[Transient ischemic accidents during pregnancy secondary to congenital protein C deficiency].
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Adult↗
Biomedical subjects
V Bauer
Publications and source records attributed to V Bauer.
Influence of acute stress on lipid peroxidation in vivo.
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Animals↗
Role of extra- and intracellular calcium in the contractile action of agonists in the guinea-pig ileum.
The effects of Ca2(+)-channel blockers (nifedipine and verapamil), EGTA, caffeine or the removal of external Ca2+ on the contractile action of different agonists and transmural electrical stimulation were examined in isolated segments of the proximal and terminal part of the guinea-pig ileum. The effects of agonists and nerve stimulation on membrane potential were also studied by means of the sucrose gap method. Acetylcholine-elicited contractions in both parts and noradrenaline- as well as histamine-induced contractions in the terminal part of the ileum were composed of an initial phasic and a sustained tonic component. Single pulse transmural nerve stimulation elicited smooth muscle twitches, whereas addition of CaCl2 to the tissue bath containing Ca2(+)-free and high-K+ medium elicited a sustained contraction. Both verapamil and nifedipine were more potent in inhibiting the tonic phase of the responses to the agonists or CaCl2 than inhibiting the phasic contractions elicited by transmural nerve stimulation, acetylcholine or noradrenaline. The excitatory junction potentials (e.j.p.s.) as well as smooth muscle twitches were reduced only by high nifedipine concentrations. The effects of acetylcholine on membrane potential and input membrane resistance were affected minimally by the omission of extracellular Ca2+, while the contractions gradually disappeared on repetitive agonist application in the absence of external Ca2+ and were blocked by caffeine preexposure. In Ca2(+)-free solution noradrenaline and histamine partially reduced each other's motor effect, while neither of them changed the contractile action of acetylcholine, yet the contraction induced by noradrenaline was prevented and that of histamine significantly reduced by preexposure to acetylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcholine↗
Angiosarcoma in postsurgical lymphedema. An unusual occurrence in a man.
A 63-year-old man underwent partial left axillary node dissection for metastatic melanoma of unknown primary. Lymphedema of his left upper extremity developed after surgery. Eight years later, extensive cutaneous angiosarcoma developed in the edematous limb. The occurrence of cutaneous angiosarcoma in postsurgical lymphedema is extremely rare in men; to our knowledge, our case is the fifth such case thus far reported.
Arm↗
Effect of potassium channel blocking agents on the actions of phenylephrine in rabbit taenia caeci.
The effects of tetraethylammonium, apamin, 4-aminopyridine and holding potential on the phenylephrine-evoked outward currents in dispersed smooth muscle cells of the rabbit taenia caeci were analyzed using the whole cell patch clamp method. Phenylephrine (10 mumol/l) under the double sucrose gap condition, substantially hyperpolarized the smooth muscle membrane and reduced the input membrane resistance. This concentration of phenylephrine enhanced the frequency and amplitude of spontaneous transient outward currents (s.t.o.c.s) and elicited a low amplitude sustained outward current which were voltage and temperature dependent. In addition, phenylephrine (10 mumol/l) reduced the outward current evoked by voltage steps. Tetratehylammonium (1-5 mmol/l) attenuated the depolarization-evoked outward current, blocked the appearance of s.t.o.c.s, and fully abolished the phenylehrine induced changes in membrane currents. Apamin (0.1-10 mumol/l) only slightly affected the evoked outward current and s.t.o.c.s. However apamin did not change the phenylephrine-induced outward currents. Pretreatment with 4-aminopyridine (0.5-2 mmol/l) did not reduce the phenylephrine-induced sustained outward current and s.t.o.c.s but prevented the phenylephrine induced reduction of the depolarization-evoked outward current. These results are in favour of assumption that the phenylephrine induced hyperpolarization and reduction in the input membrane resistance are consequences of an enhanced potassium current via tetraethylammonium-sensitive, apamin and 4-aminopyridine resistant potassium channels.
4-Aminopyridine↗
Effects of phenylephrine in single isolated smooth muscle cells of rabbit and guinea pig taenia caeci.
Spontaneous transient and evoked outward currents were studied using the whole cell patch-clamp technique with freshly dispersed smooth muscle cells isolated from rabbit and guinea pig taenia caeci. Phenylephrine induced a low amplitude sustained outward current in both tissues. Simultaneously, the frequency and amplitude of spontaneous transient outward currents were increased. However, there were differences between the effects of phenylephrine on the evoked outward currents recorded from smooth muscle cells of rabbit (reduction) and guinea pig (enhancement) taenia caeci.
Animals↗
Effect of stobadine and histamine H1 and H2 blockers on histamine-induced contraction of guinea pig airways in vitro.
