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Biomedical subjects

J C Hybbinette

Publications and source records attributed to J C Hybbinette.

11 recordsLinked to original sources
PubMed1995

Continuous intrathoracic pressure monitoring with a new esophageal microchip catheter in sleep-related upper airway obstructions.

A new small-diameter microchip catheter, especially developed for continuous intrathoracic pressure monitoring to assess the degree of respiratory obstruction and effort in patients with sleep-related upper airway obstructions, was investigated. The technical performance and clinical applicability of the catheter was tested in a simplified screening study comprising 122 sleep recordings in patients with varying complaints of snoring and daytime tiredness. In six obese snorers, sensitivity of the catheter to apneas, hypopneas, and nonapneic snoring was compared to the traditional assessment of respiratory events by conventional polysomnography. The catheter was found to be easy to handle and introduce, with technical qualities meeting the demands for overnight recordings of intrathoracic pressure variations. Patient tolerance was high (93%), and sensitivity to apneas and hypopneas was equivalent to that of traditional polysomnography. Periods with upper airway obstruction and increased respiratory effort on the borderline between asymptomatic obstructions and obstructions resulting in significant blood-gas changes could be detected primarily with intrathoracic pressure monitoring. Monitoring the intrathoracic pressure variations in the esophagus has been shown previously to reflect respiratory effort. Increased respiratory effort might be one of the explanations for the fragmented sleep patterns and sleep related daytime symptoms sometimes seen in patients without a pathologic respiratory index. In addition to being applicable for the detection of apneas and hypopneas, continuous nocturnal monitoring of the intrathoracic pressure variations also detects small increases in respiratory effort and thus may constitute a valuable tool for the understanding and diagnosis of upper airway resistance syndrome and obstructive sleep apnea syndrome.

Adult↗
PubMed1995

Intrathoracic pressure variations in obese habitual snorers.

Six obese patients with complaints of snoring and daytime fatigue were monitored with polysomnography (PSG) and continuous recording of esophageal pressure (Pes) during 1 night. Nonapneic episodes in different sleep stages, with and without snoring, were selected and analysed. Peak to peak pressure was found to be significantly increased during snoring in sleep stages 2 and 3/4 with blood gas variations within the limits of normal unobstructed breathing, indicating increased respiratory effort. The present investigation supports the assumption that daytime tiredness in nonapneic patients can be linked to increased respiratory effort during sleep and that continuous esophageal pressure measuring may contribute to assessment of this condition.

Adult↗
PubMed1985

Effects of nicotine bitartrate on mucociliary activity.

The in vivo effect of nicotine bitartrate on mucociliary (mc) activity in the rabbit maxillary sinus was investigated. An animal model was used, which permitted administration of drugs directly into the artery feeding the sinus and simultaneous recording of changes in the mc activity. When nicotine was given ia (0.5-10.0 micrograms/kg) it resulted in a brief (1 min at most) acceleration of the mc wave frequency. The response was dose-dependent and a maximum increase of 34.9% was recorded at a dose of 10.0 micrograms/kg. The response was inhibited by a preceding injection of the ganglionic blocker hexamethonium (0.2 mg/kg) or the cholinergic antagonist atropine (0.2 mg/kg). The alpha and beta-adrenoceptor antagonists phentolamine (0.2 mg/kg) and propranolol (0.2 mg/kg) did not influence the response to nicotine injection. It is concluded that the acceleration of mc wave frequency after nicotine administration is probably mediated via stimulation of nicotinic receptors on postganglionic parasympathetic nerve cells.

Adrenergic Agonists↗
PubMed1984

Mucolytic agents and mucociliary activity.

The three substances bromhexine, NA 872 (bromhexine metabolite VIII) and the beta 2-receptor agonist NAB 365 (clenbuterol) and their effect on the mucociliary activity have been studied in vivo in rabbits. The substances were given parenterally in increasing dosages and 519 records were obtained from 12 rabbits. Not even at dosages in excess of recommended human dosages has any effect on the mucociliary activity been observed for any of the substances during the first 30 minutes after administration. The conclusion to be drawn is that the three substances have no effect on the mucociliary activity in rabbit in vivo, but that this does not exclude an effect on mucociliary transport or clearance.

Adrenergic beta-Agonists↗
PubMed1982

Parasympathetic and sympathetic influences on mucociliary activity in vivo.

An in vivo test model has been developed to measure the influence of pharmacological substances on mucociliary activity in the rabbit maxillary sinus. Test solutions are administered via the feeding vessel to the investigated mucous membrane. The model permits administration of test substances and simultaneous recording of the obtained effects under conditions that closely mimic the normal situation. The parasympathomimetic agonist methacholine accelerates the mucociliary wave frequency dose-dependently. Atropine has no influence on the resting mucociliary activity but reduces or abolishes the effect of methacholine. The sympathomimetic beta 2-adrenoceptor agonist salbutamol accelerates the mucociliary activity dose-dependently whereas beta 1-adrenoceptor stimulation with prenalterol is without effect. Agonists acting on alpha 1- and alpha 2-adrenoceptors, phenylephrine and oxymetazoline, retard the mucociliary activity dose-dependently. beta- and alpha-adrenoceptor antagonists (propranolol and phentolamine, respectively) have no influence on the resting mucociliary activity but reduce the effect of beta- and alpha-adrenoceptor agonists, respectively. It is concluded that the resting mucociliary activity during anesthesia functions independently of parasympathetic and sympathetic nervous activity, and that the role of the parasympathetic and sympathetic innervation is to increase the mucociliary activity.

Animals↗
PubMedDate not supplied

Effects of neuropeptides on mucociliary activity.

