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PubMed1982

Duration of pulmonary function adaptation to ozone in humans.

The duration of pulmonary function adaptation subsequent to cessation of a 5-day repeated ozone (O3) exposure was studied in 24 nonsmoking human subjects. A three-week, 3 hr/day study was conducted. The subjects received filtered air on Week 1 and 0.4 ppm O3 on Week 2. During Week 3, 13 subjects were re-exposed to O3 on Friday and 11 were re-exposed to O3 on Tuesday. Spirometric measurements (FVC and FEV1) and bronchial reactivity to methacholine showed adaptation within 2-3 days of the repeated daily exposures (Week 2). Although the duration of adaptation seen with bronchial reactivity appears longer than 7-days, the FVC and FEV1 clearly demonstrated complete loss of adaptation by 7 days, with a trend toward significance by 4 days. We conclude, therefore, the loss of ozone adaptation in pulmonary function is a gradual phenomenon lasting less than 7 days following cessation of repeated daily exposures.

Adaptation, Physiological↗
PubMed1984

Sulfur dioxide and ammonium sulfate effects on pulmonary function and bronchial reactivity in human subjects.

The effect of exposures to 1 ppm sulfur dioxide (SO2) and 500 micrograms/m3 respirable ammonium sulfate [(NH4)2SO4] was studied in 20 nonsmoking subjects to determine if a response can be measured at these atmospheric levels and if the response is additive or synergistic. Four-hour separate and combined exposures were employed. Each subject acted as his or her own control and performed two light-to-moderate exercise stints (612 kg-m/min) for 15 minutes on each day's confinement in the environmental chamber. Pulmonary function tests (body plethysmography and spirometry) and bronchial reactivity to methacholine were performed to assess the response of these exposures. No significant changes in pulmonary function or bronchial reactivity were observed in the individual exposures [(NH4)2SO4 or SO2], the combined exposure [(NH4)2SO4 and SO2], or 24 hours post-exposure. This study design and the observed results did not demonstrate any readily apparent risk to healthy subjects with these exposures. Since no significant changes were measured, it was not possible to conclude if these two pollutants in combination produce an additive or synergistic response.

Adult↗
PubMed1967

Cholinesterase activity of nodal and internodal regions of myelinated nerve fibers of frog.

The distribution of cholinesterase (Ch-esterase) in isolated myelinated fibers of the frog has been investigated. Quantitative microgasometric measurements have confirmed the previous histochemical observations. Both approaches indicate that in frog nerve fibers acetylcholinesterase (ACh-esterase) is the only or the predominant enzyme when selective inhibitors and different substrates are used: acetylcholine (ACh), butyrylcholine, and acetyl-B-methylcholine (Mecholyl). By means of the microgasometric technique, a significant difference in ACh-esterase activity between axons isolated from ventral (37.2 +/- 1.7 micromole x 10(-5) ACh/mm(2)/hr) and dorsal roots (2.0 +/- 0.9 micromole x 10(-5) ACh/mm(2)/hr) was found. In the region of the node of Ranvier the enzyme activity (50.4 +/- 4.4 micromole x 10(-5) ACh/mm(2)/hr) appears to be considerably higher than in the internodal area (36.6 +/- 2.1 micromole x 10(-5) ACh/mm(2)/hr). The findings are discussed in relation to the theory of saltatory conduction and the ACh system.

Acetylcholine↗
PubMed1973

The effect of Bordetella pertussis on lymphocyte cyclic AMP metabolism.

Bordetella pertussis culture fractions produce decreased metabolic responses to isoproterenol and epinephrine in mice and rats, suggesting the possibility of systemic beta adrenergic blockade. The present study was undertaken to elucidate the mechanism of the alteration in adrenergic responsiveness and to clarify its relationship to other biological effects of the organism. Lymphocytes were selected as a suitable tissue because of the marked alteration in lymphocyte distribution in pertussis-treated mice and rats, suggesting a change in the surface properties of these cells. Human peripheral blood lymphocytes, purified by nylon fiber chromatography, were studied. In short incubation experiments (20 min or less) B. pertussis did not alter the cyclic AMP response to isoproterenol, prostaglandin E (PGE(1)), or methacholine. However, when cells were preincubated with B. pertussis for 90 min at 37 degrees C, the responses to all three agents were markedly inhibited. Although these observations provide direct confirmation of the ability of B. pertussis to inhibit catecholamine responsiveness, the fact that PGE(1) and methacholine responses were also inhibited suggests that blockade at the level of the beta adrenergic receptor is doubtful. The inhibitory activity was localized in a nondialyzable, protein-rich fraction that is precipitated from B. pertussis culture fluid by ammonium sulfate at 90% of saturation. The bulk of the activity was obtained in the load volume after 50,000 g centrifugation in a cesium chloride gradient, density 1.2-1.5 (fraction 4). Fraction 4 produced a change in lymphocyte hormonal responsiveness at concentrations as low as 5 ng/ml. The relationship between cyclic AMP inhibitory activity in isolated human cells and leukocytosis-producing activity in intact mice was studied. The two activities seemed to parallel one another quite closely until the final Sephadex G-150 fractionation step, in which the two activities were obtained in the same column fraction, but a greater recovery of the leukocytosis-producing activity was obtained. Additional purification will be required to establish conclusively whether the same macromolecule is responsible for both activities. The availability of a bacterial product that markedly inhibits cyclic AMP accumulation in purified lymphocytes may help to clarify the role of cyclic AMP in lymphocyte activation by antigen and nonspecific mitogens.

