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Biomedical subjects

R G DeLaney

Publications and source records attributed to R G DeLaney.

11 recordsLinked to original sources
PubMed1985

Circulatory adaptation to bimodal respiration in the dipnoan lungfish.

In the dipnoan lungfish, Protopterus aethiopicus, P. annectens, and Lepidosiren paradoxa, the ductus is a short powerful muscular vascular trunk forming a channel for communication between the systemic and pulmonary circulations. In structure, the dipnoan ductus is very similar to the ductus arteriosus (Botalli) in the mammal. Innervation is abundant, consisting of myelinated and nonmyelinated nerve fibers issuing, at least in part, from the vagus. Neurons are present in the adventitia, and numerous nerve profiles, filled with small agranular vesicles, are closely associated with the myocytes, suggesting strong cholinergic control. Perfusion of the ductus in vitro using hypoxic saline causes it to dilate; conversely it is constricted by alpha-agonists. Dopamine and prostaglandin E2 are potent dilators, whereas the beta-agonist, isoproterenol, and acetylcholine are less powerful. A vasomotor segment has been identified on the pulmonary artery (PAVS) close to its junction with the ductus. Its location and structure are similar to the corresponding segment in amphibians and reptiles. It is innervated by endings filled with small clear vesicles. Granular vesicle cells are also present within the adventitia. The PAVS is constricted by acetylcholine. As in amphibians, alpha-agonists and hypoxic saline are without vasomotor effects. Based on the anatomic and physiological observations, a concept of cyclic perfusion of the gas exchangers in Dipnoi is proposed. During the alternation between air breathing (emersion) and apneic phases (immersion), the pattern of the circulation in the lungfish oscillates between that of a tetrapod and a fish.

Animals↗
PubMed1983

Pulmonary mechanoreceptors in the dipnoi lungfish Protopterus and Lepidosiren.

Pulmonary mechanoreceptors in the dipnoi lungfish Protopterus aethiopicus and Lepidosiren paradoxa were identified and characterized both in vivo and in vitro. Both slowly adapting receptors (SAR) and rapidly adapting receptors (RAR) were found, with the majority of receptors being of the slowly adapting type. The SAR discharged during inflation once their threshold volume was exceeded, and this activity persisted during prolonged lung inflation. For most of the SAR, interaction between the rate of inflation and lung volume was involved in setting the firing rate of the receptor. Increase in intrapulmonary carbon dioxide partial pressure decreased the activity of the SAR during sustained inflation at a constant intrapulmonary pressure. The RAR also discharged during inflation once the threshold volume was exceeded. However, in contrast to the SAR, the RAR became silent within 1.5 - 15 s after the end of inflation. The activity of these receptors during inflation was influenced predominantly by the rate and influenced little by the volume of inflation. According to these observations, the behavior of lungfish pulmonary mechanoreceptors closely resembles that of pulmonary mechanoreceptors in amphibians but differs from that of mechanoreceptors in the swim bladder of teleosts.

Acclimatization↗
PubMed1983

Response of pulmonary rapidly adapting receptors during lung inflation.

Studies were conducted to establish the factors that determine the response of canine pulmonary rapidly adapting receptors (RAR) during lung inflation. Inflations of the lung were performed at several constant rates during which the activity of individual RAR was counted. At each rate of inflation tested multiple identical tests were performed. The volume of each test inflation was controlled. Data obtained in all tests at each flow rate were averaged to give the mean response of the receptor at that rate of inflation. These studies indicate the major response characteristics of RAR during lung inflation in conditions of relatively constant lung mechanics. First, at a constant rate of inflation, the activity of RAR augments increasingly as the lung is expanded. Second, their activity is influenced markedly by the rate of inflation. However, this sensitivity is nonlinear. Specifically, at low rates of inflation increases in flow rate produce more marked augmentation of RAR firing than do identical increases in flow at higher rates of inflation. The major difference between receptors is in their threshold; however, this too is a function of flow rate. With increasing flow rate the threshold, whether measured as the inflation volume or transpulmonary pressure at which receptors begin to fire, declines. The response of receptors, however, with thresholds over the entire range show the major features discussed above. The present results provide quantitative information which are necessary to begin to eludicate the transduction properties of this receptor type.

Animals↗
PubMed1981

Augmentation of phrenic neural activity by increased rates of lung inflation.

