-ch., non-adr. e.j.p.s but had no effect on i.j.p.s. Generation of non-ch., non-adr. e.j.p.s was not restored under conditions of repolarization of the membrane to the resting level by application of inward current.8. Bradykinin (BK; 10(-8)-10(-5) M) hyperpolarized the membrane and suppressed the generation of i.j.p.s in the cells of longitudinal (non-ch., non-adr. i.j.p. type) and circular muscle layers. However, when the membrane potential was displaced to the control level by outward current in the presence of BK, field stimulation evoked the i.j.p. In cells of non-ch., non-adr. e.j.p. type of the longitudinal muscle layer, BK depolarized the membrane, increased the spike activity, generated slow waves and blocked the generation of non-ch., non-adr. e.j.p.s. Displacement of the membrane potential to the control level by inward current did not restore the non-ch., non-adr. e.j.p.s.9. These results suggest that in the guinea-pig ileum ATP and adenosine probably do not contribute to the generation of non-ch., non-adr. e.j.p.s and i.j.p.s, as transmitter substances. The actions of other possible candidates such as SP and BK, are discussed.

Action Potentials↗