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PubMedDate not supplied

Clinical outcome of laryngotracheal separation for intractable aspiration pneumonia.

OBJECTIVES: To confirm that laryngotracheal separation (LTS) is a satisfactory treatment for patients with intractable aspiration pneumonia, even though it does not require tracheoesophageal anastomosis. STUDY DESIGN: Retrospective. METHODS: Nine patients with intractable aspiration pneumonia underwent LTS at our institution from 1996 to 1999. Two patients underwent postoperative barium swallow radiography. RESULTS: Neither halitosis nor stimulation of the cough reflex occurred due to pooled secretions in the blind pouch of the proximal tracheal segment. Barium swallow radiography confirmed that the secretions drained within 40 min by swallowing or a change in patient position. CONCLUSION: LTS is a satisfactory solution to the problem of chronic aspiration. Neither pooled secretions in the proximal tracheal segment nor fistula formation were significant postoperative problems.

Adolescent↗
PubMed2001

Modulatory effect of protein kinase C activator on contractility of rat vas deferens.

The modulatory effect of the protein kinase C activator was examined on contraction of rat isolated vas deferens induced by constrictive agonists, noradrenaline (NA), ATP, BaCl2 and high K+. Phorbol 12,13-diacetate (PDA, 1 micromol/l) induced a transient extracellular Ca(2+)-dependent contraction while the inactive analogue, 4alpha-phorbol (1 micromol/l) had no effect. PDA significantly enhanced the peak amplitude of the contractile response to NA (0.1-10 micromol/l), ATP (100 micromol/l), Ba2+ (3 mmol/l) or high K+ (30 mmol/l). Staurosporine at 30 nmol/l reduced the enhancing effect of PDA on the agonist-induced contraction. NA (10 micromol/l) produced a phasic contraction followed by a sustained contraction, while ATP induced monophasic contraction. Pretreatment with nifedipine (10 nmol/l) had no effect on the phasic contraction induced by NA, but it significantly reduced ATP- or high K(+)-induced contraction. Staurosporine (30 nmol/l) alone attenuated the peak contractile response induced by NA or ATP but not by Ba2+. NA produced a transient contraction in Ca(2+)-free Krebs solution, and PDA (1 micromol/l) markedly enhanced this effect. These novel data indicate that activation of a protein kinase C-dependent mechanism not only affects contraction mediated by Ca2+ influx through voltage-sensitive Ca2+ channels, but also promotes intracellular Ca2+ release or intracellular Ca(2+)-mediated contractile mechanism in rat vas deferens.

Adenosine Triphosphate↗
PubMed2001

Antidiarrheal activity of wood creosote: inhibition of muscle contraction and enterotoxin-induced fluid secretion in rabbit small intestine.

Wood creosote has long been used as an antidiarrheal agent, but its mechanism of action is not well understood. To elucidate the mechanism of its antidiarrheal activity, we have addressed questions whether it inhibits fluid secretion induced by Escherichia coli heat-stable enterotoxin (STa) in rabbit jejunum in vivo, and whether it inhibits muscle contraction of isolated rabbit ileum ex vivo. Wood creosote (10-100 mg/l) instilled in a ligated loop of jejunum inhibited STa-induced fluid secretion (p < 0.05). It also inhibited the spontaneous phasic, acetylcholine-induced tonic and Ba2+-induced tonic contractions of longitudinal and circular muscles of ileum dose-dependently with IC(50) values of 130-530 mg/l. These data provide further evidence that the antidiarrheal activity of wood creosote is attributable to its antisecretory and antimotility effects.

Acetylcholine↗
PubMed1985

Motor responses of cyproterone acetate-treated rat vas deferens to electrical field stimulation, noradrenaline and barium chloride.