Studies were conducted in anesthetized paralyzed dogs using a cycle-triggered constant-flow ventilator, which ventilated the animal in phase with the recorded phrenic neural activity. Intermittently tests were performed in which the animal was ventilated with a different airflow for a single breath. Increased airflows, within the range generated during spontaneous breathing, caused an increased rate of rise of the moving average phrenic neurogram and a shortening of the duration of the nerve burst. The magnitude of the increase in the rate of rise of the neurogram was related to the level of inspiratory airflow. Tests with brief pulses of airflow showed that an increase in the rate of rise of the phrenic neurogram could be produced without inflating the lung above the resting tidal volume of the animal. Similar results were obtained with negative-pressure ventilation and the effects were abolished by vagotomy. This vagally mediated augmentation of phrenic neural output may accelerate the inspiratory volume change in the lung during spontaneous breathing at hyperpneic levels.

Animals↗
PubMed1977

Acid-base balance and plasma composition in the aestivating lungfish (Protopterus).

Upon entering into aestivation, Protopterus aethiopicus develops a respiratory acidosis. A slow compensatory increase in plasma bicarbonate suffices only to partially restore arterial pH toward normal. The cessation of water intake from the start of aestivation results in hemoconcentration and marked oliguria. The concentrations of most plasma constituents continue to increase progressively, and the electrolyte ratios change. The increase in urea concentration is disproportionately high for the degree of dehydration and constitutes an increasing fraction of total plasma osmolality. Acid-base and electrolyte balance do not reach a new equilibrium within 1 yr in the cocoon.

Acclimatization↗
PubMed1977

Analysis of lung ventilation in the aestivating lungfish Protopterus aethiopicus.

During aestivation, the breathing pattern of the lungfish changed from the usual aquatic pattern of a single breath followed by prolonged apnea to the pattern of alternating tachypnea and apnea that characterizes Cheyne-Stokes breathing. As aestivation continued, the number of breaths per tachypneic period increased gradually to reach a steady level at about the 3rd mo. During the bouts of tachypnea, minute ventilation increased because of the increase in respiratory frequency even though tidal volumes decreased. Ventilation of the lungs during aestivation appeared to involve the same mechanism as during life in water, i.e., a buccal force pump. The breathing cycle began with the aspiration of air into the mouth as the buccal cavity enlarged. Lung deflation then occurred abetted by contraction of the abdominal muscles. Lung inflation followed and involved the "swallowing" of air form the posterior buccal region into the lungs. Cycles of deflation and partial inflation of the lungs were repeated 8-40 times (tachypneic period). At the end of the tachypneic cycle, after the last deflation, a series of larger buccal force-pump maneuvers reinflated the lungs before the start of the apneic period.

Adaptation, Physiological↗
PubMed1975

Stimulus interaction in the responses of carotid body chemoreceptor single afferent fibers.

The characteristics of steady-state responses of single afferent fibers of carotid chemoreceptors to independent changes in arterial Po2, and Pco2 were investigated in cats. The arterial blood pressure was maintained within the normal limits (115-130 torr). Single chemoreceptor afferent fibers responded to changes both in arterial Po2 and Pco2. The relationship between the activity of chemoreceptors and changes in arterial Pco2 was linear at a constant arterial Po2. The two stimuli showed multiplicative interaction. The activity approached zero (threshold) as arterial Pco2 was decreased at a constant arterial Po2; a decrease in arterial Po2 decreased the arterial Pco2 threshold. These response characteristics of a single fiber suggest that the sensory receptor may be activated through a single mechanism by the two stimuli. The data fit into an idea that the mechanism may involve a conformational change in the membrane-bound polymeric chromophore group which reacts with O2 reversibly and shows a Bohr-shift.

Animals↗
PubMed1975

Relationship between carotid chemoreceptor activity and ventilation in the cat.

The steady-state stimulus-response relations between arterial P02 and PCO2 and the mean activity of carotid chemoreceptors (single and multi-fiber) and ventilation were simultaneously recorded in 48 anesthetized cats. The carotid chemoreceptor activity varied linearly with the increase of arterial PCO2, below and above the normal value, at any given level of arterial P02. A decrease in arterial P02 increased the activity of the carotid chemoreceptors and increased its sensitivity to changes in arterial PCO2, showing multiplicative stimulus interaction. The authors also found that the response in ventilation during hypoxia to changes in arterial PCO2 below the normal value was smaller than that to changes above it, unlike the response of carotid chemoreceptors. This arterial PCO2 quasi-threshold for ventilation was, therefore, not due to a corresponding threshold for the activity of the carotid chemoreceptors but to a central mechanism. Above the central PaCO2 threshold, the ventilatory response to changes in PaCO2 and Pa02 resembled that of chemoreceptors but the ventilation dependent on hypoxia was greater than that could be directly accounted for by the activity of peripheral chemorecepors. A multiplicative interaction between the activity of peripheral chemoreceptors and central CO2 excitation appears to play a role in the regulation of ventilation.

Animals↗