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PubMed1987

Antagonist discrimination of two muscarinic responses elicited by applied agonists and orthodromic stimuli in superior cervical ganglion of rabbit.

Pirenzepine and gallamine selectively and differentially antagonized two muscarinic responses, in the superior cervical ganglion of the rabbit, whether elicited by the muscarinic agonist methacholine or by orthodromic stimulation. Methacholine elicited a biphasic ganglionic response, consisting of hyperpolarizing and depolarizing components that were the agonist-induced equivalents of the slow-inhibitory and slow-excitatory postsynaptic potentials elicited by orthodromic stimulation. Superfusion of ganglia with pirenzepine resulted in a concentration-dependent suppression of depolarization induced by methacholine with no suppressant action on ganglionic hyperpolarization. In contrast, superfusion of ganglia with gallamine resulted in a concentration-dependent suppression of ganglionic hyperpolarization and the slow-inhibitory postsynaptic potential. These effects occurred without appreciable suppression of ganglionic depolarization or the slow-excitatory postsynaptic potential. The action of gallamine was specific for muscarinic hyperpolarization. Hyperpolarizations produced by superfusion with dopamine or norepinephrine were unaffected by gallamine, at concentrations that suppressed the muscarinic slow-inhibitory post-synaptic potential. Incubation with anti-cholinesterases produced a parallel shift, to the right, of concentration-response curves for suppression by gallamine of the slow-inhibitory postsynaptic potential. This was presumably the consequence of an increase in the acetylcholine available for interaction with the muscarinic receptor. The evidence suggests that the ability of gallamine and pirenzepine to suppress selectively the slow-inhibitory and slow-excitatory postsynaptic potentials, as previously demonstrated, is through an action at muscarinic receptors. Furthermore, the data suggest that these pharmacological agents produce their effects by interaction at different muscarinic recognition sites.

Animals↗
PubMed1990

Differential effects of the muscarinic M2 antagonists, AF-DX 116 and gallamine, on single neurons of rabbit sympathetic ganglia.

Intracellular recording techniques were used to compare the effects of the M2 muscarinic antagonists, AF-DX 116 and gallamine, on membrane potential (Vm), input resistance (Ri), responses induced by methacholine, muscarinic slow postsynaptic potentials and action potentials in the superior cervical ganglion of the rabbit. Gallamine or AF-DX 116 antagonized methacholine-induced or synaptically-evoked muscarinic hyperpolarization, without having significant effect on depolarization induced by methacholine or synaptically. The drug AF-DX 116 reduced evoked muscarinic hyperpolarizing potentials, without significant change in Vm or Ri, recorded in the absence of muscarinic stimulation. In contrast to AF-DX 116, gallamine elicited a concentration-dependent depolarization of the membrane, with a corresponding increase in Ri, when tested in the absence of muscarinic stimulation. These effects of gallamine were accompanied by an increase in duration and decrease in the slope of the descending phase of the action potential. Blockade by gallamine of evoked hyperpolarization was independent of membrane depolarization and readily occurred when gallamine-induced depolarization was prevented by clamping Vm at its pre-gallamine level. The effects of gallamine were maintained during its presence and reversed upon washing with gallamine-free physiological solution. These results indicate that AF-DX 116 and gallamine have a specificity for antagonism of muscarinic responses, mediated by receptors of the M2 type in the superior cervical ganglion. However, gallamine, while an effective antagonist of M2 responses, also has the ability to modify the electrical characteristics of ganglion cells and thus may modify ganglionic transmission by mechanisms other than antagonism of receptors.

Action Potentials↗
PubMed1985

Pharmacology of the erectile tissue of the canine penis.

To assess the role of different neuroeffector systems in penile erection, pharmacological agents were tested in vitro using strips of corpus cavernosum tissue from the dog. Alpha-adrenoceptor agonists, K+ or histamine caused concentration-dependent contraction. Tyramine caused a poorly sustained contraction, as did nicotine in some cases. In precontracted preparations, relaxation was caused by beta2-adrenoceptor or muscarinic cholinoceptor agonists, or by vasoactive intestinal peptide. The results suggest that a noradrenergic alpha-adrenoceptor system maintains penile flaccidity in the dog. Penile erection may result from the activation of inhibitory beta2-adrenergic, muscarinic and/or peptidergic systems.

Adrenergic beta-Agonists↗
PubMed1985

Effect of propranolol on pulmonary function and bronchoconstrictor responsiveness in guinea pigs and rats.

