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Biomedical subjects

M A Lung

Publications and source records attributed to M A Lung.

25 records · Page 2Linked to original sources
PubMed1987

Nasal venous drainage in the dog.

In the dog, blood from the nasal mucosa may drain via several passageways. Venous outflow measured from the dorsal nasal veins was 30 +/- 1.4 ml/min (of both sides; n = 10) while that from the sphenopalatine veins was 12 +/- 1.0 ml/min (of both sides; n = 10). Nasal venous pressure measured from the dorsal nasal veins was 20 +/- 1.2 mm Hg (n = 10) while that from the sphenopalatine veins was 10 +/- 0.7 mm Hg (n = 10). Occlusion of the dorsal nasal venous outflow increased significantly the sphenopalatine venous outflow whereas occlusion of the sphenopalatine venous outflow had no effect on the dorsal nasal venous outflow. These findings suggest that there are probably two venous systems in the nose; a system of high flow and high pressure draining the anterior nasal cavity and a system of low flow and low pressure draining the posterior nasal cavity.

Animals↗
PubMed1986

Effects of hypercapnia and hypoxia on nasal vasculature and airflow resistance in the anaesthetized dog.

The experiments were performed on anaesthetized dogs which breathed spontaneously or were artificially ventilated and paralysed. The spontaneous nasal arterial blood flow was measured on one side of the nose while nasal vascular resistance was determined on the other side simultaneously. Nasal arterial blood flow was measured by means of an electromagnetic flow sensor placed around the terminal branch of the internal maxillary artery, the main arterial supply to the nasal mucosa. Nasal vascular resistance was measured by constant-flow perfusion of the terminal branch of the internal maxillary artery. Nasal airway resistance was assessed by monitoring the transnasal pressure at constant airflow through each side of the nose simultaneously. Hypercapnic gas challenge (8% CO2, 30% O2 in N2) to the lungs increased nasal vascular resistance and decreased nasal airway resistance. Similar gas challenge to the nose did not affect nasal vascular resistance but decreased nasal airway resistance. Hypoxic gas challenge (6% O2 in N2) to the lungs did not affect the nasal vascular resistance but decreased nasal airway resistance only when the nasal vascular bed was under controlled perfusion. Similar gas challenge to the nose did not affect either nasal vascular or airway resistance. Arterial chemoreceptor stimulation by intracarotid injection of sodium cyanide increased nasal vascular resistance and decreased nasal airway resistance. The nasal vascular response to hypercapnia and arterial chemoreceptor stimulation was reflex in nature, being abolished by nasal sympathectomy. The nasal airway response to hypercapnia, hypoxia and arterial chemoreceptor stimulation was reflex in nature, being partially or completely abolished by nasal sympathectomy. Hypercapnia probably induced a local vasodilatatory effect on the capacitance vessels whereas hypoxia had no direct action on the vasculature.

Airway Resistance↗
PubMed1984

Control of nasal vasculature and airflow resistance in the dog.

Nasal vascular and airflow resistances have been measured in dogs, simultaneously on both sides separately. Vascular resistance was measured either by constant flow perfusion of the terminal branch of the maxillary artery (which supplies, via the sphenopalatine artery, the nasal septum, most of the turbinates and the nasal sinuses) or by measuring blood flow through this artery, maintained by the dog's own blood pressure. Airflow resistance was assessed by inserting balloon-tipped endotracheal catheters into the back of each nasal cavity via the nasopharynx, and measuring transnasal pressure at constant airflow through each side of the nose simultaneously. Preliminary experiments indicated that there was 5-10% collateral anastomosis between the two sides. Close-arterial injection of drugs showed different patterns of response. Adrenaline, phenylephrine, chlorpheniramine and low doses of prostaglandin F2 alpha increased vascular resistance and lowered airway resistance. Salbutamol, methacholine and histamine lowered vascular resistance and increased airway resistance. Dobutamine decreased airway resistance with a small increase in vascular resistance. Prostaglandins E1, E2 and F2 alpha (high dose) decreased both vascular and airway resistances. Substance P, eledoisin-related peptide and vasoactive intestinal polypeptide lowered vascular resistance with little change in airway resistance. The results are interpreted in terms of possible drug actions on precapillary resistance vessels, sinusoids and venules, and arteriovenous anastomoses. It is concluded that nasal airway resistance cannot be correlated with vascular resistance or blood flow, since the latter has a complex and ill-defined relationship with nasal vascular blood volume.

Adrenergic Agonists↗
PubMedDate not supplied

The role of the autonomic nerves in the control of nasal circulation.

Patients suffering from allergic or vasomotor rhinitis usually show nasal mucosal hyperaemia, engorgement, hyperrhinorrhoea and obstruction of the nasal airway. The nasal mucosa is drained by two venous systems which are anatomically and functionally separate. The nasal mucosa receives tone discharges from the sympathetic nerves but not from the parasympathetic nerves. Sympathetic nerve stimulation causes constriction of the resistance vessels via the alpha-adrenergic mechanism and constriction of the capacitance vessels via the alpha-adrenergic mechanism and some non-adrenergic and non-cholinergic mechanism; the capacitance vessels are under more prominent sympathetic influence than the resistance vessels. Parasympathetic nerve stimulation causes non-cholinergic dilatation of both resistance and capacitance vessels; dilatation is more pronounced in the posterior venous system. Simultaneous optimal stimulation of the autonomic nerves resulted in vasoconstriction, especially of the capacitance vessels. Hence, nasal congestion may be related more to a withdrawal of sympathetic discharge than to an overactivity of the parasympathetic nerves.

Animals↗
PubMedDate not supplied

Nasal blood flow and airway resistance. Canine study.

Nasal blood flow was measured in anesthetized dogs by an electromagnetic flow sensor placed around the terminal branch of the internal maxillary artery, the major arterial supply to the nasal mucosa. Nasal airway resistance was monitored simultaneously by recording the transnasal pressure when airflow through the nasal cavity was maintained constant. Phenylephrine decreased nasal blood flow and airway resistance while albuterol (salbutamol) did the opposite. Prostaglandin E1 increased nasal blood flow but decreased airway resistance. The present study demonstrates that nasal vascular and airway resistance may change in parallel or opposite directions, implying that nasal airway resistance cannot be used to assess the vascular situation in the nose.

Airway Resistance↗
PubMedDate not supplied

Nasal airway response to mucosal perfusion and outflow resistance in the dog and rat.

Simultaneous measurements of nasal airway resistance and vascular perfusion of the nasal mucosa were carried out in the dog and rat. Nasal blood flow (perfusion pressure) and nasal venous pressure (jugular venous pressure) were found to have a linear correlation with nasal airway resistance. The slope of the percentage change in nasal airway resistance to perfusion pressure was 0.03 to 0.04%/mmHg and resistance to nasal venous pressure, 1.15 to 1.28%/mmHg. The results therefore indicate that alterations in venous outflow resistance are more effective than alterations in arterial inflow in changing nasal airway resistance.

Airway Resistance↗