The effect of cyproterone acetate (CA) was studied on the autonomic transmission and smooth muscle function of the rat vas deferens. In the CA-treated vas deferens, the endogenously released noradrenaline (NA) in response to electrical field stimulation or exogenously administered NA produced rhythmic contractions (lacking a tonic component) which were abolished by prazosin - a preferential postjunctional alpha-adrenoceptor blocker. The biphasic nature of the nonadrenergic response elicited on electrical field stimulation in CA-treated rats remained unaltered. Like in controls, yohimbine potentiated this response thereby demonstrating the presence of functional presynaptic alpha-adrenoceptors (inhibitory in nature). The postjunctional alteration on the membrane function appears to be specific to adrenergic stimulation alone, since both tonic and phasic components were demonstrated in the responses resulting from nonadrenergic stimulation or those produced by barium chloride.

Animals↗
PubMed1986

Comparison of the effects of nifedipine, diltiazem and verapamil on the mechanical activity of rabbit papillary muscles induced by barium chloride.

Isolated rabbit papillary muscles that do not present pacemaker activity under physiological conditions develop a spontaneous activity in the presence of 2 mmol/l BaCl2. Ba-induced contractions were unaffected by high concentrations of the Na antagonist procainamide (10(-5) mol/l). Tetrodotoxin (10(-5) mol/l), a specific blocker of the fast Na current, only slightly increased the amplitude of contractions. In contrast, the calcium entry blockers nifedipine, diltiazem, and verapamil strongly depressed the mechanical activity in a time- and dose-dependent manner. The concentrations that decreased the amplitude and frequency of contractions by 50% were determined. The order of potency was nifedipine much greater than diltiazem greater than or equal to verapamil. Ba-induced automaticity is a particularly useful model on which the potency of calcium entry blockers could be assessed.

Animals↗
PubMed1989

Effect of induced thyroid dysfunction upon uterine responsiveness in strips from pregnant and nonpregnant rats.

The influence of thyroid dysfunction on rat myometrial responsiveness to oxytocin, acetylcholine, CaCl2 and BaCl2 was assessed in uterine strips from pregnant and nonpregnant rats. In preparations obtained from hypothyroid nonpregnant rats, oxytocin and acetylcholine concentration-response curves were significantly displaced to the left, whereas myometrial strips from hyperthyroid nonpregnant rats were only supersensitive to acetylcholine. In relation to the pregnant state, T3 treatment caused an increased myometrial sensitivity to both oxytocin and acetylcholine. In this condition, concentration-response curves for oxytocin did not differ from nonpregnant control animals, whereas acetylcholine was about 300-fold more potent at the ED50 levels compared with those in nonpregnant animals. Either in pregnant or nonpregnant state, maximal responses and ED50 to BaCl2 did not differ. In addition, thyroid dysfunction did not modify the pattern of CaCl2-induced contractions in isolated myometrial strips from pregnant rats. This data extended to the myometrium, previous evidence in the literature indicating that thyroid dysfunction may affect uterine responsiveness to agonists.

Acetylcholine↗
PubMed1994

Vascular reactivity to vasoconstrictors in aorta and renal vasculature of hyperthyroid and hypothyroid rats.

Vascular reactivity to vasoconstrictors in relation to altered thyroid function was studied in two preparations: aortic strips and the isolated perfused kidney. To assess whether the possible alterations in vascular reactivity were restricted to a specific agonist or whether they involved the contractile system, receptor-mediated and nonspecific smooth muscle stimulants were used. Male Wistar rats were divided into three groups: control, hyperthyroid and hypothyroid rats. Aortic strips from hypothyroid rats were less sensitive to phenylephrine and KCl when the data were expressed in absolute values or as percentages of the maximum responses. Sensitivity and reactivity in strips from hyperthyroid rats were similar to those observed in control strips. Renal vasculature obtained from hypothyroid rats also showed a markedly reduced sensitivity to phenylephrine, with normal maximal responses. The response to vasopressin at 3-10(-11) mol/l was also decreased, as was the reactivity to barium chloride. In contrast, renal vasculature of hyperthyroid rats showed markedly enhanced reactivity to all agonists: the concentration-response curves were characterized by a similar threshold and a greater maximal response. These results demonstrate that hypothyroidism is accompanied by a marked decrease in sensitivity to vasoconstrictors in large arteries as well as in resistance vessels. This decrease may be secondary to a generalized alteration in the contractile system of vascular smooth muscle cells and may play a role in the decreased blood pressure in these animals. In contrast, isolated perfused kidneys of hyperthyroid rats showed increased vascular reactivity to vasoconstrictors, which may play a role in the maintenance of elevated blood pressure in these animals.