Histamine, a nonselective histamine receptor agonist, activates simultaneously both H1 and H2 receptors in the guinea pig trachea and lung strip. The resulting contraction is due to the prevalence of H1 receptors, because they are blocked by the selective H1 antagonist diphenhydramine. The H2 receptor antagonists cimetidine and ranitidine increased the sensitivity of both tissues to histamine by affecting primarily the amplitude of contractions induced by high histamine concentrations. Since the lung strips were more sensitized by ranitidine and low concentrations of the other studied antagonists (diphenhydramine, dithiadene, stobadine) than the tracheal smooth muscle, it is inferred that the density of H2 receptors is higher in peripheral than central airways. From all the studied histamine receptor antagonists only dithiadene was able to unmask the relaxation induced by H2 receptor activation indicative of its highest H1 selectivity. In the light of the concentration-dependent antihistaminic effect of stobadine, i.e. potentiation in low and inhibition in high concentrations, stobadine is suggested to belong to antihistaminics with no histamine receptor subtype selectivity.
Animals↗
[Invasive cervix cancer stage I and II in women less than 35 years old].
The results of a retrospective study of 74 women under the age of 35, treated invasive cervical cancer, stage I and stage II, between 1973 and 1985, were compared with those obtained in 547 women over 35, treated during the same period of time for a similar cervical cancer. The treatment consisted of: association radium therapy-surgery for stages IB less than 25 mm and II A moderately extended and an association radiotherapy-radium therapy for stages IB greater than 25 mm and II A extended, II B and II C. A better distribution per stage is found in women under 35, identical regarding the histological type with 5-year survival identical in both groups at the same stage. Relapses or recurrences occur much earlier in younger women. In the literature, the age as a prognosis factor is very much controverted. On the contrary, other factors should be taken into consideration: clinical stage, node invasion, size and volume of the tumor, depth of infiltration of the cervix.
Adult↗
Trachealis responses induced by vincamine and vinpocetine; inhibition by indomethacin and Ca2+ dependence.
Vincamine in low concentrations induced a sustained contraction of the isolated guinea pig trachealis with long latency and slow onset and, in high concentrations, it induced relaxation which was potentiated in the precontracted trachealis. Vinpocetine had actions similar to those of vincamine on trachealis, however its relaxant effect was more pronounced. The vincamine-induced trachealis contraction was not changed by substance P desensitization, was reduced by tetrodotoxin, nifedipine and low Ca2+ high Mg2+ solution and increased in nominally Ca2+-free solution. The vincamine-induced relaxation of precontracted trachealis was increased by guanethidine and was not affected by propranolol, high Mg2+-low Ca2+ solution and tetrodotoxin. Vincamine- and vinpocetine-induced trachealis contraction as well as vinpocetine-induced relaxation at basal tension were abolished by indomethacin. Vincamine in a low concentration shifted to the left the concentration-effect curve for CaCl2 in the K+-depolarized trachealis, and shifted it to the right at a high concentration. Our results indicate that the contractile and relaxant actions of vincamine and vinpocetine on the guinea pig trachealis may be due to the generation of prostaglandins and to changes in the membrane Ca2+ fluxes and/or the intracellular Ca2+ distribution.
Acetylcholine↗
Calcitonin gene-related peptide action on intestinal circular muscle.
Isolated segments of the guinea pig small intestine were used to examine the effect of calcitonin gene-related peptide (CGRP) on the motor activity of the circular muscle. CGRP (0.3-30 nM) initiated phasic contractions of the circular muscle due to stimulation of cholinergic neurons. Peristalsis, however, was inhibited by CGRP. A further analysis of this effect showed that CGRP had no inhibitory influence on the main, cholinergic, pathway of the ascending enteric reflex (AER) contraction, whereas the hexamethonium- and atropine-resistant pathways of the AER were blocked. The inhibition of the atropine-resistant AER resulted from an action of CGRP on nerves and, since it was antagonized by apamin, might be explained by a CGRP-induced activation of enteric inhibitory neurons. The direct relaxant action of CGRP on the longitudinal muscle was not affected by apamin. These findings indicate a heterogeneity and topical selectivity in the motor actions of CGRP on the gut and suggest that this peptide, when released from nerve endings within the intestine, plays a specific role in the regulation of intestinal motility.
Animals↗
Interactions of neurogenic responses of longitudinal and circular muscle in the guinea-pig ileum.
The relationship between neurogenic responses of longitudinal and circular muscle was studied by measuring contractions and EMG or nonadrenergic, non-cholinergic (NANC) relaxations and NANC inhibitory junction potentials in different preparations of the guinea-pig ileum. NANC relaxation of longitudinal muscle was observed also without any preceding or concomitant circular muscle contraction ruling out the possibility that the latter might be the cause of the NANC relaxation. Circular muscle twitches or powerful contractions were absent if there was no preceding neurogenic or myogenic excitation of longitudinal muscle; in preparations with myenteric plexus-longitudinal muscle layers removed only small residual responses were seen although still under neurogenic influences. Thus excitation of longitudinal muscle seemed a prerequisite for synchronized and powerful contractions of circular muscle to occur. Cholinergic contraction and NANC relaxation of longitudinal muscle evoked by field stimulation were partly inhibited if the submucous plexus was also present suggesting the involvement of a more complex neuronal circuitry in these responses.
