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Biomedical subjects

M A Lung

Publications and source records attributed to M A Lung.

At least 19 recordsLinked to original sources
PubMed1998

Autonomic nervous control of venous pressure and secretion in submandibular gland of anesthetized dogs.

In dogs anesthetized with pentobarbital sodium, hilar venous pressure (Phv) and secretion were measured from the submandibular gland receiving spontaneous blood flow or vascular perfusion at the normal resting flow rate. Parasympathetic nerve stimulation and ACh-induced secretion increased Phv and its pulse pressure; Phv also showed an obvious arterial (or perfusion pressure)-like waveform. Vasoactive intestinal polypeptide (VIP) exerted similar effects on Phv but produced negligible secretion. Sympathetic nerve stimulation, phenylephrine, and clonidine did not induce secretion and had no significant action on Phv, whereas isoproterenol provoked secretion and changed Phv as with parasympathetic stimulation. Background or superimposed sympathetic nerve stimulation reduced the parasympathetic nerve-induced responses; the sympathetic inhibition was abolished by phentolamine and yohimbine but not by prazosin and propranolol. The results suggest a direct relationship between Phv and secretion during parasympathetic salivation: the elevation in Phv was primarily independent of the concurrent blood flow response, mediated via muscarinic and peptidergic mechanisms, and related to an opening of arteriovenous anastomoses. Sympathetic inhibition of parasympathetic salivation may be related to prevention of an increased Phv exerted primarily via the alpha2-adrenergic mechanism.

Acetylcholine↗
PubMed1994

Mechanisms of sympathetic enhancement and inhibition of parasympathetically induced salivary secretion in anaesthetized dogs.

1. The effects of superimposed and continuous sympathetic nerve stimulation on submandibular parasympathetic salivation were investigated in anaesthetized dogs. 2. Superimposed sympathetic nerve stimulation (1-2 min) initially enhanced and later inhibited salivary secretion induced by parasympathetic nerve stimulation (2-8 Hz) in glands with uncontrolled blood supply or constant-flow vascular perfusion. Propranolol (0.05 mg kg-1, i.a.) did not affect the diphasic sympathetic action whereas phentolamine (0.1 mg kg-1, i.a.) abolished it. Prazosin (0.025 mg kg-1, i.a.) greatly lessened the initial enhancement while yohimbine (0.025 mg kg-1, i.a.) alleviated the late inhibition. 3. Salivary secretion, induced by parasympathetic nerve stimulation (4 Hz) or acetylcholine infusion (10 micrograms kg-1 min-1, i.a.), was abolished by atropine (0.05 mg kg-1, i.a.), increased by phenylephrine infusion (0.25 microgram kg-1 min-1, i.a.) and depressed by clonidine infusion (0.75 microgram kg-1 min-1, i.a.). Hexamethionium (12.5 mg kg-1, i.a.) abolished the nerve-induced secretion but had no effect on the acetylcholine-induced secretion. 4. Continuous background sympathetic nerve stimulation decreased parasympathetic nerve-induced salivary secretion in glands with uncontrolled blood supply or constant-flow vascular perfusion. 5. These results show that parasympathetic salivation can be modified by the sympathetic system at the postsynaptic level; enhancement is via alpha 1-adrenoceptors whereas inhibition is via alpha 2-adrenoceptors.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1994

Increase or decrease in nasal airway resistance induced by acetylcholine in anesthetized dogs: vascular mechanisms.

In sodium pentobarbital-anesthetized dogs with spontaneous nasal blood flow or constant-flow vascular perfusion of the nasal mucosa, we measured nasal airway resistance, vascular resistance, and arterial inflow and outflow of the anterior and posterior venous systems. Acetylcholine in low doses (< 5 micrograms/kg per minute, intraarterially) increased nasal airway resistance, and the response was greater in dogs with spontaneous blood flow. Nasal vascular resistance was decreased. However, the posterior venous outflow was increased and the anterior venous outflow was decreased in dogs with constant-flow vascular perfusion. Acetylcholine in higher doses (> 5 micrograms/kg per minute, intraarterially) decreased nasal airway resistance, and vascular resistance fell further, but both venous outflows were increased in dogs with spontaneous blood flow or constant-flow vascular perfusion. The results indicate that acetylcholine may increase or decrease nasal airway resistance, depending on the dose administered, probably via a dose-dependent differential action on different components of the nasal vascular bed.

