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Biomedical subjects

A M Roberts

Publications and source records attributed to A M Roberts.

At least 55 records · Page 3Linked to original sources
PubMed1985

Pulmonary C-fibers reflexly increase secretion by tracheal submucosal glands in dogs.

Stimulation of bronchial C-fibers evokes a reflex increase in secretion by tracheal submucosal glands, but the influence of pulmonary C-fibers on tracheal gland secretion is uncertain. In anesthetized dogs with open chests, we sprayed powdered tantalum on the exposed mucosa of a segment of the upper trachea to measure the rate of secretion by submucosal glands. Secretions from the gland ducts caused elevations (hillocks) in the tantalum layer. We counted hillocks at 10-s intervals for 60 s before and 60 s after we injected capsaicin (10-20 micrograms/kg) into the right atrium to stimulate pulmonary C-fiber endings. Right atrial injection of capsaicin increased the rate of hillock formation fourfold, but left atrial injection had no significant effect. The response was abolished by cutting the vagus nerves or cooling them to 0 degree C. We conclude that the reflex increase in tracheal submucosal gland secretion evoked by right atrial injection of capsaicin was initiated as capsaicin passed through the pulmonary vascular bed, and hence that pulmonary C-fibers, like bronchial C-fibers, reflexly increase airway secretion.

Animals↗
PubMed1985

Reflex tracheal contraction evoked in dogs by bronchodilator prostaglandins E2 and I2.

Bronchodilator prostaglandins E2 and I2 may cause airway irritation and bronchoconstriction in human subjects. These experiments were designed to test the hypothesis that this paradoxical bronchoconstriction is a vagal reflex triggered by stimulation of airway afferents. We recorded smooth muscle tension in an innervated upper tracheal segment in anesthetized dogs and injected prostaglandins into the general circulation or into a bronchial artery or administered them as aerosol to the lungs. Prostaglandins usually caused tracheal contraction, which survived vagal cooling to 5-7 degrees C but was abolished at 0 degrees C. Vagally mediated tracheal contraction was also evoked when prostacyclin was injected into the pulmonary circulation of dogs whose pulmonary and systemic circulations were independently pump perfused. Recordings of afferent vagal impulses indicated that bronchial arterial injection of prostaglandins stimulated bronchial C-fibers; aerosols of prostaglandin stimulated pulmonary and bronchial C-fibers and C-fibers in extrapulmonary airways. We postulate that in susceptible human subjects concentrations of these prostaglandins too low to have direct bronchodilator effects may cause reflex bronchoconstriction by stimulating afferent vagal C-fibers in the lower airways.

Action Potentials↗
PubMed1985

Vagal chemoreflex coronary vasodilation evoked by stimulating pulmonary C-fibers in dogs.

We performed experiments on anesthetized, open-chest dogs to determine whether the pulmonary chemoreflex (bradycardia and systemic hypotension) evoked by stimulating pulmonary C-fibers also involves reflex changes in coronary vascular resistance. We perfused the circumflex coronary artery at constant pressure (usually 100 mm Hg) and recorded mean circumflex blood flow. Stimulation of pulmonary C-fibers by right atrial injection of capsaicin (10 micrograms/kg) decreased arterial blood pressure and heart rate and increased circumflex blood flow by 32-109% (P less than 0.001). Circumflex blood flow also increased, by 26-100% (P less than 0.001), when heart rate was kept constant by pacing. Coronary vasodilation was not secondary to the reflex decrease in arterial blood pressure. Injecting capsaicin (10 micrograms/kg) into the left atrium did not increase circumflex blood flow. Reflex coronary vasodilation could still be evoked when myelinated nerve fibers were blocked selectively by cooling the cervical vagus nerves to 7-8 degrees C but was abolished by cooling to 0 degrees C, by cutting the pulmonary vagal branches, or by giving atropine. Reducing coronary perfusion pressure shifted the stimulus (dose of capsaicin)-response (increase in coronary blood flow) curve to the right, but, even at low perfusion pressures, significant reflex vasodilation still occurred. Regional (transmural) distribution of myocardial blood flow was measured by the microsphere technique at various perfusion pressures. The endocardial:epicardial blood flow ratio decreased significantly as perfusion pressure was reduced, but was not altered by right atrial injection of capsaicin at any perfusion pressure. Our results indicate that stimulation of pulmonary C-fibers triggers reflex cholinergic vasodilation in all layers of the myocardium.