Acetylcholine↗
PubMed1988

Systemic blood pressure and intraocular pressure relationship.

The relationship between intraocular pressure (IOP) and arterial blood pressure (BP) was analyzed in response to two pressor agents (norepinephrine and angiotensin II) and two depressor agents (methacholine and isoproterenol) in pentobarbital anesthetized cats. Both IOP and BP were measured manometrically in the same animals. Intravenous norepinephrine and angiotensin II produced dose-dependent increases, whereas intravenous methacholine and isoproterenol produced dose-dependent decreases of both BP and IOP. The IOP response to methacholine was biphasic, with an initial decrease followed by an increase above the pre-drug level. In some experiments a cannula loop was inserted into a carotid artery in order to separate the direct ocular effect of drugs on IOP from that contributed by the changes in systemic BP. Intravenous administration of norepinephrine and angiotensin II produced a larger increase in IOP on the side where drugs were delayed by the loop. Conversely, methacholine produced a larger fall in IOP on the cannulated side while the effect of isoproterenol was essentially unchanged. In other experiments injections were made directly into the ocular arterial blood supply. Norepinephrine and angiotensin II produced a decrease in IOP, methacholine produced a rise of IOP and isoproterenol was not active by this route. The present findings indicate that IOP is largely influenced by arterial BP changes in the acute phase and that the IOP response to drugs is the algebraic sum of effects on systemic BP and their direct ocular effects.

Angiotensin II↗
PubMed1988

An assessment of methacholine inhalation tests in elderly asthmatics.

We have assessed the feasibility and value of measuring nonspecific bronchial responsiveness to methacholine in investigation of asthma in the elderly. Results from duplicated tests in 20 subjects aged 65-82 years were expressed as dose provoking a 20% decrement in 1 second forced expiratory volume (PD20.FEV1) or peak expiratory flow (PD20.PEF). Repeatability for PD20.FEV1 was satisfactory but less good than in younger subjects, 95% confidence limits being 0.39-2.57 and 0.52-1.91, respectively, x initial PD20. For PD20.PEF, confidence limits were wider (0.26-3.91 x initial PD20) but multiple PEF measurements were better tolerated than those of FEV1, which commonly caused fatigue and dizziness. PD20.FEV1 and PD20.PEF correlated closely (r = 0.95, P less than 0.0001) and both predicted bronchodilatation following a 6-week course of inhaled corticosteroid and beta agonist. This was not predicted by the response to a single dose of beta agonist. We conclude that measurement of bronchial responsiveness is feasible and clinically valuable in elderly subjects.

Aged↗
PubMed1982

Methacholine pupillary responses in third nerve palsy and Adie's syndrome.

In order to examine the clinical usefulness of methacholine in assessing the site of ocular parasympathetic lesions, pupillary responses in man were measured in postganglionic (Adie's syndrome) and preganglionic third nerve lesions involving the pupil and in controls. From previous work with methacholine it might have been expected that greater constriction would occur in the postganglionic lesions but similar responses were found in both. Corneal hypoxia due to ptosis appeared unlikely to affect corneal permeability significantly and it is probable that these results reflect an increase responsiveness of the iris at, or distal to, the site of muscarinic acetylcholine receptors. Pupils contralateral to third nerve palsy, when tested on a separate occasion, also constricted by an amount approximately proportional to that of the clinically abnormal pupil. The possibilities that this may result in some way from reduction in total retinal illumination, or from retrograde changes in preganglionic pupilloconstrictor neurons affecting contralateral pupilloconstrictor neurons via central pathways, are discussed. It is concluded that supersensitivity to methacholine, tested carefully in the manner described, is a useful guide to the presence of parasympathetic denervation or decentralization, but that it is not reliable in distinguishing between the two sites.

Adie Syndrome↗
PubMed1975

Pure pan-dysautonomia with recovery. Description and discussion of diagnostic criteria.