Acetylcholine↗
PubMed1993

An investigation of the vascular organisation of the canine submandibular gland.

It is known that parasympathetic nerve stimulation elevates venous pressure in the dog submandibular gland, and that the venous pressure wave is transformed to that of the arterial pulse. The vascular arrangements and histological characteristics of the dog submandibular gland were therefore examined to establish which anatomical structures are responsible for the change in venous pressure during salivation induced by parasympathetic stimulation. The acinar and ductal circulations were found to be arranged in parallel and arteriovenous anastomoses were identified in both. Microsphere injection studies demonstrated the opening of arteriovenous anastomoses in actively secreting glands. Smooth muscle cells were rarely found in venous blood vessels but venous valves were abundant in both circulations. Dense connective tissue was observed to enclose the ductal system and its accompanying structures (blood vessels, lymphatic vessels and nerves); it was most abundant in the hilum and diminished aborally. The mechanism responsible for elevating venous pressure during parasympathetic salivation is thus probably related to opening of the arteriovenous anastomoses; the increase in the amount of surrounding dense connective tissue in a central direction may facilitate the preservation of the transmitted arterial pressure and pulse in the venous system.

Animals↗
PubMed1991

Mechanical stimulation of canine respiratory tract and nasal vascular and airway resistances.

Mechanical irritation of the upper airways (nose and larynx) decreased nasal vascular and airway resistances in anaesthetized dogs; the responses were probably due to dilatation of the nasal resistance and venous outflow blood vessels via stimulation of irritant receptors. Mechanical irritation of the lower airways (bronchi) increased nasal vascular resistance but decreased nasal airway resistance; the responses were probably due to constriction of nasal resistance and venous sinusoidal blood vessels via stimulation of cough receptors.

Airway Resistance↗
PubMed1990

Variations in blood flow on mandibular glandular secretion to autonomic nervous stimulations in anaesthetized dogs.

1. Continuous stimulation of the preganglionic parasympathetic nerve (the ramus communicans of the mandibular ganglion) for 1-2 min at supramaximal voltage (5 V) and pulse duration (1 ms) increased salivary gland arterial inflow and this was accompanied by copious salivary secretion. The responses were recorded continuously during the period of stimulation. The frequency for initiating the responses was 0.5 Hz. Maximal responses occurred at 16 Hz. The response coefficient of arterial inflow to stimulus frequency was 0.17 ml min-1g-1 Hz-1 and that of secretion to stimulus frequency was 0.016 ml min-1g-1 Hz-1. 2. The secretory response to low and moderate levels of parasympathetic nerve stimulation (below 8 Hz) was not affected by a reduction or cessation in arterial inflow whereas the response to high level parasympathetic nerve stimulation (above 8 Hz) was significantly alleviated if blood flow to the gland was maintained (via controlled vascular perfusion) at a level less than that of the resting arterial inflow. However, when the gland was already secreting near-maximally (stimulated at 8 Hz), sudden cessation of blood flow for a short period of time (0.5-2 min) had no effect on the salivary flow. 3. Continuous stimulation of the cervical sympathetic nerve for 1-2 min at supramaximal voltage (20 V) and pulse duration (1 ms) decreased arterial inflow and this was accompanied by scanty salivary secretion. The vascular response persisted during the period of stimulation. The secretory response was 15 s late in onset and might continue for 1 min after stimulation. The frequency for initiating the responses was 1-4 Hz. Maximal responses occurred at 16-32 Hz. The response coefficient of arterial inflow to stimulus frequency was -0.04 ml min-1g-1Hz-1 and that of salivary secretion to stimulus frequency was 0.001 ml min-1g-1Hz-1. 4. The secretory response to sympathetic nerve stimulation at different frequencies in glands with blood flow maintained at resting rate (via controlled vascular perfusion) resembled that in glands with spontaneous blood flow. 5. Sympathetic nerve stimulation was found to retard salivary secretion caused by parasympathetic stimulation, irrespective of whether the gland received spontaneous arterial inflow or controlled vascular perfusion at a resting flow rate. 6. The results suggest that the salivary secretion to stimulation of parasympathetic nerve is independent of blood flow over a wide range of stimulus frequencies; however, the response to high frequency stimulation of the parasympathetic nerve may be affected by fluctuations in blood flow.(ABSTRACT TRUNCATED AT 400 WORDS)

Anesthesia, Intravenous↗
PubMed1989

Autonomic nervous control of nasal vasculature and airflow resistance in the anaesthetized dog.