Adenosine Triphosphate↗
Action of histamine on nerve mediated responses of the guinea-pig ileum.
The effect of histamine on the responses of the guinea-pig ileum to stimulation of intramural nerves and to some potential nonadrenergic, noncholinergic (NANC) neurotransmitters was analysed. During sustained tonic histamine contraction, electrical stimulation of all intramural nerves elicited a biphasic response (contraction followed by after-relaxation) and application of ATP and bradykinin caused relaxation of the ileum in contrast to their contractile effect on basal tension. Histamine reduced contractile and augmented relaxatory NANC responses, and prevented capsaicin from producing any contractile effect and from significantly influencing the NANC contractions. The present results suggest that, besides its direct effect, histamine activates intramural nerve fibres, mainly the sensory ones, and unmasks NANC relaxation thus modifying the mechanical activity.
Animals↗
Action of pentacaine on gastric acid secretion.
The action of pentacaine, a new prospective antiulcer drug with gastric cytoprotective activity, on gastric acid secretion was analysed and compared with the action of other antisecretory drugs. The drugs were given orally or intraduodenally to Wistar rats after pylorus ligation. The gastric acid secretion was studied under basal or stimulated (histamine, pentagastrin, carbachol) conditions. Oral administration of pentacaine, oxethazaine and procaine, in contrast to atropine, had no influence either under basal or stimulated conditions. However, intraduodenal administration of pentacaine significantly suppressed both the basal and stimulated gastric secretion. The present study suggests that the mechanism of antisecretory activity of pentacaine differs from that of anticholinergic and antihistaminergic drugs.
Animals↗
Calcium and the activation of the alpha 1-adrenoceptors in the guinea-pig taenia caeci.
1. The actions of phenylephrine (0.1-100 mumol l-1) and methoxamine (0.1-100 mumol l-1) were compared with that of adrenaline (0.01-10 mumol l-1) using the single sucrose gap method and mechanical recording in the guinea-pig taenia caeci. Drugs were applied for variable periods of time. 2. The characteristics of the inhibitory effects of alpha-adrenoceptor agonists were the same when exposure time did not exceed 5 min. When the exposure was prolonged, in contrast to the sustained effects of adrenaline (0.1-3 mumol l-1), phenylephrine and methoxamine (1-10 mumol l-1) produced a transient inhibitory action. 3. During the delayed recovery phase of phenylephrine, adrenaline preserved its ability to suppress the spontaneous electrical and mechanical activities of the taenia both when phenylephrine was replaced by adrenaline or when adrenaline was applied in addition to phenylephrine. All the above effects were found in untreated preparations, as well as during blockade of muscarinic cholinoceptors by atropine (1.4 mumol l-1), beta-adrenoceptors by propranolol (3 mumol l-1) and release of endogenous catecholamines by guanethidine (2.5 mumol l-1). 4. In the presence of phorbol 12,13-dibutyrate adrenaline ceased to be effective, while the inhibitory action of phenylephrine was converted to a contraction. 5. In calcium-free conditions in the presence of EGTA (0.4 mmol l-1) the initial hyperpolarization induced by adrenaline and phenylephrine was significantly reduced and with repeated applications of the agonists the inhibitory response disappeared. Similar results were obtained using tissues treated with nifedipine (1 and 10 mumol l-1). When caffeine (30mmolI 1) was present in the calciumfree solution the alpha-agonists studied were unable to produce any membrane potential changes. 6. The present results imply that the inhibitory effect of alpha-adrenoceptor agonists is mediated by the opening of potassium channels, which are activated by calcium derived from an intercellular source supplied from the extracellular space via a nifedipine-sensitive mechanism.
Animals↗
Effect of calcium entry blockade on the actions of phenylephrine on the taenia of the guinea pig caecum.