The patient described in this report appears to have had a unique, severe, pure pan-dysautonomia, and has been investigated in sufficient detail to specify precisely the disorders of functions subserved by the autonomic nervous system. Though we cannot rule out the possibility of an unknown autonomic toxin, we have no evidence for it and suggest that our patient's disorder be considered an acute polyneuritis, restricted to the autonomic system. Comment is made on tests of autonomic dysfunction and on the reliance which can be placed upon the results.

Blood Pressure↗
PubMed1986

Effects of adrenergic and muscarinic receptor stimulation on serum potassium concentrations and myocardial electrical stability.

The influence of adrenergic and muscarinic receptor activation on cardiac electrical stability and on serum potassium concentrations was studied in 23 anaesthetised dogs. The ventricular fibrillation threshold was assessed using the single stimulus technique. Adrenaline (1.0 microgram X kg-1 X min-1) caused a brief rise and a subsequent prolonged fall in serum potassium concentration, which was accompanied by a decline in ventricular fibrillation threshold when baroreceptor activation was prevented. After pretreatment with the beta1 adrenoceptor blocking agent metoprolol (0.5 mg X kg-1), adrenaline did not alter vulnerability to ventricular fibrillation but still elicited hypokalaemia. In contrast, selective beta2 adrenoceptor blockade (ICI 118551, 100 micrograms X kg-1) prevented the adrenaline induced lowering of serum potassium concentration but not of ventricular vulnerability. Muscarinic receptor activation by methacholine (3.0 micrograms X kg-1 X min-1) had no effect on serum potassium concentration but increased the ventricular fibrillation threshold by 30%. When methacholine was administered concomitantly with adrenaline the decline in serum potassium concentration persisted, but the increase in ventricular vulnerability was completely prevented. It is concluded that in the normal canine myocardium adrenaline produces an increase in vulnerability that is mediated through beta 1 adrenoceptors and that the beta 2 adrenoceptor mediated hypokalaemia is dissociated from electrophysiological effects of adrenaline. Parasympathetic nervous system activation does not influence serum potassium concentrations but opposes the effects of adrenaline on susceptibility to ventricular fibrillation.

Adrenergic beta-Antagonists↗
PubMed1980

Changes in vagal activity and response to muscarinic receptor agonists with age.

The response to vagal nerve and muscarinic receptor stimulation was evaluated in young (90 day), adult (365 day) and old (730 day) male F-344 rats anesthetized with urethane. Bilateral vagotomy produced a significant increase in heart rate in the young and adult animals (p < 0.05), while no change in heart rate occurred in the old animals. Stimulation of the right vagus nerve produced a frequency dependent decrease in response to right vagus nerve stimulation with age (p < 0.05; analysis of variance), i.e., old animals had a smaller decrease in heart rate over the same frequency range of nerve stimulation than either the young or adult animals. The effect of age on the response of the muscarinic receptor was examined using cumulative doses of methacholine administered by bolus injection. Methacholine produced a dose dependent decrease in heart rate and blood pressure. The heart rate response to methacholine was diminished in the older animals (p < 0.05; analysis of variance). Similar results were obtained after atropine although the doses of methacholine employed were much greater. In contrast, although methacholine decreased blood pressure in all animals at each age there was no change in the hypotensive response to methacholine with age. These data indicate that there is a diminution in vagal control of heart rate with age as well as the response of the vagus nerve to stimulation. Furthermore, the response of the muscarinic receptor in the heart declines with age while that in the peripheral vasculature does not.

Age Factors↗
PubMed1982

Bronchial reactivity in experimental infections with influenza virus.

In an attempt to develop an objective, quantitative test to assess the reactogenicity of candidates for attenuated influenza virus vaccines, the clinical responses and bronchial reactivity to methacholine were assessed in 36 normal volunteers lacking antibody to both hemagglutinin and neuraminidase (doubly seronegative) who were inoculated with either wild-type or temperature-sensitive attenuated influenza A (H1N1) virus by intranasal droplets. Five of six volunteers infected with wild-type virus developed systemic and/or febrile illness that lasted for a mean of five days. Nineteen of 30 persons who received attenuated virus developed infection without febrile or systemic illness. In the six recipients of wild-type virus, bronchial reactivity appeared to increase after inoculation and persist for four weeks. This trend was not observed in infected or noninfected vaccinees. Analysis of variance provided suggestive (but not significant) evidence that the different trends in bronchial reactivity manifested by the wild-type virus and vaccine groups were distinct (P = 0.075).

Airway Resistance↗
PubMed1987

Enhanced cAMP accumulation after termination of cholinergic action in the heart.

