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PubMedDate not supplied

[Effect of prolonged beta-adrenergic treatment on the ventilatory response to sympathomimetics].

Ventilatory adrenergic responsiveness induced by long-term beta-mimetic treatment over three years were analysed in a study carried out in two groups of asthmatics. In group I, 11 patients received theophylline and oral beta-2-agonists; in group II, 7 patients received the same drugs and corticosteroids. Pulmonary function tests were serially performed with a body plethysmograph (Jaeger). The effect of beta adrenergic stimulation with 400 micrograms fenoterol was measured using variations of flow-volume curves. The mean increase of FEV1 after fenoterol was: in group I, 0.680 +/- 0.200 1 before treatment and 0.500 +/- 0.340 1 after beta adrenergic therapy; in group II, it was 0.550 +/- 0.340 1 before treatment and 0.510 +/- 0.350 1 after treatment (difference not statistically significant). For each patient, FEV1 variations were expressed in percent of optimum improvement. In most cases, there was a significant correlation between the two parameters (0.38 less than r less than 0.59), but the slopes of the regression curves differed from one patient to another. Intra-individual variation coefficient of the improvement of FEV1 has been calculated and showed large variations of the adrenergic pulmonary responses: from 34% to 98% of the mean improvement. Four patients only exhibited a significant and definitive decrease of their adrenergic response, which could be due to tachyphylaxis. But a transient loss of responsiveness to adrenergic stimulation has been found in all patients. Those cases were related to viral infections or allergen inhalations.

Adrenal Cortex Hormones↗
PubMed1986

Human vascular vasopressin receptors: analysis with selective vasopressin receptor antagonists.

The vascular activity of arginine vasopressin (AVP) and selective AVP receptor antagonists was investigated in isolated arterial ring segments from human superior mesenteric arteries. AVP elicited a potent and concentration-dependent contraction in human mesenteric arterial rings with an EC50 value of 2.01 X 10(-9) M. The presence or absence of the vascular endothelium did not affect significantly AVP-induced contraction. AVP induced slight, although significant, tachyphylaxis in human mesenteric arteries. The selective vascular (V1) receptor antagonist [d(CH2)5 1Tyr(Me)2]AVP (SK&F 100273) shifted the concentration-response curves for AVP-induced vascular contraction to the right in a parallel manner (KB = 2.23 X 10(-9) M). A mixed V1/V2 receptor antagonist, [d(CH2)5 1D-Tyr(Et)2Val4desGly9]AVP (SK&F 101926), was also a potent antagonist of AVP-mediated vascular contraction; however, inhibition was marked by a nonparallel shift of the concentration-response curves with depression of maximum contraction. Furthermore, a relatively renal (V2) selective receptor antagonist [d(CH2)5 1D-Ile2Val4]AVP (SK&F 101485) was approximately 100-fold less potent at inhibiting AVP-induced vascular contraction (KB = 1.37 X 10(-7) M). These studies illustrate for the first time the in vitro effects of selective vasopressin receptor antagonists in isolated human blood vessels. Studies of other blood vessels and the design of therapeutically useful antagonists should proceed with the hypothesis that the vasopressin receptors mediating vascular contraction in human mesenteric arteries are of the V1 subtype.

Arginine Vasopressin↗
PubMed1986

Leukotriene B4 and 20-hydroxyleukotriene B4 contract guinea-pig trachea strips in vitro.

In contrast to its established myotropic effect on guinea-pig lung parenchyma, the myotropic action of leukotriene B4 on the trachea is uncertain. Our characterization of its effects on the latter organ indicates that leukotriene B4 contracts guinea-pig trachea zig-zag strips in a concentration-dependent manner from 5 X 10(-9) to 5 X 10(-7) M. Leukotriene B4 was at least 10 times more potent than histamine, but 10 times less potent than leukotriene C4. Similar effects were evident with 20-hydroxyleukotriene B4; however, this metabolite contracted the trachea less forcefully. Tracheas developed tachyphylaxis after cumulative administration of leukotriene B4, but not 20-hydroxyleukotriene B4. The myotropic effect of leukotriene B4 was attributable to an indirect mechanism involving formation of cyclooxygenase metabolites of arachidonic acid. For example, the levels of prostaglandin E2 and prostaglandin F2 alpha released into the incubation medium correlated with the contractile response, and suppression of their biosynthesis with cyclooxygenase inhibitors eliminated that response. We conclude that myotropic effects of leukotriene B4 occur in central airways in addition to peripheral airways. The contribution of leukotriene B4 to tracheal bronchospasm is not necessarily negligible.