The beta-blocker propranolol was studied for its effects on basal pulmonary functions and on bronchoconstrictor responses to methacholine and histamine in mechanically ventilated guinea pigs and rats. Using doses that blocked the antibronchoconstrictor (bronchodilator) effects of the beta 2-agonist salbutamol, propranolol had no measurable effect on basal airway resistance and dynamic lung compliance in both guinea pigs and rats. However, bronchoconstrictor responses to methacholine and histamine were augmented by propranolol in guinea pigs. In contrast, propranolol did not change bronchoconstrictor responses to methacholine in rats. These results are discussed in terms of the functional role of pulmonary beta-receptors in guinea pigs and rats.

Airway Resistance↗
PubMed1978

Occlusion pressure in acute bronchospasm induced by methylcholine.

We measured resting minute ventilation, the pressure developed by the inspiratory muscles during the first 0.1 sec of inspiratory effect against an occluded airway (P0.1), FRC and airway resistance in normal subjects during bronchoconstriction induced by methylcholine inhalation and again after the bronchoconstriction had been reversed by inhaled isoproterenol. Methylcholine resulted in a 2- to 3-fold increase in airway resistance, FRC rose in 5/6 subjects and ventilation changed in variable fashion. P0.1 increased in all subjects with methylcholine and decreased after isoproterenol. When the subjects were considred as a group, P0.1 correlated positively with airway resistance. Normal subjects respond to bronchoconstriction as they do to external resistance loading, by increasing inspiratory muscle activity. During bronchoconstriction, all subjects demonstrated an increase of breathing frequency and a decrease in the duration of expiration; inspiratory duration did not change significantly. This response may have been due to activity of pulmonary irritant receptors. Breathing frequency and expiratory duration returned to control levels with isoproterenol, so we could not show that this response was independent of changes in lung mechanics.

Adult↗
PubMed1984

Effects of bronchoconstriction on breathing during normoxia and hypoxia in anesthetized cats.

The effect of an increase in bronchomotor tone on control of breathing during both normoxia and hypoxia, and the role of vagal afferents in regulating these responses were studied in 15 anesthetized cats. Minute ventilation (VE) was measured with a pneumotachograph connected in series with a tracheal cannula. Total diaphragmatic EMG activity per minute (means p X f, peak EMG moving average X respiratory frequency) was measured to assess the central inspiratory drive. Bronchoconstriction was generated by inhalation of methacholine aerosol (10-30 breaths, 0.5% solution) which increased total lung resistance to approximately 400% of the control value. Transient hypoxia was induced by allowing the cats to rebreathe a hypoxic gas mixture (4.5% O2 balanced N2) for approximately 1 min. During normoxia, bronchoconstriction increased VE from a baseline of 100 to 129 +/- 7% (mean +/- SEM; P less than 0.05) and increased (means p X f) from 100 to 174 +/- 16% (P less than 0.01). During hypoxia, the response of (means p X f) to bronchoconstriction (404 +/- 40%) was still greater than without bronchoconstriction (306 +/- 35%; P less than 0.01), but the responses of VE were not significantly different between these two conditions (P greater than 0.05). After sectioning both vagus nerves the bronchoconstriction-induced increase in central inspiratory drive was either reduced (during normoxia) or abolished (during hypoxia). These results suggest that stimulation of vagal bronchopulmonary afferents are involved in regulating the ventilatory responses to bronchoconstriction. Other non-vagal factors, such as intrinsic properties and reflex responses of the respiratory muscles, may also contribute, in part, to the observed responses.

Anesthesia↗
PubMed1984

The relationship between bronchial hyperresponsiveness to methacholine and airway smooth muscle structure and reactivity.

The airway responsiveness of a group of 25 patients scheduled for lung resection was studied. 10 of 25 patients had a greater than or equal to 20% fall in FEV1 in response to inhaled methacholine (responders), with PD20 FEV1 values ranging from 0.6 to 7.3 mumol. Methacholine did not induce a 20% fall in FEV1 in 15 patients (non-responders). The sensitivity to carbachol and histamine of the bronchial smooth muscle resected from these patients was similar in tissue from responders and non-responders. There was no correlation between in vivo responsiveness to methacholine and in vitro sensitivity to carbachol or histamine. The volume of smooth muscle in some of these airway preparations was quantitated. There was a significant correlation between the maximum tension change in response to histamine and the volume of smooth muscle in each airway. There was no similar correlation for carbachol. The in vivo responsiveness to methacholine and in vitro sensitivity to histamine or carbachol was not related to the degree of inflammation in the airways studied. It is concluded that in vivo responsiveness cannot be explained in terms of smooth muscle sensitivity and that there may be differences between histamine and carbachol in the mechanism of contraction of airway smooth muscle.