1. In pentobarbitone-anaesthetized dogs with constant-flow vascular perfusion of nasal mucosa on both sides, nasal airway resistance, vascular resistance, vascular capacitance (via changes in total venous outflow) and blood flow in the anterior and posterior venous systems were measured. 2. Electrical stimulation of the cut peripheral ends of the cervical sympathetic trunk, caudal nasal nerve, or major palatine nerve increased vascular resistance and decreased vascular capacitance and airway resistance. Propranolol and atropine had no effect on the responses while bretylium completely abolished them; phentolamine greatly lessened the vascular resistance response and partially decreased the vascular capacitance and airway responses. Hence, sympathetic stimulation causes constriction of the resistance vessels via alpha-adrenergic mechanism and constriction of capacitance vessels via alpha-adrenergic as well as some non-adrenergic and non-cholinergic mechanisms. 3. Denervation of the cervical sympathetic trunk, caudal nasal nerve and major palatine nerve decreased nasal vascular resistance and increased vascular capacitance and airway resistance, suggesting tonic sympathetic discharge to nasal mucosa via caudal nasal and major palatine nerves. 4. Electrical stimulation of the nerve of pterygoid canal decreased vascular resistance but increased vascular capacitance (in the posterior venous system) and airway resistance to low-voltage stimulation (below 10 V), and decreased vascular capacitance (in the anterior venous system) and airway resistance to high-voltage stimulation (above 10 V). Hexamethonium reversed the vascular resistance response as well as vascular capacitance and airway responses to high-voltage stimulation. Bretylium and phentolamine enhanced the vascular resistance response and reversed vascular capacitance and airway resistance responses to high-voltage stimulation. Hence, low-voltage stimulation results in parasympathetic dilatation of resistance and capacitance vessels whereas high-voltage stimulation results in parasympathetic dilatation of resistance vessels and sympathetic constriction of capacitance vessels. The parasympathetic vasodilatation was atropine resistance and the sympathetic vasoconstriction was partially via alpha-adrenergic mechanisms. 5. Denervation of the nerve of pterygoid canal did not affect vascular resistance, vascular capacitance or airway resistance suggesting negligible tonic parasympathetic and sympathetic discharges to nasal blood vessels via the nerve. 6. Simultaneous optimal stimulation of sympathetic and parasympathetic nerves resulted in vasoconstriction, especially in capacitance vessels, suggesting sympathetic predominance over parasympathetic control.

Airway Resistance↗
PubMed1989

An anatomical investigation of the nasal venous vascular bed in the dog.

Physiological experiments have demonstrated that the canine nasal mucosa has two venous systems that differ in blood pressure and flow. An investigation of the vascular arrangements and histological characteristics of the nasal venous vascular bed was performed to search for anatomical structure(s) responsible for their functional separation. Parietal bicuspid valves were found to be present in both venous systems, being particularly abundant at the two extremities of the nasal cavity and less frequently found over the turbinates. Ostial valves were found to be present guarding the entries of tributaries into the periosteal venous plexus, collecting veins and outflow veins of the nasal mucosa. The collecting veins of the posterior venous system were found to be much larger and to contain a greater amount of muscle than those of the anterior venous system. The parietal valves are suggested to be the anatomical structures responsible for the functional separation of the two venous systems whereas the ostial valves might act as a throttle mechanism, regulating blood flow into the cavernous periosteal venous plexus and the collecting veins of the posterior venous system. The physiological significance of the presence of venous valves and their distribution in the nasal mucosa as well as the probable functions of the collecting veins of the posterior venous system are discussed.

Animals↗
PubMed1987

Lung reflexes and nasal vascular resistance in the anaesthetized dog.