The interaction between phenylephrine and calcium entry blockers was studied on the taenia of the guinea-pig caecum using the double sucrose gap method. Sustained hyperpolarization, relaxation and attenuation of evoked electrical and mechanical activity were induced by non-cumulative addition of phenylephrine (0.1 to 250 mumol.1-1) for 2 to 4 min. When the alpha 1-adrenoceptor agonist was applied for a prolonged period (20 to 60 min) the initial inhibitory response gradually disappeared both at room temperature and at 32 degrees C. The renewed action potentials were accompanied by a positive afterpotential. The initial hyperpolarization and its delayed recovery in course of the phenylephrine effect were significantly reduced in calcium-free medium containing EDTA (2 mmol.1-1), after pretreatment with nifedipine (0.1 to 1 mumol.1-1), verapamil (10 to 100 mumol.1-1) or procaine (0.5 to 2 mmol.1-1). In contrast sodium nitroprusside (10 to 100 mumol.1-1) which produced biphasic changes similar to those of phenylephrine, did not affect the initial and delayed phase of phenylephrine action. Ba2+(5 mmol.1-1) could substitute for Ca2+ in the generation of action potentials but could not substitute for Ca2+ in the mechanisms responsible for the initial and delayed recovery phase of phenylephrine effects. In the presence of La3+ and Mn2+ (0.5 to 3 mmol.1-1) the phenylephrine effects were reduced. In contrast, in the presence of extracellular Ca2+, pretreatment with Mg2+ (12 mmol.1-1) or Ba2+ (5 mmol.1-1) did not affect the action of phenylephrine. It is concluded that activation of alpha 1-adrenoceptors results in the release of Ca2+ from an intracellular store, which leads to the opening od TEA-sensitive potassium channels, causing the initial phase of alpha 1-adrenoceptor action. Ca2+ is loaded into this intracellular store by entering the cell through the potential sensitive calcium channels. Although the mechanisms responsible for the delayed phase could not be clarified, its dependence on the presence of the initial phase is apparent.
Action Potentials↗
The effects of methylxanthines, ethymizol, ephedrine and papaverine on guinea pig and dog trachea.
The study was aimed to compare the effects of pentoxyphylline, aminophylline, choline theophyllinate and ethymizol on guinea pig and dog trachea with those of theophylline, papaverine and ephedrine. The effects of these drugs on the basal tension, on dose-response curves for muscle contraction produced by histamine and on cAMP level were investigated in guinea pig trachea, together with their influence on the resting and histamine-evoked mechanical and membrane activities of dog trachea. Like papaverine, pentoxyphylline did not alter the resting membrane potential, although it relaxed both tracheal preparations, and it antagonised the effects histamine and raised the cAMP level of the smooth muscle. The effects of ethymizol were similar to those of theophylline and its water soluble derivatives (aminophylline and choline theophyllinate). Whereas, ephedrine although it decreased the basal tension and inhibited histamine-evoked responses, also elicited substantial hyperpolarization of the smooth muscle membrane with no effect on the cAMP level. These findings are consistent with the hypothesis that cAMP has an important role in the action of some bronchodilator drugs; however, it is concluded that the possibility of contributing of their action on membrane potential to their action needs to be considered. The similarity of the potencies of ethymizol and pentoxyphylline to that of classical bronchodilators in inhibiting contraction of guinea pig and dog tracheal smooth muscle suggests that they may have a therapeutic value.
Animals↗
The action of adrenoceptor agonists and antagonists on the guinea pig and dog trachea.
The action of beta- and alpha-adrenoceptor agonists (isoprenaline, orciprenaline, noradrenaline, phenylephrine and ephedrine) and antagonists (propranolol, metipranolol, exaprolol, BL 445 and phentolamine) on the resting tension and cAMP level of the guinea pig and the mechanical and electrical activities of the dog trachea were studied. By activating beta 2-adrenoceptors, isoprenaline and orciprenaline relaxed the smooth muscle, elevated the membrane potential and attenuated the excitatory effect of histamine on membrane potential and muscle tension. Noradrenaline and phenylephrine, acting on alpha 1-receptors, did not affect the membrane potential and increased the basal tension of the dog trachea only insignificantly. Ephedrine, in high concentrations, however, hyperpolarized the smooth muscle membrane and relaxed the dog trachea, while it did not alter the cAMP level in the guinea pig preparations. It is, therefore unlikely that alpha 1-adrenoceptors play a major role in the excitation of the dog trachea under resting conditions whereas the participation of alpha 2-receptors in the mechanisms of adrenergic relaxation could not be ruled out. All the beta-adrenoceptor antagonists studied enhanced the action of low isoprenaline concentrations and competitively antagonized it in high concentrations. The order of their antagonistic potency in the guinea pig trachea was as follows: metipranolol greater than propranolol = exaprolol greater than or equal to BL 445. It was suggested that metipranolol and exaprolol are nonselective beta-adrenoceptor antagonists, similarly as propranolol, whereas BL 445 shown some beta 1-selectivity. In contrast to their antagonistic effects on the membrane activities and muscle tension, both histamine and isoprenaline increased the level of cAMP in smooth muscle cells and, when present simultaneously, their effect was additive. The mechanism of histamine-induced cAMP level elevation and the possible involvement of different subcellular compartments in the action of isoprenaline and histamine in relation to the contraction-relaxation cycle is discussed.
Adrenergic alpha-Agonists↗