Animals↗
PubMedDate not supplied

An investigation of the adrenergic uptake specificity of phenyl-2-aminoethyl sulfides.

In earlier work we have demonstrated that a novel series of phenylethylamine analogs (phenyl-2-aminoethyl sulfides) cause a potent antihypertensive effect in spontaneously hypertensive rats. In addition, we have shown in vitro that these compounds are facile substrates for dopamine beta-hydroxylase, the terminal enzyme of norepinephrine synthesis. While the mechanism of action of these derivatives is as yet hypothetical, we have proposed that, if they are capable of gaining entrance into adrenergic nerve endings and neurotransmitter storage vesicles, these compounds may reduce norepinephrine synthesis by competing with dopamine for oxygenation. In this report, we present results of preliminary studies designed to examine this hypothetical mechanism of action. We find that all derivatives of this series are classical indirect-acting sympathomimetics whose initial cardiovascular activity is blocked by cocaine. These results suggest that compounds of this type gain entrance to adrenergic neurons via the normal norepinephrine uptake mechanism on adrenergic nerve endings. We also present data which demonstrate that the methylated derivative was not only the most potent indirect-acting sympathomimetic, but also the only derivative capable of producing a marked tachyphylaxis. In addition, we find these compounds affect a specific pool of intraneuronal norepinephrine, distinct from that affected by tyramine, a well-known indirect-acting sympathomimetic agent.

Anesthesia↗
PubMed1988

[Role of vasopressin in the development of arterial hypertension and the search for ways to correct it].

The sensitivity of the vessel smooth muscles to vasopressin and their contractile responses were obviously increased in hypertensive rats, whereas the vasopressin inhibitory effect and tachyphylaxis were decreased. These changes seem to be connected with the prevalence of V1-activating over V2-inhibitory vasopressin receptors in hypertensive rats' vessel smooth muscles. Administration of lithium oxybutyrate for 4 weeks normalized central hemodynamics and decreased the sensitivity to vasopressin. The findings suggest a possible role of the inositol pathway in transmission of hormonal signal (vasopressin) to hypertensive rats' vessel smooth muscles as well as participation of vasopressin in pathogenesis of arterial hypertension and the possibility of using lithium oxybutyrate for its correction.

Animals↗
PubMed1988

Long-term bupivacaine infusion does not alter the acute seizure threshold to bupivacaine in rats.

Rats were given a continuous subcutaneous infusion of either bupivacaine (n = 18) or placebo (n = 17) for 4 days. On the 5th day the acute seizure threshold to intravenous bupivacaine was determined in both groups. Blood and brain concentrations of bupivacaine at the onset of seizures showed no difference between the two groups, whereas the seizure dose was decreased in the bupivacaine group. The tachyphylaxis observed when bupivacaine is used for a regional nerve blockade does not seem to evolve for the central nervous system effects.

Acute Disease↗
PubMed1986

The role of interleukin-1 in neutrophil leukocyte emigration induced by endotoxin.

Chemotactic factors induce neutrophil emigration into tissues. Interleukin-1 (IL-1) was found to be several log times more potent in this respect than C5a des Arg, leukotriene B4, and f-Met-Leu-Phe and of comparable potency to endotoxin. Kinetic studies revealed a rapid and transient neutrophil influx, with the peak rate at 30-90 minutes. Cross tachyphylaxis was observed between IL-1 and endotoxin; and this, together with its high potency and rapid onset of action, suggest that IL-1 mediates endotoxin-induced neutrophil emigration.