Animals↗
PubMed1984

Further observations on dental parameters of trigeminal and atypical facial neuralgias.

One hundred thirty-one patients with primary trigeminal neuralgia and 77 patients with atypical facial neuralgia or pain were treated by oral surgical procedures, with complete or almost complete pain remission in 88% of the cases and without persistent residual anesthesias, dysesthesias, or dysalgesias. The following conditions were related to patients' pain perceptions: cavities in alveolar bone at tooth extraction sites, bone fistulas, periodontal infections, and maxillary sinus infections draining into alveolar bone. The bone cavities and fistulas mentioned above were usually not visualized by standard x-ray diagnostic procedures, and their detection required a new diagnostic approach which is described. Microbiologic findings indicated involvement of a mixed, variable flora in the above conditions. Histopathologic observations of scrapings from involved bone showed a variable incidence of bone necrosis, predominantly chronic inflammatory cell populations and fibrous tissue.

Adult↗
PubMed1984

Aortic wall properties and baroreceptor behaviour at normal arterial pressure and in acute hypertensive resetting in dogs.

In order to throw light on the mechanism of acute hypertensive baroreceptor resetting, we examined the relationship between aortic baroreceptor firing and aortic wall properties in anaesthetized dogs as pressure was varied in a number of ways. We recorded baroreceptor impulses from the left aortic nerve, and measured aortic pressure with a catheter-tip transducer and external aortic diameter with ultrasonic transit-time transducers. Narrow anticlockwise hysteresis loops were evident in the pressure-diameter relationship of the upper thoracic aorta, both during the rapid pulsatile pressure changes of the cardiac cycle and during the slow excursions of mean pressure imposed for construction of baroreceptor pressure--response curves. In contrast to the 'phase-lag' response of diameter to pressure, the baroreceptor response was 'phaselead' in character, decreasing when stress-induced creep occurred in the aortic wall. When the mean arterial pressure set-point was increased from 100 to 125 mmHg for 20 min, the hysteresis loops relating mean diameter to mean pressure in the range 60-200 mmHg were displaced along the diameter axis in the direction of wall creep. A reduction in the baroreceptor response to pressure (i.e. resetting) always accompanied this displacement. Administration of ouabain (25-35 micrograms/kg) had no consistent effect on baroreceptor resetting. It has been suggested that acute baroreceptor resetting is akin to adaptation. To investigate the possibility that the two processes are accompanied by similar changes in aortic wall properties, we converted the aorta into a closed sac and distended it with a square wave of pressure. Like resetting, adaptation of the baroreceptor response to maintained pressure was associated with a small degree of creep of the aortic wall. Our results are compatible with the hypothesis that acute hypertensive resetting of aortic baroreceptors is similar to adaptation, both phenomena being attributable to relaxation of viscoelastic coupling elements, leading to a reduction of strain at the receptor membrane. Whether viscoelastic processes alone can account for acute resetting, or whether changes in ionic balance are involved also, baroreceptor responsiveness is a function of the stress history of the wall, the pressure-response curve moving along the pressure axis in the direction of the prevailing set-point. Hence, in early hypertension physiological resetting of baroreceptors will precede pathological resetting, and may even promote an upward movement of set-point.

Action Potentials↗
PubMed1984

Pulmonary C-fibers evoke both apnea and tachypnea of pulmonary chemoreflex.