The effects of four neuropeptides, vasoactive intestinal polypeptide, enkephalin, bombesin, and substance P, on mucociliary activity in the rabbit maxillary sinus were investigated in vivo. The peptides were administered via the feeding artery (arteria maxillaris), and the resulting effects were registered with a noninvasive photoelectric technique. The peptides were tested in the dose range 0.0001 to 10 micrograms/kg body weight. The following results were observed: 1) vasoactive intestinal polypeptide and enkephalin did not influence mucociliary activity; 2) bombesin had only a slight accelerating effect on the mucociliary activity at doses of 0.1 to 10 micrograms/kg; and 3) substance P markedly accelerated the mucociliary activity in a dose-dependent manner in the dose range 0.01 to 10 micrograms/kg, the maximal increase being about 50%. The effect of substance P was atropine-resistant, and probably acted directly on the mucosa.

Animals↗
PubMedDate not supplied

Effects of sympathomimetic agonists and antagonists on mucociliary activity.

The effect on the mucociliary (m.c.) wave frequency of sympathomimetic agonists and antagonists was studied in the maxillary sinus in anesthetized rabbits. The non-selective beta-adrenoceptor agonist isoprenaline (0.005-10 micrograms/kg i.a.) and the selective beta2-adrenoceptor agonist salbutamol (0.01-10 micrograms/kg, i.a.) induced a dose-dependent acceleration of the m.c. wave frequency, whereas the beta1-adrenoceptor agonist prenalterol (1-200 micrograms/kg, i.a.) did not influence the basal m.c. activity. The selective alpha1-adrenoceptor agonist phenylephrine (0.01-20 micrograms/kg, i.a.) and the selective alpha2-adrenoceptor agonist oxymetazoline (0.001-1 microgram/kg, i.a.) both induced a dose-dependent retardation of the m.c. wave frequency. The non-selective beta-adrenoceptor antagonist propranolol (2-200 micrograms/kg, i.a., and 1 mg/kg, i.v.) and the non-selective alpha-adrenoceptor antagonist phentolamine (0.1-1 000 micrograms/kg, i.a.) had no influence on the basal m.c. wave frequency. Propranolol (1-2 mg/kg, i.v.) reduced the effect of isoprenaline and salbutamol (both in the dose range of 0.01-10 micrograms/kg, i.a.) and similarly phentolamine (0.2 and 1 mg/kg, i.a.) reduced the effect of oxymetazoline (0.01-10 microgram/kg, i.a.). It was concluded that during basal conditions in the anesthetized rabbit the m.c. activity functions independently of sympathetic activity and that sympathomimetic agonists acting on beta2-adrenoceptors accelerate the wave frequency, whereas sympathomimetic agonists acting on alpha1 and alpha2-adrenoceptors have a retarding effect, all in a dose-dependent manner.

Albuterol↗
PubMedDate not supplied

A pharmacological evaluation of the short-term effect of cigarette smoke on mucociliary activity.

The effect of whole cigarette smoke on mucociliary (m.c.) activity was recorded in the maxillary sinus in anesthetized rabbits. Puffs of cigarette smoke were delivered in a way that imitates the normal smoking habit in man. Cigarette smoke from nicotinic cigarettes was found to accelerate the m.c. wave frequency in proportion to the nicotine content. Smoke from nicotine-free cigarettes and exposure to oxygen did not influence the m.c. activity. The stimulating effect of smoke drawn from nicotine cigarettes was inhibited by hexamethonium (0.2 mg/kg i.a.) and by atropine (0.2 mg/kg i.a.). It is concluded that the accelerating effect on the m.c. activity of short-term exposure to cigarette smoke might be explained by stimulation of ganglion nicotinic receptors situated on parasympathetic postganglionic nerve cells.

Animals↗
PubMedDate not supplied

A method for evaluating the effect of pharmacological substances on mucociliary activity in vivo.

A test model for in vivo studies of the effect of pharmacological substances on mucociliary activity in the rabbit maxillary sinus is presented. The method permits administration of pharmacological substances and recording of the mucociliary activity under conditions that mimic the physiological situation very closely. The test substances are given intra-arterially. Using a photoelectric technique the mucociliary activity is recorded from a small and limited area of the mucous membrane. There is minimal exposure to external stimuli since normal sinus ventilation is retained. Various factors which may influence the results, e.g. the anesthesia, movements from cardiac and respiratory activity, and the volumes and injection velocities of test doses, are analysed and discussed. When the animal model was tested with serotonin, ATP, and certain cholinergic and adrenergic agents, it was found to be reliable. It permitted easy detection of changes in the mucociliary activity and gave reproducible results.

Animals↗
PubMedDate not supplied

Effects of the parasympathomimetic drug methacholine and its antagonist atropine on mucociliary activity.

The effect on the mucociliary (m.c.) activity of the parasympathomimetic drug methacholine and its antagonist atropine was studied with the aid of a newly developed animal test model, designed for evaluating the effect of pharmacological substances on the m.c. wave frequency. Methacholine i.a. (0.01-2 micrograms/kg) was found to give a dose-dependent acceleration of the m.c. wave frequency, and the threshold dose 0.03 +/- 0.02 (+/- S.D.) micrograms/kg is suggested to be within physiological limits. The anticholinergic drug atropine i.a. (0.05-0.5 mg/kg) did not influence the basal m.c. wave frequency, but a dose of 0.2 mg/kg reduced or abolished the responses to methacholine (0.05-2 micrograms/kg). These results indicate that the basal m.c. activity functions independently of parasympathetic activity in anesthetized animals, that parasympathomimetic drugs influence the m.c. activity and that the effects of these drugs can be reduced or blocked by atropine.

Animals↗