Adult↗
PubMed1985

Alteration of airway reactivity by mucus.

In 11 beagles with permanent tracheostomies we investigated whether mucus hypersecretion alters airway reactivity to inhaled aerosols. Mucus was collected from the dogs while awake by resting a cytology brush on the lower tracheal mucosa; the mucus collection rate was used as an index of mucus flux. Mucus linear velocity was determined under light sedation by bronchoscopically observing the rate of particle clearance in the trachea. Mucus depth was then computed from the flux and velocity. On a separate occasion, under pentobarbital anesthesia, methacholine aerosols (1 min duration) were given at 10 min intervals in doubling doses up to at least 2 mg/ml. Pulmonary resistance RL was determined prior to and 2 min after each dose. After a 1 h pause, methacholine was infused at a constant rate of 40 micrograms X kg-1 X min-1 for 10 min. This dose produced a plateau in RL after approximately 3 min; the mean rise in RL was similar to that achieved with the 2 mg/ml aerosol. The infusion response Rinf was defined as the change in RL 4-5 min post infusion; the aerosol response Raer was defined as the change in RL 2 min post 2 mg/ml aerosol. There was no significant correlation between Rinf and Raer, nor between either Rinf or Raer and mucus flux. There was, however, a strong positive association between Rinf/Raer and mucus flux and a similar positive association between Rinf/Raer and mucus depth. These associations indicate that dogs with elevated secretion levels are relatively unresponsive to aerosolized as opposed to infused methacholine. Thus, to the extent that infusion reactivity reflects innate airway reactivity, the reactivity to inhaled aerosol may underestimate the true value when mucus hypersecretion occurs.

Aerosols↗
PubMed1986

Airway responses to methacholine and histamine in basenji greyhounds and other purebred dogs.

To investigate whether airway hyperresponsiveness is a general characteristic of either the basenji or the greyhound ancestry of the basenji-greyhound (BG) dog and to determine whether airway hyperresponsiveness of the BG dogs in specific for methacholine, we compared pulmonary responsiveness to increasing doses of aerosols of histamine and methacholine in 17 BG dogs, 5 unrelated purebred basenjis and 5 unrelated greyhounds. BG dogs were hyperresponsive to both methacholine and histamine compared to basenjis and greyhounds. There was a significant correlation between histamine compared to basenjis and greyhounds. There was a significant correlation between histamine and methacholine responsiveness (r = 0.70, P less than 0.0001) in the dog population. We conclude that airway hyperresponsiveness characteristic of the BG dog is not a general characteristic of the basenji or greyhound breed and occurs to histamine as well as to methacholine.

Aerosols↗
PubMed1986

Mechanisms of gas loss from normal and hyperinflated excised guinea pig lungs.

Increased pulmonary gas trapping was produced by in vivo inhalation exposures of guinea pigs to bronchoconstrictive aerosols. Both normal (filtered air-exposed) and hyperinflated excised lungs lost about 20% of their initial volume by 4 h; gas loss was more rapid during the first 60 min (early period) than the following 180 min (late period). During both periods, absolute rates of gas loss were positively correlated (P less than 0.001) with initial excised lung gas volumes (ELGVs). Tracheal foam movement was observed in most of the hyperinflated lungs, but only during the early period. Occlusion of the trachea reduced gas loss during the early period, but not the late. Gas volumes increased in lungs of animals exposed to SF6:O2 (tracheas tied), and decreased most rapidly in lungs of animals exposed to He:O2 (tracheas tied). Our results suggest that a major part of the early gas loss from excised guinea pig lungs occurs via the trachea and may be influenced by airway foam or menisci formation. After 60 min, airways may be closed and gas loss may occur via transpleural diffusion.

Airway Resistance↗
PubMedDate not supplied

Unequal pupils. A flow chart for sorting out the anisocorias.

When anisocoria is present, the ophthalmologist knows that something is wrong. However, location of the lesion and diagnosis of the problem can be difficult. A step-by-step flow chart for diagnosis of unequal pupils is presented, with explantation of various signs and descriptions of appropriate diagnostic tests.

Adie Syndrome↗