Pulmonary C-fibers initiate the prompt apnea evoked by pulmonary arterial injections of capsaicin, but their role in the subsequent rapid shallow breathing of the pulmonary chemoreflex is disputed. To determine whether this reflex tachypnea is triggered by pulmonary C-fibers rather than by afferents further downstream, we separately perfused the pulmonary and systemic circulation in anesthetized dogs. When the lungs were rhythmically inflated, injection of capsaicin (0.5-20.0 micrograms X kg-1) into the isolated pulmonary circulation evoked an immediate cessation of phrenic nerve firing ("apnea") and when phrenic bursts resumed, a reduction in their amplitude. Phrenic burst frequency was usually entrained to the ventilator cycle and did not increase. By contrast, when entrainment of phrenic bursts was avoided by statically inflating the lungs at a transpulmonary pressure of 3 cmH2O, the injection of capsaicin evoked apnea, followed by a prolonged increase in phrenic burst frequency and a decrease in amplitude ("rapid shallow breathing"). The infusion of capsaicin (10-20 micrograms X kg-1 X min-1) also evoked rapid shallow breathing, but without apnea. Our results are consistent with the hypothesis that in spontaneously breathing animals, stimulation of pulmonary C-fibers evokes rapid shallow breathing.

Animals↗
PubMed1983

Rapid shallow breathing evoked by selective stimulation of airway C fibres in dogs.

1. We have examined the reflex changes in breathing evoked in anaesthetized dogs by stimulation of the afferent vagal C fibres that supply the intrapulmonary and lower extrapulmonary airways. We stimulated bronchial (intrapulmonary) C fibres selectively by injecting bradykinin into the right bronchial artery (the chest had been opened briefly for insertion of a bronchial arterial catheter).2. Bronchial arterial injection of bradykinin (0.15-1.5 mug in 3-6 sec) usually caused a brief bout of rapid shallow breathing, which was sometimes preceded by apnoea. Infusion of bradykinin (0.2-2.0 mug min(-1) for 2-12 min) caused prolonged rapid shallow breathing, the breathing frequency (f) increasing by 19-102% and tidal volume (V(T)) decreasing by 13-87%; end-tidal P(CO2) decreased by 2-9 mmHg in several experiments. Rapid shallow breathing was also evoked by administration of bradykinin aerosol through a lower tracheal cannula.3. Cutting the vagus nerves or cooling them to 0 degrees C abolished the prolonged rapid shallow breathing evoked by bradykinin, but intermittent disturbances of breathing could still be elicited in some dogs. These residual effects often consisted of irregular spasmodic inspirations, which were abolished by avulsion of the right upper thoracic sympathetic chain.4. Rapid shallow breathing was accompanied by contraction of airway smooth muscle in an innervated segment of the upper trachea; contraction was abolished by cutting or cooling the vagus nerves.5. Arterial blood pressure often decreased briefly when bradykinin was injected into the bronchial artery; changes in pressure were smaller and less frequent when bradykinin was infused slowly, and pressure was usually unaltered when bradykinin was administered as an aerosol. Rapid shallow breathing occurred whether pressure decreased, increased or was unchanged. A number of other observations indicated that the changes in breathing were independent of the changes in blood pressure. Changes in heart rate were complex and appeared to result from the interplay of several reflexes. Marked cardiac slowing was evoked by bradykinin aerosol.6. Bradykinin injected into a bronchial artery is known to stimulate bronchial (intrapulmonary) C fibres. Results of recording afferent vagal impulses in the present study indicated that bradykinin administered as an aerosol stimulated bronchial C fibres and also C fibres with endings in the lower trachea and extrapulmonary bronchi. Irritant and pulmonary stretch receptors were not stimulated unless aerosols were administered repeatedly and in higher concentration. Hence airway C fibres appeared to be responsible for the reflex effects of bradykinin aerosol.7. Bronchial C fibres are stimulated by substances (bradykinin, prostaglandins and histamine) known to be released by the lungs and airways in a variety of pathophysiological circumstances. Results of this and previous studies are compatible with the hypothesis that stimulation of bronchial C fibres plays a major role in evoking the rapid shallow breathing, bronchoconstriction and increased secretion by airway submucosal glands that are part of the pulmonary defence response.