Animals↗
PubMed1981

Angiotensin induction of active responses in cultured reaggregates of rat aortic smooth muscle cells.

Electrical activity was studied in cultured reaggregates of vascular smooth muscle cells prepared from the aortas of normotensive (WKY) and spontaneously hypertensive (SHR) rats. There were no significant differences between the resting membrane potentials of WKY (- 44.7 +/- 0.5 mV) and SHR (- 45.6 +/- 0.5 mV) reaggregates. Electrical field stimulation elicited active responses that consisted of two components: an initial spike component (amplitude, 30-40 mV; +Vmax 1-3 V/s) and a plateau component (amplitude, 10-30 mV; duration 3-5s; +Vmax, 0.1-0.3 V/s). Often the spike component was absent. Both components of the response were abolished by verapamil, Mn++, and Na+-free solutions indicating that Na+ and Ca++ currents may be associated with them. Addition of 10 mM TEA increased the duration of the response, and addition of 0.5 mM BaCl2 to the TEA solution increased the duration even further. The spike component always occurred in the presence of TEA and Ba++. No differences were observed between responses in WKY and SHR reaggregates. A bolus of angiotensin II (AII) (bolus concentration of 1 micro M) elicited a transient depolarization. In some cells an active membrane response was triggered by the depolarization and sometimes included the spike component. Replacing all the Na+ in the solution with either Tris or choline resulted in loss of the response to AII, and in some cells a hyperpolarization was actually seen on addition of the AII. The response to AII was insensitive to verapamil (up to 10(-5) M), but was blocked by 1 mM MnCl2. Reaggregates from both WKY and SHR animals gave similar responses to AII. The data indicates that cultured reaggregates of vascular smooth muscle are electrically excitable and are sensitive to angiotensin. Therefore functional angiotensin receptors must be present in the cultured cells.

Angiotensin II↗
PubMed1985

Inhibition of barium-induced constriction of cerebral surface arterioles by blockers of calcium channels.

Barium ion, applied as BaCl2 to the cerebral surface, produces marked constriction of pial arterioles. The present data demonstrate that this constriction is inhibited by the calcium channel blockers verapamil and nimodipine. Verapamil in concentrations as low as 10)-7) M was effective in local administration. Verapamil in milligram per kilogram doses and nimodipine in microgram per kilogram doses were effective 30 min after intraperitoneal injection without producing dilation. The basis for the inhibitory action of the calcium channel blockers is not established by the data. However, in view of barium's known ability to depolarize membranes, it may be that the constriction which results is related to inward passage of ions and is facilitated by inward movements of calcium.

Animals↗
PubMedDate not supplied

Modulatory role of endothelium-derived relaxing factors on the response to vasoconstrictors and flow-pressure curve in the isolated perfused rat kidney.

The aim of this study was to compare the effects of the blockade of nitric oxide (NO) and of endothelium-derived hyperpolarizing factor (EDHF) on the response to vasoconstrictors (VC) and on the flow-pressure curve in the isolated perfused rat kidney. To this end, dose-response curves to phenylephrine and BaCl2 were studied in the renal vasculature under basal conditions and after the infusion of N(omega)-nitro-L-arginine methyl ester (L-NAME) and tetraethylammonium (TEA) in endothelium-intact and endothelium-denuded (CHAPS-treated) preparations. In another experiment, renal flow-pressure curves were obtained under basal conditions and after the infusion of L-NAME or TEA. The flow-pressure curve was obtained by increasing renal perfusion flow (RPF) from 2.5 to 15 ml/min/g kidney weight (KW) over the basal level (5 ml/min/g KW). L-NAME or TEA produced a leftward shift of the dose-response curves of both VC, and the simultaneous administration of L-NAME and TEA produced a greater shift to the left in the pressor response curves. CHAPS treatment produced a leftward shift of the dose-response curves of both VC, and the dose-response curves were not significantly modified by the infusion of L-NAME or TEA. L-NAME markedly shifted the flow-pressure curve upward, especially at higher levels of RPF. However, the administration of TEA, perfusate solution (Tyrode) or D-NAME did not significantly change the flow-pressure curve. These results suggest that NO is released in response to VC as well as to increased perfusion flow in the isolated renal vascular bed. However, EDHF release seems to be stimulated by VC but not by increased perfusion flow.

