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Biomedical subjects

H D Schultz

Publications and source records attributed to H D Schultz.

48 records · Page 3Linked to original sources
PubMed1986

Stimulation of pulmonary vagal afferent C-fibers by lung edema in dogs.

In anesthetized, open-chest dogs we examined the effect of pulmonary edema on the firing frequency of afferent vagal fibers arising from the lung. We recorded impulses from slips of the cervical vagus nerves and infused isotonic Krebs-Henseleit solution (20% of body weight) intravenously to increase net filtration pressure in the lung microvasculature. Measurement of extravascular lung water (6.0 +/- 0.4 g/g dry lung), and morphological examination of lung tissue (revealing various degrees of perivascular and peribronchial cuffing) confirmed that edema was present. At the end of the infusion when the lungs were congested (lung microvascular pressure, 37 cm water) and edematous, the impulse frequency of pulmonary and bronchial C-fibers and rapidly adapting receptors had increased 5-6 times. The only significant change in slowly adapting receptor activity was an increase during deflation. When lung water was still elevated but lung microvascular pressure had been restored to control by withdrawal of blood, impulse activity of rapidly and slowly adapting receptors reverted to or below control. Pulmonary C-fiber activity, although less than during congestion, remained significantly above control, several C-fibers being stimulated by interstitial edema in the absence of alveolar edema. Bronchial C-fibers were stimulated in severely edematous lung showing pronounced peribronchial cuffing and alveolar edema, but were not stimulated in milder grades of edema. Our results support the hypothesis (Paintal, 1969) that pulmonary C-fibers (J-receptors) are stimulated by an increase in interstitial pressure secondary to edema.

Action Potentials↗
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↗
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

Arterial baroreceptors have minimal physiological effects on adrenal medullary secretion.

The influence of arterial baroreceptors on secretion of catecholamines from the adrenal medulla was evaluated by several methods. Conscious mongrel dogs with surgically denervated hearts were hemorrhaged until an estimated 16% of their blood volume had been removed. On a separate day they were anesthetized and their blood pressure was lowered with intravenous nitroglycerin. Neither of these maneuvers produced appreciable increases in heart rate in these dogs. In contrast, in a group of sham-operated control dogs, hemorrhage induced a mean increase in heart rate of 20 beats/min (P less than 0.05), and nitroglycerin-induced hypotension induced an increase of 50 beats/min (P less than 0.05). In a separate group of conscious dogs with aortic arch denervation but intact cardiac nerves, occlusion of the common carotid arteries for 5 min increased blood pressure and heart rate significantly but elicited only small, insignificant increases in plasma epinephrine and norepinephrine; the peak concentration of epinephrine achieved was considerably less than the amount necessary to cause appreciable effects on blood pressure and heart rate as determined in another experiment by infusing varying amounts of epinephrine into conscious, cardiac-denervated dogs. We conclude that the arterial baroreceptor reflex, within the range of activity likely to occur during most physiological and pathophysiological adjustments in the conscious dog, exerts only minimal effects on the secretion of catecholamines from the adrenal medulla.

Adrenal Medulla↗
PubMed1982

Effects of left atrial stretch in cardiac-denervated and intact conscious dogs.

We monitored cardiovascular and renal function in conscious dogs with surgically denervated hearts during two experimental procedures: 1) inflation of a balloon in the left atrium and 2) intravascular volume expansion. The results obtained were compared with results from identical experiments on sham-operated control dogs. Left atrial balloon inflation in the sham-operated dogs produced an increase in left atrial pressure, heart rate, urine flow, and sodium excretion; central venous pressure decreased. These changes were absent in the cardiac-denervated dogs. Infusion of 6% dextran in isotonic saline (16% of estimated blood volume) increased the heart rate significantly in the control dogs but not in the cardiac-denervated dogs; other hemodynamic measurements were comparable in the two groups. Urine flow and sodium excretion increased significantly in both the cardiac-denervated and control dogs; the responses did not differ significantly between the two groups. These experiments demonstrate that inflation of a balloon in the left atrium of a conscious dog elicits diuretic and natriuretic responses that are dependent on intact cardiac neural pathways, presumably specifically dependent on afferent neural impulses from left atrial receptors. On the other hand, an increase in circulating blood volume induced by the intravenous infusion of an isotonic, isoncotic solution elicits diuretic and natriuretic responses in the cardiac-denervated dog that are similar to the renal responses produced in a control dog. Thus, although cardiac receptors are capable of eliciting reflex changes in both hemodynamics and renal function, it is not clear what role they play in mediating the renal responses evoked by increases in blood volume.

Animals↗
PubMed1982

Reflexes elicited by acute stretch of atrial vs. pulmonary receptors in conscious dogs.

