Airway epithelium modulates the responsiveness of porcine bronchial smooth muscle

1988 ◽  
Vol 65 (2) ◽  
pp. 721-727 ◽  
Author(s):  
K. Stuart-Smith ◽  
P. M. Vanhoutte
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Airway Epithelium ◽  
Maximal Response ◽  
Physiological Salt Solution ◽  
Bronchial Smooth Muscle ◽  
Peak Response ◽  
Rightward Shift ◽  
Effect Curve ◽  
Fifth Order

The effect of epithelium removal on the responses of porcine airways to exogenously applied agonists and nerve stimulation was examined. Paired rings of third- (segmental), fourth- and fifth-order (subsegmental) bronchi, with and without epithelium, were placed in organ chambers in physiological salt solution (95% O2-5% CO2, 37 degrees C). Removal of the epithelium caused a leftward shift in the concentration-effect curve for acetylcholine (3rd and 4th order). A similar shift occurred for histamine (3rd and 5th order). The relaxation to isoproterenol was reduced by epithelium removal in a similar fashion in the three orders. Removal of the epithelium reduced the maximal response to KCl (3rd and 4th order) and acetylcholine (5th order). The peak response to nerve stimulation showed a significant rightward shift in the absence of epithelium. In fifth-order bronchi, tissues with epithelium showed a significantly greater degree of fade of the response to sustained electrical stimulation. Thus both epithelium-derived relaxing and contracting factors may be released in porcine airways.

Physiological and pharmacological response of canine bronchial smooth muscle in situ

1983 ◽  
Vol 54 (1) ◽  
pp. 215-224 ◽  
Author(s):  
S. G. Hendrix ◽  
N. M. Munoz ◽  
A. R. Leff
Keyword(s):  
Smooth Muscle ◽  
Electrical Stimulation ◽  
Maximal Response ◽  
Repeated Injection ◽  
Third Order ◽  
Bronchial Smooth Muscle ◽  
Pure Nitrogen ◽  
Parasympathetic Ganglion ◽  
The Right

We studied the isometric response of bronchial smooth muscle in a single third-order bronchus of 24 dogs in situ. Length-tension studies were performed in six dogs by repeated injection of 10(-5) mol acetylcholine (ACh) into the right bronchoesophageal artery, and the resting tension (30.6 +/- 6.9 g/cm) and length (0.76 +/- 0.14 cm) permitting maximal contraction were determined. In eight other dogs, dose-related bronchial contraction was obtained with 10(-10) to 10(-5) mol intra-arterial (ia) ACh. Supramaximal electrical stimulation of the right cervical vagus nerve and bronchial parasympathetic ganglion stimulation with ia 1–1-dimethyl-4-phenylpiperazinium (DMPP) also caused bronchial contraction. The maximal response to ia ACh (28.5 +/- 1.7 g/cm), supramaximal electrical stimulation (15.2 +/- 1.1 g/cm), and ia DMPP (10.5 +/- 3.0 g/cm) was blocked by an ia dose of atropine (1–5 micrograms/kg) that did not alter the sympathetic relaxation response in the trachea. In four dogs, the bronchial response to sympathetic activation was studied by intravenous (iv) bolus injection of DMPP after cholinergic blockade with atropine. DMPP (25 micrograms/kg iv) caused 9.5 +/- 2.2 g/cm bronchial relaxation, which was blocked completely by 2–4 mg/kg iv propranolol. In six other dogs, hypoxia induced by ventilation with pure nitrogen caused bronchial contraction, which was blocked by vagotomy, atropine, and hexamethonium. We report a sensitive method for selective measurement of bronchial smooth muscle response in a single resistance bronchus. This preparation preserves regional innervation and circulation and permits selective physiological stimulation in situ.