Animals↗
PubMed1984

Protective effects of ketotifen on guinea pig trachea.

We have studied the effects of ketotifen (Ke), an effective antiallergic drug, on guinea pig trachea. Ke (10(-6)-5 X 10(-5) M) inhibits contractions induced in this preparation by acetylcholine, prostaglandin F2 alpha, barium chloride, potassium chloride and electrical stimulation. These results provide evidence for protective effects of Ke in airways. Furthermore, Ke exerts also a neural inhibitory effect on postganglionic parasympathetic fibers of guinea pig trachea. These findings resemble the effects reported previously for disodium cromoglycate by us and might be relevant for antiasthmatic and antiallergic properties of Ke.

Acetylcholine↗
PubMed1994

Enhancement of the responsiveness of vas deferens and ileum smooth muscle in sensitized guinea pigs: in vitro study.

Changes in the reactivity of the ileum (to histamine and barium chloride) and vas deferens (to acetylcholine and barium chloride), isolated from actively egg albumen-sensitized guinea pigs, have been investigated. The study was performed on 2 guinea pig strains: the Dunkin-Hartley strain, usually used as an airway allergic model, and the BFA strain. In actively sensitized guinea pigs of both strains, concentration-response curves exhibited a significant dose-dependent upward shift compared to those obtained in control guinea pigs. The maximal contraction strength calculated from these curves was significantly enhanced in both sensitized guinea pig strains, without a change in EC50 values. This study showed that the active antigen sensitization procedure involved several smooth muscle functions, and not exclusively the trachea.

Acetylcholine↗
PubMed1995

Strain-related differences in the tracheal responsiveness of sensitized guinea pig.

The purpose of this study was to evaluate the strain-related differences in tracheal hyperresponsiveness in control and egg albumen-sensitized guinea pigs. Concentration-response curves to acetylcholine and barium chloride were established from tracheal rings of Dunkin-Hartley and BFA strain guinea pigs. In the Dunkin-Hartley strain, sensitization did not significantly increase the tracheal responsiveness to acetylcholine and barium chloride. By contrast, in the BFA strain, significant sensitization-induced hyperreactivity was achieved as the maximal contractions induced by acetylcholine and barium chloride, were enhanced from 6.5 +/- 1.2 and 3.2 +/- 0.4 mN in control to 10.0 +/- 1.4 and 5.6 +/- 0.8 mN, respectively, in sensitized animals. However, antigen challenge, performed in vitro, exhibited a similar amplitude of contraction in tracheal rings from both strains (Dunkin-Hartley 5.1 +/- 0.8 mN; BFA 5.9 +/- 0.5 mN). Finally, while the two guinea-pig strains developed specific sensitization to allergen, only tracheal rings from the BFA strain developed hyperresponsiveness to acetylcholine and barium chloride. The strain-related difference appears to be partly explained by a lower basal reactivity in the BFA strain both acetylcholine (Em 7.3 +/- 1.7 and 6.5 +/- 1.2 mN for Dunkin-Hartley and BFA, respectively) and barium chloride (Em 9.4 +/- 2.6 and 3.2 +/- 0.4 mN for Dunkin-Hartley and BFA, respectively). As the same procedure of sensitization provides different results in the genesis of hyperreactivity between the two guinea-pig strains used for asthma models, the BFA guinea-pig strain seems to be a better model because sensitized non-challenged animals could easily be dissociated from control ones, similar to that which occurs in asthmatic patients during provocation tests with cholinergic drugs.

Acetylcholine↗
PubMed1987

Effects of disopyramide on detrusor muscle contraction: in vitro experiment and report of 3 cases with disopyramide-induced urinary retention.