Animals↗
PubMedDate not supplied

[On the hypotensive activity of carrageenan iota in the rat (author's transl)].

1. Carrageenan iota and dextran sulfate deplete the plasmatic stores of kininogens in the Rat. 2. A slow intravenous infusion of carrageenan iota in the anaesthetized Rat produces a lowering of blood pressure which is only transient because of the development of tachyphylaxy. At this stage the cardio-vascular system which fails to respond to carrageenan iota injection is also refractory to ellagic acid administration. After depletion of the plasmatic stores of kininogens by dextran sulfate, glandular kallikreins or ellagic acid, carrageenan iota has lost its hypotensive properties. It is concluded that the cardio-vascular effects of carrageenan iota are mainly due to activation of the kininogenskinins system. 3. Indomethacin curtails the hypotensive effects of kinins by inhibition of the release of prostaglandins by these polypeptides. It also reduces the duration of the hypotensive response to carrageenan. Carrageenan iota is neither a histamine nor a 5-hydroxytryptamine liberator.

Albinism↗
PubMedDate not supplied

The pharmacological effects of acute and chronic clenbuterol treatments after lesions of central noradrenergic nerve terminals.

Acute administration of clenbuterol, a lipophilic beta-adrenergic agonist, decreases motor activity and antagonizes the reserpine-induced hypothermia in mice. After chronic administration of clenbuterol, the acute effect on motor activity disappears (tachyphylaxis) and the acute effect on reserpine hypothermia is potentiated (facilitation). These effects of clenbuterol (either acute or chronic + acute treatments) are not abolished after specific lesions of the noradrenergic system by the neurotoxin DSP-4 which reduces the cerebral levels of norepinephrine to 30% of controls. Although it cannot be excluded that a 70% lesion may be insufficient, another explanation is that beta-adrenergic receptors involved in hypomotility and in reserpine-induced hypothermia may not be located on noradrenergic neurons or may be different from the post-synaptic beta-adrenergic receptors which become hypersensitive after DSP-4 denervation.

Animals↗
PubMedDate not supplied

Absence of habituation of airway dilation following lung inflation.

In order to test the possibility that airway dilation following lung inflation (ADFLI) could exhibit habituation, partial and complete maximum expiratory flow-volume curves were obtained in 12 healthy individuals before and after inhaling methacholine aerosol in a dose that reduced in each individual the partial expiratory flows to approximately 50% of baseline values. Following methacholine inhalation, the difference in flows between complete and partial flow-volume curves at 40% VC was 64 +/- 22% (mean +/- SD) of partial curves after a single full lung inflation and 79 +/- 36% after 12 consecutive full inflations (p = NS). The absence of demonstrable habituation (tachyphylaxis) of ADFLI makes it unlike that ADFLI is due to a release of mediators and supports the view that it may be due to the intrinsic properties of the airway smooth muscle.

Adult↗
PubMedDate not supplied

[Microcirculation in the brain during controlled arterial hypotension. Experimental study of the effect of nipruton].

The effect of nipruton (sodium nitroprusside)-induced controlled arterial hypotension on the intracerebral microcirculatory channel was studied on 4 rabbits with transplanted induced tumors (anaplastic astrocytomas) and 7 intact rabbits under general anesthesia. It was found that nipruton injected in doses necessary for marked reduction of arterial pressure (35-45 mm Hg) for a sufficient duration (30-55 minutes) causes no circulatory disorders in the brain. In animals with tachyphylaxis to nitropruton, in which the amount of the injected agent must be increased to 9-10 mg/kg, controlled arterial hypotension even of lesser depth (60-65 mm Hg) and lesser duration (20-25 minutes) can lead to partial obstruction of the intracerebral microcirculatory channel. i. e. to the no-reflow phenomenon.

Animals↗
PubMed1979

Tachyphylactic action of high doses of pentagastrin.

The study of the human LES was performed with manometrical methods for atropine action on gastrine tachyphylaxis. Our study points out that there is a complex self regulating neuronal circuit in the LES contraction. We discuss some hypothesis for the LES control. In particular ACh could activate an inhibitory adrenergic muscarinic receptor.