Noncholinergic vasodilator innervation in the feet of ducks

1979 ◽  
Vol 237 (2) ◽  
pp. H112-H117
Author(s):  
D. D. McGregor
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Anas Platyrhynchos ◽  
Gallus Domesticus ◽  
Krebs Solution ◽  
Vasomotor Responses ◽  
Pekin Ducks ◽  
Stimulation Of

Vasomotor responses to nerve stimulation were studied in the feet of Pekin ducks (Anas platyrhynchos) and domestic chickens (Gallus domesticus). The birds were killed and the feet isolated and perfused with a Krebs solution. Electrical stimulation of pedal nerves gave vasoconstrictor responses that were abolished by injecting guanethidine and by treating birds with reserpine. After guanethidine or reserpine, nerve stimulation resulted only in vasodilatation, which was unaffected by hexamethonium. Vasodilator responses to nerve stimulation were not blocked by hyoscine or atropine, which blocked responses to acetylcholine, nor by metiamide, which blocked vasodilatation in response to histamine. Responses to nerve stimulation were blocked by tetrodotoxin. Isoprenaline produced vasoconstriction that was blocked by phentolamine and also weak vasodilator responses that were antagonized by propranolol. It is concluded that the vasoconstrictor innervation is adrenergic. The identy of the vasodilator neurotransmitter is unknown; it is apparently not acetylcholine, a catecholamine, or histamine.

Magnetically Evoked Facial Nerve Potential

1989 ◽  
Vol 100 (4) ◽  
pp. 345-347 ◽  
Author(s):  
Ian M. Windmill ◽  
Serge A. Martinez ◽  
Christopher B. Shields ◽  
Markku Paloheimo
Keyword(s):  
Electrical Stimulation ◽  
Facial Nerve ◽  
Nerve Stimulation ◽  
Magnetic Stimulation ◽  
Electrical Current ◽  
Facial Muscle ◽  
Facial Nerve Stimulation ◽  
Muscle Responses ◽  
Stimulation Of

Facial nerve stimulation by electrical current is painful and tends to discourage serial studies. Transcutaneous magnetic stimulation of the facial nerve is painless, easily reproducible, and elicits facial muscle responses identical to electrical stimulation.

Cholinergic stimulation and blockade on urinary bladder

1961 ◽  
Vol 201 (2) ◽  
pp. 325-328 ◽  
Author(s):  
Laszlo Gyermek
Keyword(s):  
Electrical Stimulation ◽  
Urinary Bladder ◽  
Nerve Stimulation ◽  
Mode Of Action ◽  
Relative Potency ◽  
Peak Activity ◽  
Cholinergic Stimulation ◽  
Pelvic Nerve ◽  
Parasympathetic Nerve

The relative potency and mode of action of some cholinomimetics were investigated on the pelvic nerve-bladder preparation of the dog and cat. Most of the cholinomimetic agents used proved to be considerably more potent than acetylcholine (ACh). The peak activity was shown by muscarine and dl-muscarone, which were 100–300 times more potent than ACh. Atropine did not markedly influence the effect of the electrical stimulation on the pelvic nerve. Atropine also proved to be ineffective against the actions of 1,1-dimethyl,4-phenyl piperazinium iodide, serotonin, histamine, and BaCl2. It antagonized the effects of ACh only moderately, but completely inhibited the effects of muscarine and methacholine. After atropinization, hexamethonium inhibited the effects of nerve stimulation and ACh. ACh has a significant ganglionic component of its action on the bladder. It is postulated that part of the parasympathetic effector sites of the bladder functionally resemble autonomic ganglions. These ganglionic type of receptors seem to play an important role in the effects of parasympathetic nerve stimulation and in the action of ACh.