Three cases of disopyramide-induced urinary retention were reported and effects of disopyramide on agonist-induced contraction of detrusor muscle were studied in vitro. Muscle strips were obtained from rabbit bladder body and changes in isometric contraction of the strips were monitored. Acetylcholine, prostaglandin F2-alpha, potassium chloride, barium chloride, adenosine triphosphate and Ca2+ were used as agonists for detrusor muscle contraction. Disopyramide relaxed the contraction elicited by acetylcholine in normal Krebs solution, but exhibited no relaxing effect on contractions induced by prostaglandin F2-alpha, potassium chloride, barium chloride and adenosine triphosphate. In Ca2+-free Krebs solution, basal tension of the strips declined and spontaneous contractile activity was eliminated. Replenishment of 3 mM Ca2+ induced a slow contraction and redevelopment of spontaneous contraction of the strips. Pretreatment of the strips with disopyramide had no inhibitory effect on the Ca2+-induced contraction or on the spontaneous contractile activity in Ca2+-free solution. In normal Krebs solution, acetylcholine (10(-9)-10(-2)M) caused dose-dependent contractions of the detrusor muscle strips. Pretreatment of the strips with disopyramide (10(-5)-10(-3)M) dose-dependently inhibited the acetylcholine-induced contraction in a competitive way. The inhibitory effect of disopyramide on acetylcholine-induced contraction was less potent than that of atropine. We conclude that disopyramide may inhibit detrusor contractile activity mostly by its anticholinergic effect, resulting clinically in micturition disturbance.

Acetylcholine↗
PubMed1983

A simple and sensitive cAMP phosphodiesterase assay using a modification of the Ba(OH)2-ZnSO4 precipitation method.

A modification of the zinc-barium precipitation method is described for the measurement of phosphodiesterase activity. This method differs from the previous precipitation method in that it measures the appearance of the 5'-AMP product in the precipitate rather than the disappearance of the cAMP substrate from the supernatant. The method is simple, rapid, accurate and possesses a high sensitivity. It can be used to measure both the calmodulin activatable and nonactivatable forms of the enzyme. The procedure can be applied to monitoring phosphodiesterase activity throughout the purification of the enzyme from various tissues.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1986

The monophasic action potential upstroke: a means of characterizing local conduction.

The upstrokes of monophasic action potentials (MAPs) recorded with an extracellular pressure electrode were characterized in isolated canine tissue preparations in vitro. The characteristics of the MAP upstroke were compared with those of the local action potential foot as well as with the characteristics of approaching electrical activation during uniform and asynchronous conduction. The upstroke of the MAP was exponential during uniform conduction. The time constant of rise of the MAP upstroke (TMAP) correlated with that of the action potential foot (Tfoot): TMAP + 1.01 Tfoot + 0.50; r2 = .80. Furthermore, changes in Tfoot with alterations in cycle length were associated with similar changes in TMAP: Tfoot = 1.06 TMAP - 0.11; r2 = .78. In addition, TMAP and Tfoot both deviated from exponential during asynchronous activation; the inflections that developed in the MAP upstroke correlated in time with intracellular action potential upstrokes that were asynchronous in onset in these tissues. Finally, the field of view of the MAP was determined and was found to be dependent in part on tissue architecture and the space constant. Specifically, the field of view of the MAP was found to be greater parallel compared with transverse to fiber orientation (6.02 +/- 1.74 vs 3.03 +/- 1.10 mm; p less than .01). These data suggest that the MAP upstroke may be used to define and characterize local electrical activation. The relatively large field of view of the MAP suggests that this technique may be a sensitive means to record focal membrane phenomena in vivo.

Action Potentials↗
PubMed1996

Modulation of the hyperpolarization-activated current (I(f)) by adenosine in rabbit sinoatrial myocytes.