Adult↗
PubMed1983

Effects of somatostatin on mammalian cortical neurons in culture: physiological actions and unusual dose response characteristics.

Somatostatin was applied to rat cortical neurons grown in dispersed cell culture while electrophysiological effects were monitored with intracellular recordings. The effects of somatostatin were predominantly excitatory, but they varied and were dose dependent. Somatostatin at concentrations between 100 pM and 1 microM depolarized 30 of 87 neurons, often with a concomitant increase in spontaneous action potentials and a small increase in membrane input resistance. Somatostatin also increased the frequency of synaptic activity coming into the recorded neuron in 45 of 78 recordings, an effect which was seen even in the absence of direct effects. In six of nine neurons, somatostatin decreased the amplitude of large ongoing inhibitory synaptic potentials, concomitant with an increase in membrane input resistance. Somatostatin occasionally caused inhibition of neuronal activity, an effect predominantly associated with the application of higher concentrations. The unpredictability of the response of an individual neuron to somatostatin is partially explained by three phenomena: a marked tachyphylaxis, an inverted U-shaped dose response curve for membrane depolarization, and qualitatively different responses depending on the concentration of somatostatin. These findings show that somatostatin is predominantly an excitatory agent when applied to cortical neurons, but it may cause several different changes in membrane properties. The dose response data suggest a considerable complexity of the actions of somatostatin at a cellular level.

Action Potentials↗
PubMed1984

Electrophysiological basis of excitation of canine colonic circular muscle by cholinergic agents and substance P.

The circular muscle layer of the canine colon exhibits omnipresent rhythmic periodic waves of depolarization (slow waves), acting as pacemaker activity. The electrophysiological and motor responses of this layer to the muscarinic agonists acetylcholine and carbachol, and to the excitatory peptide substance P, were studied using the sucrose-gap technique. In addition, changes in the contractile activity were examined in organ bath experiments. The slow waves consisted of an initial potential followed by a plateau potential. All substances depolarized the membrane and increased dramatically the duration of the plateau potential resulting in a decrease of the slow wave frequency. In addition, the amplitude of the plateau potential was often increased significantly. Carbachol and substance P readily evoked spiking activity whereas acetylcholine did not. Both spiking activity and the plateau potential generated contractile activity. The prolongation of the slow wave duration caused a profound alteration of the pattern of contractions. Long-lasting tachyphylaxis to the effect of substance P, but not to acetylcholine or carbachol, occurred. The electrophysiological and motor effects of the drugs were due to a direct action on the smooth muscle cell membrane. This study provides an electrophysiological basis for prolonged circular muscle contractions of the colon, and it emphasizes the pacemaker activity of gastrointestinal smooth muscle as an important site of drug action.

Acetylcholine↗
PubMed1984

Postjunctional Origin of the indirect-like sympathomimetic effect of metanephrine and normetanephrine on blood pressure.

The effects of metanephrine and normetanephrine have been compared with those from equiactive doses of the origin compounds, adrenaline and noradrenaline, on the pressor responses in rat, in order to determine whether their effects are owed, at least partially, to a releasing presynaptic action of the catecholamines in normal animals as well as those pretreated with reserpine, guanethidine and 6-OH-dopamine. Their effects have likewise been studied in isolated perfused renal arteries both in normal and reserpinized rats. None of the adrenolytic agent used were able either to reduce the duration of the hypertensive response or to accelerate tachyphylaxis. Identical results were obtained in renal artery preparations. It is thus concluded that the catecholamines stored in presynaptic endings are not involved in the observed phenomena and it is suggested that they might depend on the high doses required to produce effects equiactive to those of the origin substances.

Animals↗
PubMed1984

Selectivity of histamine for the proximal muscle loop of the cat pylorus.