Animals↗
PubMed1982

Tracheal contraction and relaxation initiated by lung and somatic afferents in dogs.

Capsaicin injected into the right heart of dogs causes reflex bronchoconstriction by stimulating pulmonary C-fibers, but injected into the left heart it is said to have little effect even though it stimulates bronchial C-fibers, which are known to cause contraction of airway smooth muscle. Attempting to resolve this apparent contradiction, we recorded smooth muscle tension in an innervated tracheal segment in anesthetized dogs and examined the reflex effects of injecting capsaicin intravascularly at different sites. Right atrial injection of capsaicin (10 micrograms/kg) caused tracheal contraction, as did bronchial arterial injection (0.15-5.0 micrograms); left atrial injection (10 micrograms/kg), however, caused relaxation or slight contraction, or a combination of the two. Contraction but not relaxation was abolished by cutting or cooling (0 degree C) the cervical vagus nerves. Femoral arterial injection (10-100 micrograms) caused tracheal relaxation, which was abolished by cutting hindlimb nerves. We conclude that both pulmonary and bronchial C-fibers evoke tracheal contraction, but when capsaicin is injected into the left atrium any effects of stimulating bronchial C-fibers are masked by the reflex action of somatic afferents, which cause tracheal relaxation.

Animals↗
PubMed1982

Reflex tracheal gland secretion evoked by stimulation of bronchial C-fibers in dogs.

We examined the effect of stimulating bronchial C-fibers on tracheal submucosal gland secretion in anesthetized dogs with open chest and lungs ventilated through the lower trachea. We opened the upper trachea in the midline, retracted the cut edges, and sprayed powdered tantalum onto the exposed mucosa. Secretions from the ducts of submucosal glands caused elevations (hillocks) in the tantalum layer, which were viewed through a microscope and recorded on videotape with a television camera. We counted the hillocks (greater than 0.2 mm diam) in an area of mucosa (1.2 cm2) before and after injecting capsaicin (3 micrograms) into a bronchial artery to stimulate bronchial C-fibers. In the minute before capsaicin was injected 7 +/- 2 (mean +/- SE; n = 20) hillocks appeared and in the minute after 40 +/- 2 hillocks. Bradykinin (1.5 micrograms) had similar effects. Secretion was accompanied by contraction of the trachealis muscle. Effects were abolished by cooling (0 degree C) or cutting the vagus nerves. Since capsaicin and bradykinin stimulate bronchial C-fibers selectively when injected in these small doses, we conclude that bronchial C-fibers furnish the afferent arm of an airway secretory reflex.

Animals↗
PubMed1981

Prostacyclin (PGI2) mediates hypoxic relaxation of bovine coronary arterial strips.

Bovine coronary arterial strips (BCA) exhibiting spontaneous tone, relax in response to a decrease in the pO2 of the bathing medium. Experiments were performed to determine if prostaglandins (PGs) mediate the oxygen-induced changes in tension. BCA were equilibrated in Krebs-bicarbonate solution at 37 degrees C gassed with 95% O2, 5% CO2 and tension was measured isometrically. When the pO2 of the bathing medium was decreased, BCA exhibited reversible reductions in tension. Switching from 95% O2, 5% CO2 to 95% N2, 5% CO2 (anoxia) elicited an initial relaxation followed by a contraction. In contrast, a change to 5% O2, 5% CO2, 90% N2 (hypoxia) was followed by a sustained relaxation. Re-introduction of O2 to anoxic strips produced a biphasic response: relaxation followed by contraction. Indomethacin or eicosatetraynoic acid (EYA) increased tone and inhibited the relaxation produced by anoxia or hypoxia. Indomethacin or EYA did not inhibit the relaxation of anoxic strips during re-introduction of O2, but did inhibit the contraction partially. Relaxation of arterial strips to arachidonic acid (AA) was similar to relaxation to prostacyclin (PGI2). Anoxia limited the relaxation to AA but not to PGI2. We conclude that PG synthesis contributes to the basal tone and the hypoxia-induced relaxation of BCA. In addition, hypoxia, unless severe, does not prevent the conversion of AA to PGI2.