We measured hemodynamics and renal function in conscious dogs while partially obstructing blood flow at various sites within the thorax. Inflation of a balloon in the left atrium increased left atrial pressure (LAP) by 9 mmHg and caused a parallel increase in pulmonary arterial pressure (PAP); heart rate, arterial pressure, and total peripheral resistance increased; stroke volume and right atrial pressure decreased; and cardiac output remained unchanged. The increase in LAP was accompanied by a fourfold increase in urine flow and a threefold increase in sodium excretion. Plasma vasopressin (AVP) and renin activity (PRA) decreased. On the other hand, partial occlusion of the pulmonary veins or the main pulmonary artery produced similar increases in PAP without affecting LAP, systemic hemodynamics, renal function, or plasma AVP. Similarly, inflation of a balloon in the right atrium failed to alter renal function, plasma AVP, or PRA. Finally, constriction of the thoracic inferior vena cava decreased LAP and increased PRA. In summary, these data emphasize that inflation of a balloon in the left atrium of the conscious dog produces a composite response consisting of alterations in cardiovascular function, renal function, and circulating hormones. Moreover, our data indicate that the response is mediated by a reflex initiated from receptors located in the left atrium; we detected no evidence that receptors located in the pulmonary vasculature or right heart contribute to this response.

Animals↗
PubMed1982

Central and peripheral adrenergic modulation of carotid sinus-induced renin release.

To study central and peripheral mechanisms that regulate the level of circulating renin during activation of the carotid sinus baroreflex, both carotid sinuses were isolated and perfused at constant flow in chloralase-anesthetized dogs. Sinus pressure was controlled by an adjustable reservoir while systemic pressure was stabilized using an external chamber. Arterial renin activity, measured by radioimmunoassay, was increased during sinus hypotension only if systemic pressure was held constant. The renin response was eliminated by either sinus or renal denervation. Administration of propranolol (iv) or phentolamine directly into the renal artery totally blocked the increase in renin during activation of the reflex. Perfusion of a beta-adrenergic blocker (propranolol) or an alpha-adrenergic blocker (phentolamine) through the third and fourth cerebroventricles had no effect on the increase in renin during sinus hypotension, whereas centrally administered clonidine, and alpha-agonist, blocked the response. We conclude that the sinus reflex arc affecting renin release involves not only activation of peripheral alpha- and beta-adrenergic receptors in the kidney but also inhibition of central alpha-adrenergic receptors. No evidence for central beta-involvement was found.

Animals↗
PubMed1981

Alteration of the baroreceptor reflex by an effect of propranolol on the isolated carotid sinus.

The present experiments were designed to measure and characterize direct hemodynamic effects of propranolol on vascularly isolated carotid sinuses. dl-Propranolol, when restricted to the isolated carotid sinuses, inhibited in a dose-dependent manner the reflex increases in heart rate and mean arterial pressure during carotid sinus hypotension. When perfused through isolated sinuses at a concentration of 10 micrograms/ml, the drug totally abolished reflex changes to carotid sinus hypotension. Perfusion of the sinuses with d-propranolol or procaine at the same doses also totally inhibited the response. On the other hand, perfusion of the sinuses with sotalol, an adrenergic blocker without membrane stabilizing effects, did not alter resting levels of arterial pressure or heart rate and did not affect reflex changes during sinus hypotension. These results suggest that propranolol at high doses may affect baroreceptor afferents and inhibit the baroreceptor reflex through membrane-stabilizing and local anesthetic properties rather than through hypothesized beta receptors. It seems unlikely that these pathways contribute to the antihypertensive actions of the drug.

Animals↗
PubMedDate not supplied

Neural regulation of sympathetic nerve activity in heart failure.

One of the hallmarks of chronic congestive heart failure is an increase in sympathetic tone to the peripheral circulation and to the heart. A correlation between plasma norepinephrine and the severity of the heart failure state has been demonstrated. One mechanism that has been proposed to account for this sympathoexcitation is a depression in the baroreflex and, perhaps, cardiac reflex control of sympathetic nerve activity. This review summarizes work from several laboratories, including our own, that documents a depressed baroreflex control of heart rate and sympathetic nerve activity in both animals and humans with heart failure. The mechanism of the depressed baroreflex most likely is caused by reduced baroreceptor sensitivity as well as enhanced input to the central nervous system from cardiac receptors that are chemosensitive. Although sympathetic tone and arterial baroreflex sensitivity are altered in heart failure, there have been no studies showing a cause-and-effect relationship. Increases in plasma norepinephrine are similar in baroreceptor-denervated and intact dogs paced into heart failure. This latter observation cells into question the traditional concept of baroreceptor-mediated increases in sympathetic tone in heart failure.

Animals↗