Most drugs stimulate tonic and phasic muscular activity of the gastroduodenal junction to similar degrees except for histamine which enhances purely phasic contractions. The present study examined whether this selective histamine effect is due to a preferential action of histamine on the proximal muscle loop of the pylorus (PPL) which, unlike the distal loop (DPL), generates mostly phasic contractions. Strips were cut so as to represent the mechanical activity of muscle from the antrum, the PPL and the DPL of the cat stomach. All strips responded to acetylcholine with a combination of tonic and phasic activity. Histamine increased the frequency and the amplitude of phasic contractions in most strips from the antrum and the PPL; it increased the tonic contraction of a few DPL strips. In all types of strips, maximal histamine effects were only a fraction of the effects occurring with acetylcholine. Exposure to histamine produced no mechanical response in one fifth of the antral strips and in more than one third of the strips from both the PPL and the DPL. Histamine tachyphylaxis was marked, and sometimes irreversible. Histamine also led to phasic interruptions of flow across the isolated gastroduodenal junction without altering baseline flow. The present study demonstrates that histamine acts preferentially on those parts of the gastroduodenal junction that generate phasic rather than tonic muscular activity.

Acetylcholine↗
PubMed1981

Characteristics of succinylcholine-produced phase II neuromuscular block during enflurane, halothane, and fentanyl anesthesia.

The characteristics of phase II neuromuscular block following repeated intravenous injections of succinylcholine (SCh) were determined in 15 adult patients during enflurane, halothane, or fentanyl-nitrous oxide anesthesia. The onset of phase II block (train-of-four ratio (T4) equal to 0.5) occurred following a cumulative SCh dose of 4.4 +/- 0.3 (SEM) mg/kg of enflurane, 5.1 +/- 0.5 mg/kg of halothane, or 6.4 +/- 0.5 mg/kg of fentanyl. The cumulative SCh dose producing phase II block during fentanyl-nitrous oxide anesthesia was significantly greater than during enflurane (p less than 0.01) or halothane (p less than 0.05) anesthesia. Based on these data it is predicted that the likelihood of phase II block developing is less during fentanyl administration than during enflurane or halothane anesthesia. An abrupt transition from phase I to phase II neuromuscular block, as evidenced by an accelerated decrease in the T4 ratio, was observed during enflurane or halothane anesthesia as the cumulative SCh dose approached 3 to 5 mg/kg. The transition phase was delayed during fentanyl-nitrous oxide anesthesia, occurring after a cumulative SCh dose of 4 to 7 mg/kg. Following this transition, tachyphylaxis (decreased time between SCh injections) was observed in each study group. The T4 ratio in all three study groups stabilized at 0.15 to 0.25 after 7 to 8 mg/kg.

Adult↗
PubMed1981

Differential effects of ibuprofen and indomethacin in the regional circulation of the dog.

The effects of indomethacin and ibuprofen on aortic blood pressure and regional vascular resistances were studied in pentobarbital-anesthetized dogs. In the mesenteric vascular bed, indomethacin produced severe, acute vasoconstriction when administered by i.v. infusion as well as by i.a. injections. Tachyphylaxis developed rapidly to this response. In contrast. ibuprofen did not alter mesenteric blood flow even when a large (50 mg) i.v. bolus was rapidly injected. The mesenteric vasoconstrictor response to indomethacin was not modified when prostaglandin synthesis was inhibited or in the presence of cyproheptadine. Phentolamine exerted only a minor influence on the mesenteric vascular effect of indomethacin. The effects of indomethacin and ibuprofen on aortic blood pressure and renal blood flow were similar. Both agents increased aortic pressure and decreased renal blood flow a small but significant amount, but these responses occurred slowly and were probably not related to the acute mesenteric vasoconstricting effect or indomethacin. The present study demonstrates that these nonsteroidal anti-inflammatory agents have different effects on the mesenteric vascular bed and the data suggest that the vasoconstricting effects of indomethacin are not related to the inhibition of prostaglandin synthesis in the intestine. The data also suggest that the acute vasoconstriction in the mesenteric circulation produced by indomethacin is not mediated to a significant degree by local release of alpha adrenergic agents or serotonin.

Animals↗