Cholinergic agents decrease myocardial contractility in part by inhibiting adenylate cyclase (EC 4.6.1.1) activity. We have found that after a prolonged preincubation period (greater than 6 h), washout of cholinergic agents from embryonic chick hearts or cultured heart cells results in a persistent increase in their basal and catecholamine-stimulated cAMP content. Membranes prepared from pretreated cells have elevated basal, forskolin-, and catecholamine-stimulated adenylate cyclase activities. This myocardial adaptation to cholinergic agents is analogous to changes in nerve cells and other cell types after prolonged exposures to narcotics or other inhibitors of adenylate cyclase, respectively. A rapid (less than 5 min) adaptation response to cholinergic agents can also be demonstrated in heart cells by quickly blocking agonist action with atropine. Atropine alone has no effect, but after a brief preincubation period with agonists (methacholine or oxotremorine), the addition of atropine transiently enhances catecholamine-stimulated cAMP accumulation by 2.5-fold. These responses are absent in heart cells pretreated with pertussis toxin. The data indicate that the response is not mediated by the phosphoinositide pathway, which has been demonstrated to be insensitive to pertussis toxin in chick heart. Enhanced cAMP accumulation after termination of muscarinic agonist action may provide an explanation for the observation that acetylcholine sometimes produces biphasic contractile responses.

1-Methyl-3-isobutylxanthine↗
PubMed1990

Pulmonary reactivity to methacholine during beta-adrenergic blockade: propranolol versus esmolol.

Pulmonary reactivity to methacholine after equipotent beta-blocking doses of propranolol and esmolol was compared in seven basenji-greyhound dogs during thiopental-fentanyl anesthesia. Equipotent doses of esmolol and propranolol were determined by both heart rate effects and by isoproterenol response curves. Propranolol (2 mg/kg) was administered intravenously as a bolus dose and esmolol (0.4-0.5 mg.kg-1.min-1) was administered by continuous infusion. Both esmolol and propranolol significantly decreased heart rate and mean arterial pressure (P less than 0.001). Baseline pulmonary resistance and dynamic compliance did not change after the administration of either propranolol or esmolol. However, propranolol significantly shifted the methacholine dose-response curve to the left so that methacholine (0.3 mg/ml) increased pulmonary resistance by 7.9 +/- 0.97 cmH2O.l-1.s-1 (mean +/- SEM of seven dogs) after pretreatment with propranolol but only 4.4 +/- 0.89 cmH2O.l-1.s-1 (P less than 0.05) without propranolol pretreatment (control). Esmolol, however, did not significantly shift the methacholine dose-response curve. Methacholine (0.3 mg/ml) increased resistance 4.0 +/- 0.89 cmH2O.l-1.s-1 during esmolol administration. This study shows that at equipotent beta 1-blocking doses, propranolol, but not esmolol, produces significant increases in pulmonary reactivity to methacholine.

Adrenergic beta-Antagonists↗
PubMed1974

Inhibition of Heidenhain pouch pepsin secretion by commercial cholecystokinin and duodenal fat in dogs.

In unanesthetized dogs with Heidenhain pouches and separated duodenal pouches, intravenous infusion of commercial cholecystokinin (1.0 IDU per min) produced a significant depression of pouch acid and pepsin secretion stimulated by pentagastrin (1.0 microg per min) or by methacholine (2.0 microg per min). Acid response to methacholine was temporarily augmented. Irrigation of the duodenal pouches with emulsified fat produced similar patterns of depression of acid secretion in response to pentagastrin and pepsin secretion in response to pentagastrin or methacholine. Acid secretion stimulated by methacholine was temporarily augmented after the irrigation. It is concluded that fat releases endogenous cholecystokinin from the duodenal mucosa and that cholecystokinin, or duodenal fat, powerfully depresses Heidenhain pouch pepsin secretion in dogs. The involvment of the gastric inhibitory polypeptide (GIP) cannot be assessed from the present experiments.

Animals↗
PubMed1988

Cardiopulmonary effect of various inspiratory flow profiles during controlled mechanical ventilation in a porcine lung model.

We studied the influence of inspiratory flow (VI) patterns on gas exchange and hemodynamics after metacholine inhalation challenge (MIC) in seven swine mechanically ventilated with a constant, sinusoidal, accelerating, and decelerating flow pattern. Blood gas and expired CO2 tensions, pulmonary mechanics, and hemodynamics were measured during each pattern. Flow pattern sequence was randomized and MIC was repeated at 30 to 45-min intervals. MIC reliably reduced PaO2, and increased PaCO2 and peak tracheal pressure (PT). There was no significant difference in gas exchange or hemodynamics between various VI curves. Insufflation with an accelerated VI manifested a significantly higher PT than any other pattern. We conclude that no VI contour studied offers a unique advantage for gas exchange after MIC in swine. However, since accelerated gas flow generates significantly higher PT values, it is not recommended in the presence of significant airway resistance.

Animals↗