1. In pentobarbitone-anaesthetized dogs the nasal vasculature was perfused on both sides, and nasal vascular and airflow resistances were measured together with blood pressure, heart rate and tidal airflow. 2. Capsaicin was injected intravenously to stimulate lung C-fibre receptors, and veratrine to stimulate pulmonary stretch receptors and cardiac receptors. Injections with both drugs were repeated after pulmonary denervation and after cervical vagosympathectomy. 3. Intravenous capsaicin caused hypotension, bradycardia and rapid shallow breathing, together with a decrease in nasal vascular resistance and little change in nasal airways resistance. Denervation showed that these effects came from lung reflexes, presumably from C-fibre receptors. 4. Intravenous veratrine caused similar effects to capsaicin before denervations, presumably due to stimulation of slowly adapting pulmonary stretch receptors. Left atrial injections of veratrine caused hypotension, bradycardia and hyperpnoea, together with an increase in nasal vascular resistance and little change in nasal airways resistance. Thus cardiac receptors seem to increase nasal vascular resistance. 5. Injections of capsaicin and veratrine into the nasal circulation decreased nasal vascular resistance, with a stimulation of breathing and changes in blood pressure. Denervations indicated that these were a combination of local and reflex actions.

Animals↗
PubMed1987

Arterial supply, venous drainage and collateral circulation in the nose of the anaesthetized dog.

1. In pentobarbitone-anaesthetized dogs, nasal blood flows were measured with electromagnetic flow sensors. 2. The terminal internal maxillary artery was found to supply 22 +/- 2.2 ml min-1 (one side) to the nasal mucosa via the sphenopalatine and major palatine branches; the artery was found to receive multiple supply routes from common carotid, vertebral and subclavian arteries. 3. Nasal mucosa was found to receive collateral flow from contralateral terminal internal maxillary artery (about 5 to 10% of normal flow) and branches of subclavian arteries (about 36% of normal flow). 4. Nasal mucosa was found to have two venous systems: the low-flow (12 +/- 1.0 ml min-1; both sides) and low-pressure (7 +/- 0.6 mmHg) sphenopalatine veins draining the posterior nasal cavity and the high-flow (30 +/- 1.4 ml min-1; both sides) and high-pressure (17 +/- 1.0 mmHg) dorsal nasal veins draining the anterior nasal cavity. 5. PO2 of nasal venous blood was found to range from 62 +/- 2.9 mmHg to 65 +/- 3.4 mmHg. During nitrogen challenge to the nose, the sphenopalatine venous PO2 dropped to 35 +/- 3.0 mmHg while the dorsal nasal venous PO2 remained unchanged, suggesting that the sphenopalatine veins were responsible for draining capillary flow and dorsal nasal veins arteriovenous anastomotic flow as well. 6. Microscopic examination of the vascular casts confirmed that arteriovenous anastomoses were located only in the anterior nasal cavity.

Anesthesia, General↗
PubMed1987

Effects of lung inflation on nasal airway resistance in the anesthetized rat.

Nasal airway resistance was assessed in halothane-anesthetized rats by measuring the transnasal pressure at constant airflow through both nasal cavities. Low inflation pressures (2.5-5 cmH2O) decreased nasal airway resistance, whereas higher inflation pressures (10-20 cmH2O) caused a biphasic response: an initial increase in resistance followed by a decrease in resistance. The nasal responses to all levels of inflation were completely abolished by hexamethonium, guanethidine, or bretylium pretreatment or cervical sympathectomy and greatly lessened by cervical vagotomy or phenoxybenzamine pretreatment. Atropine and propranolol pretreatments had no effect on the responses. These findings indicate that the nasal airway resistance is related to the level of inflation through pulmonary reflexes with afferents along the vagi and efferents via the alpha-adrenergic nervous system.

Airway Resistance↗
PubMed1987

Effects of H1 antihistamines on canine nasal vascular and airway resistances.

The effects of three commonly used H1 antihistamines on the nasal vascular and airway resistances were studied in the dog. Promethazine hydrochloride decreased nasal vascular resistance but increased nasal airway resistance in a dose-dependent manner. Diphenylpyraline hydrochloride in low doses increased nasal vascular resistance without affecting much nasal airway resistance while in high doses decreased nasal vascular resistance but increased nasal airway resistance. Chlorpheniramine maleate in low doses increased nasal vascular resistance but decreased nasal airway resistance while in high doses decreased nasal vascular resistance without affecting much nasal airway resistance. It was concluded that different H1 antihistamines might exert vasoconstrictor or vasodilatatory action on both the resistance and capacitance vessels of the nasal vascular bed depending on the type and the dose of the drug used.

Airway Resistance↗
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↗