Mechanisms of airway hypercontractility in basenji-greyhound dogs

1987 ◽  
Vol 63 (5) ◽  
pp. 2008-2014 ◽  
Author(s):  
T. M. Murphy ◽  
N. M. Munoz ◽  
C. A. Hirshman ◽  
J. S. Blake ◽  
A. R. Leff
Keyword(s):  
Maximal Response ◽  
Adrenergic Blockade ◽  
Vagus Nerves ◽  
Response Curves ◽  
Bronchial Smooth Muscle ◽  
Muscarinic Response ◽  
Contractile Forces ◽  
Stimulation Of

The comparative effects of contractile agonists and physiological stimulation of the tracheal and bronchial smooth muscle (BSM) response were studied isometrically in situ in five Basenji-greyhound (BG) and six mongrel dogs. Frequency-response curves generated by bilateral stimulation of the vagus nerves (0–20 Hz, 15–20 V, 2-ms duration) elicited greater maximal contraction in mongrel trachea (36.8 +/- 8.1 vs. 26.9 +/- 4.0 g/cm; P less than 0.02) and exhibited greater responsiveness in mongrel BSM (half-maximal response to electrical stimulation 3.0 +/- 1.1 vs. 7.0 +/- 0.5 Hz; P less than 0.05) compared with BG dogs. However, muscarinic sensitivity to intravenous methacholine (MCh) was substantially greater in BG dogs; MCh caused contraction greater than 1.5 g/cm at a mean dose of 3.0 X 10(-10) mol/kg for BG dogs compared with 5.1 X 10(-9) mol/kg for mongrel controls (P less than 0.03, Mann-Whitney rank-sum test). In contrast to the muscarinic response, the contractile response elicited by intravenous norepinephrine after beta-adrenergic blockade was similar in trachea and bronchus for both mongrel and BG dogs. Our data confirm previous in vitro demonstration of tracheal hyporesponsiveness in BG dogs and demonstrate that the contraction resulting from efferent parasympathetic stimulation is less in the BG than mongrel dogs. However, postsynaptic muscarinic responsiveness of BG BSM is substantially increased. We conclude that a component of airway responsiveness in BG dogs depends directly on contractile forces generated postsynaptically that are nongeometry dependent, postjunctional, and agonist specific.

Effect of vibration on a canine cutaneous artery

1986 ◽  
Vol 250 (3) ◽  
pp. H519-H523 ◽  
Author(s):  
L. E. Lindblad ◽  
R. R. Lorenz ◽  
J. T. Shepherd ◽  
P. M. Vanhoutte
Keyword(s):  
Electrical Stimulation ◽  
Calcium Ions ◽  
Adrenergic Nerve ◽  
Potassium Ions ◽  
Calcium Entry Blocker ◽  
Plateau Phase ◽  
Sympathetic Nerve Stimulation ◽  
Peak Response ◽  
Prostaglandin F2 Alpha ◽  
Adrenergic Nerve Endings

Vibration of rings of isolated canine saphenous arteries depressed contractions induced by potassium chloride, prostaglandin F2 alpha, and activation of the adrenergic nerve endings by electrical stimulation. Peak contractions to exogenous norepinephrine were not significantly affected by vibration, being augmented, unchanged, or depressed, whereas contractions during the stable plateau phase were depressed. The calcium entry blocker diltiazem reduced the peak response but not the stable plateau phase of the contraction to norepinephrine; in the presence of diltiazem, vibration still depressed the latter. When vibration was applied during the steady state of contractions evoked by electrical stimulation, the depression was immediate, and its extent increased with both the amplitude (0.025-0.10 mm) and the frequency (30-150 Hz) of vibration. In arteries labeled with [3H]norepinephrine, vibration (120 Hz, 0.1 mm amplitude) during electrical stimulation induced a slight but significant increase in the release of labeled transmitter. It is suggested that the depression of contractions to potassium ions, prostaglandin F2 alpha, sympathetic nerve stimulation, and the plateau phase of the response to exogenous norepinephrine are caused by vibration depressing the force-generating process in vascular smooth muscle. Failure of vibration to significantly depress the peak contraction to norepinephrine may be explained by the facilitation by vibration of the influx of extracellular calcium ions.

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