BACKGROUND: Modulation of sinoatrial pacemaking by adenosine (Ado) in the absence of concomitant adrenergic stimulation (direct modulation) has been attributed to activation of a K+ conductance. In the present study, we evaluated the direct effects of Ado on the pacemaking current I(f) and tested their interaction with those of acetylcholine (ACh). METHODS AND RESULTS: Rabbit sinoatrial myocytes were patch-clamped at 35 degrees C in the presence of 1 mmol/L BaCl2 and 2 mmol/ L MnCl2, Ado (1 mumol/L) reversibly reduced I(f) by 33.1 +/- 5.7% of control (n = 5; P < .05). Ado (1 mumol/L) reversibly shifted I(f) midactivation potential by -6.63 +/- 1.18 mV (n = 4; P < .05). Fully activated I(f) conductance (0.262 +/- 0.037 versus 0.254 +/- 0.036 nS/ pF; n = 6, NS) and reversal potential (-17.35 +/- 0.99 versus -18.01 +/- 1.42 mV; n = 6, NS) were not changed by 10 mumol/L Ado. The Ado receptor antagonist 8-PST (10 mumol/L) reversed the effect of 0.3 mumol/L Ado by 64.9 +/- 4.2% (n = 6; P < .05). Ado maximally shifted the I(f) activation curve by -5.85 mV, with a half-maximal concentration of 0.0796 mumol/L (n = 93). The shifts in I(f) activation induced by Ado (0.3 mumol/L) and ACh (1 mumol/ L) separately were -4.89 +/- 0.05 and -8.84 +/- 0.51 mV, respectively; concomitant Ado and ACh superfusion shifted activation by -9.7 +/- 0.45 mV (NS versus ACh alone; n = 9). Threshold Ado concentrations dose-dependently reduced the rate of spontaneous pacemaker activity (eg, -18.8 +/- 3.4% at Ado 0.03 mumol/L). CONCLUSIONS: Submicromolar Ado directly inhibits I(f) and slows pacemaking in sinoatrial myocytes; the mode of I(f) inhibition is similar to that previously described for ACh. Thus, Ado may exert local modulation of sinus rate through signaling pathways similar to those used by ACh.

Acetylcholine↗
PubMed1999

Hyperkalemia enhances the effect of adenosine on IK,ADO in rabbit isolated AV nodal myocytes and on AV nodal conduction in guinea pig isolated heart.

BACKGROUND: The atrioventricular (AV) node is insensitive to changes in extracellular potassium concentration, [K+]o, because of the absence of the inward rectifier potassium current (IK1). However, we propose that in the presence of adenosine, elevated [K+]o should increase the adenosine-activated inward rectifier potassium current (IK,ADO) in AV nodal myocytes and hence augment the negative dromotropic effect of the nucleoside. METHODS AND RESULTS: The effects of normal (4.8 mmol/L) and high (8.0 mmol/L) [K+]o on adenosine-induced changes in resting membrane potential (Vm), IK,ADO, and membrane resistance (Rm) in rabbit isolated AV nodal myocytes and in AV nodal conduction delay (atrium-to-His bundle, AH, interval) in guinea pig isolated hearts were determined with the use of whole-cell patch-clamp and His bundle electrogram techniques, respectively. High [K+]o alone did not significantly affect membrane current, Rm, or Vm in AV nodal myocytes. However, high [K+]o in the presence of adenosine (3 micromol/L) markedly increased Im (-0. 249+/-0.038 to -0.571+/-0.111 nA, P<0.05) at -100 mV and reduced Rm (151+/-21 to 77+/-8 MOmega, P<0.02). Adenosine still hyperpolarized Vm from -48+/-2 to -65+/-1 mV (P<0.001). High [K+]o alone did not significantly affect the AH interval in isolated hearts. However, high [K+]o markedly lengthened the AH interval prolongation caused by adenosine (4 micromol/L, 7.9+/-0.8 vs 22.1+/-3.0 ms, P<0.001). The potentiating effect of high [K+]o on adenosine-induced delay in AV nodal conduction was abolished by BaCl2 (100 micromol/L). CONCLUSIONS: By increasing IK,ADO and decreasing Rm of AV nodal myocytes, elevated [K+]o, augments the depressant effect of adenosine on AV nodal conduction.

Adenosine↗