Animals↗
PubMed1981

Reflex tracheal contraction induced by stimulation of bronchial C-fibers in dogs.

Bradykinin stimulates the afferent vagal endings of bronchial C-fibers but has little effect on other pulmonary vagal afferents. In anesthetized dogs with open chest, we recorded transverse tension in the posterior wall (trachealis muscle) of an upper cervical tracheal segment and stimulated bronchial C-fibers selectively by injecting bradykinin (19 ng-3 microgram) into a bronchial artery. The recurrent and pararecurrent laryngeal nerves were cut so that the superior laryngeal nerves provided the motor supply to the segment. Bradykinin caused a dose-dependent increase in tracheal muscle tension and often a conspicuous decrease in heart rate, which were abolished by vagotomy or administration of atropine. Injection of bradykinin still evoked tracheal contraction when myelinated lung afferents were blocked by cooling the midcervical vagi to 7 degrees C, but contraction was abolished when unmyelinated lung afferents were blocked by cooling to 0-1 degrees C, the effects of cooling being reversible. Our results indicate that stimulation of bronchial C-fibers, like that of pulmonary C-fibers, evokes reflux contraction of airway smooth muscle and reflex cardiac slowing.

Animals↗
PubMed1980

Quantitation by bioassay of mixtures of prostaglandins E2 and I2.

A bioassay method is described for the simultaneous identification and quantitation of small amounts of prostaglandins E2 and I2. Strips of rabbit coeliac and bovine coronary arteries were suspended within a common chamber surrounded by a heated water bath. The tissues were coupled individually to transducers to record their length. Using a superfusion flow rate of 2.0 ml/min the rabbit coeliac and bovine coronary arterial strips responded in a highly reproducible manner to threshold doses of 0.1 ng PGE2 and 1.0 ng PGI2, respectively. This technique is more sensitive than the conventional bioassay methods to quantify and differentiate between prostaglandins.

Animals↗
PubMed1979

Etiology and treatment of idiopathic trigeminal and atypical facial neuralgias.

In a series of sixteen patients with idiopathic trigeminal neuralgia and twenty-one patients with atypical facial neuralgia, it was found that the painful phenomena associated with both disorders were, in nearly all instances, closely related to the presence of maxillary or mandibular bone cavities at previous tooth extraction sites. Standard oral surgical procedures for curettage of the cavities, together with administration of antibiotics, were employed in the successful treatment of both the trigeminal and atypical facial neuralgias, with complete pain remissions for periods varying from 2 months (for most recently treated cases) up to 9 years. The observations and results of this study suggest that dental and oral disorders may play a role in the genesis of trigeminal and atypical facial neuralgias.

Adult↗
PubMed1977

Role of prostaglandins in the mediation of systemic tachyphylaxis to angiotensin II.

Angiotensin-induced prostaglandin release has been implicated in the deveolpment of tachyphylaxis to angiotensin in vitro. Based on these findings and evidence that prostaglandins modulate the angiotensin reposne locally, experiments were done to investigate the role of prostaglandins in the systemic tachyphylaxis to angiotensin. Rats were given intravenous infusions of 1-asparaginyl-5-valyl and 1-aspartyl-5-isoleucyl andiotensin II at two different doses. Using systemic blood pressure as a parameter, varying degrees of tachyphylaxis were produced and the aspartyl analog was found to be more tachyphylactic. When rats were given indomethacin, a prostaglading synthesis inhibitors, the response to intravenous infusion of aspartyl angiotensin was not significantly altered.

Angiotensin II↗