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Biomedical subjects

F L Eldridge

Publications and source records attributed to F L Eldridge.

At least 73 records · Page 4Linked to original sources
PubMed1981

Pharmacologic study of respiratory afterdischarge.

Respiratory afterdischarge, an increased but slowly declining respiratory output lasting some minutes after cessation of a stimulus, is generated by a bulbopontine mechanism whose precise anatomic locus and neurophysiological mechanism are unknown. To determine if the mechanism responsible for the afterdischarge was due to one of the major long-acting central neurotransmitters, we studied a control group of animals and groups of animals that were pretreated with the antiserotonin agents, methysergide, parachlorophenylalanine, and 5,7-dihydroxytryptamine, the dopamine-norepinephrine antagonists alpha-methytyrosine and haloperidol, and the endorphin antagonist, naloxone. Anesthetized, paralyzed, vagotomized, and glomectomized cats were used. We measured phrenic activity before, during, and after carotid sinus nerve and calf muscle stimulation. None of the antagonists had an effect on the response to stimulation, on the magnitude of the afterdischarge, or on its time course during recovery. We conclude that these central neurotransmitters do not participate in the genesis of the respiratory afterdischarge.

5,7-Dihydroxytryptamine↗
PubMed1980

Central neural respiratory drive and afterdischarge.

Different modes of stimulation of the carotid sinus nerve were used in anesthetized cats to study development of inspiratory neural activity and respiratory afterdischarge. Continuous and inspiratory-only stimulations produced rapid rises of activity; cessation led to equally rapid initial falls followed by slowly decaying afterdischarges. Expiratory-only stimulations produced more slowly rising and smaller increases of inspiratory activity and the offset led to no rapid fall of activity; nevertheless, the time course of the afterdischarge was similar to those of continuous and inspiratory runs. During alternate cycle stimulation, the developing pattern of activity of stimulated breaths resembled that of continuous or inspiratory stimulation, whereas that of unstimulated breaths was like expiratory. The findings support conclusions that the neural network causing the afterdischarge is separate from and does not require input from inspiratory neurons in the medulla. Both the activation and decay times of this neural mechanism are relatively long.

Animals↗
PubMed1980

Prolonged stimulation of respiration by a new central neural mechanism.

The inspiratory responses to stimulation by peripheral chemoreceptor, central chemoreceptor and calf muscle afferents were studied in anesthetized, or decerebrate, paralyzed cats whose end-tidal PCO2 was servo-controlled and kept constant. All stimuli were associated with immediate increases of inspiratory (phrenic) activity and at offset were followed by a respiratory afterdischarge lasting approximately five minutes. The level of inspiratory activity following decay of the afterdischarge was the same as the prestimulation control after central chemoreceptor and calf muscle stimulation. However, after peripheral chemoreceptor afferent stimulation the stable level of inspiratory activity following the afterdischarge had increased over the prestimulation level and remained elevated for as long as it was followed, up to 90 min. Decerebration, vagotomy, and section of the spinal cord at C--T1 did not prevent this long-lasting increase in respiration. We conclude that we have demonstrated a new ponto-medullary neural mechanism which is uniquely activated by peripheral chemoreceptor afferent input; once activated, this mechanism sustains respiration at an increased level for a long period of time.

Afferent Pathways↗
PubMed1980

Mechanisms of hyperpnea induced by isoproterenol.

We injected boluses of isoproterenol (2 to 3 micrograms) into the inferior vena cava to determine the effects on phrenic activity, end-tidal PCO2, arterial pressure and aortic flow in anesthetized cerebrate and unanesthetized decerebrate cats. We studied both spontaneously breathing animals and those paralyzed and servo-ventilated to keep end-tidal PCO2 constant. Isoproterenol caused an increase of respiratory output within a few seconds if carotid bodies were intact; recordings of the carotid sinus nerves showed that the response was due to activation of carotid body chemoreceptors. After denervation of both carotid bodies isoproterenol still caused a late (approximately 16 sec) but smaller increase of respiratory output, which persisted after section of vagi and thoracic (T1-5) dorsal roots. We concluded that the major effect of isoproterenol on respiration is through its excitatory action on the carotid bodies. There is another small, late facilitatory effect, of uncertain mechanism but not caused by peripheral chemoreceptors, by other receptors in the heart and lungs or by a change in PaCO2 acting on the central chemoreceptors.

Animals↗
PubMed1980

Subthreshold central neural respiratory activity and afterdischarge.

The phrenic nerve response to identical carotid sinus nerve (CSN) stimulations was studied in anesthetized, paralyzed and vagotomized cats during apnea induced by hypocapnia. Apnea could be terminated and rhythmic phrenic activity reestablished by CSN stimulation. Magnitudes and latencies of the phrenic response were used as indices of the level of subthreshold respiratory neural activity before stimulation. Increasing hypocapnia progressively reduced the apparent magnitude of the response to a constant CSN stimulus and increased the latency. When the chemical stimulus (PCO2) was held constant at levels subthreshold for rhythmic respiration, it was found that: (1) physical calf muscle stimulation shortened the latency, (2) restimulation of the CSN led to greater magnitudes of response and shorter latencies as the time after a prior stimulation became shorter. The findings support a conclusion that even in the absence of rhythmic respiration there exists a subthreshold respiratory drive which is graded by the level of PCO2 and which is affected by neural input from limb muscles and by the mechanism that causes respiratory afterdischarge.

Animals↗
PubMed1980

Prolonged stimulation of respiration by endogenous central serotonin.

We have recently reported a new neural brainstem mechanism which is uniquely activated by stimulation of carotid body afferent input to the brain and which facilitates respiration for hours after the immediate affects of the stimulation have dissipated (Millhorn, Eldridge and Waldrop, 1980). In the present study respiratory responses to carotid body or carotid sinus nerve stimulation were measured in vagotomized, anesthetized, and paralyzed cats whose end-tidal PCO2 and temperature were servo-controlled and kept constant. The responses of animals pretreated with various serotonin antagonists and a dopamine-norepinephrine antagonist were compared to the responses of untreated control animals. All three differently acting serotonin antagonists (methysergide, parachlorophenylalanine, and 5, 7-dihydroxytryptamine) either prevented or significantly reduced the magnitude of the long-lasting respiratory response whereas the dopamine-norepinephrine antagonist (alpha-methyltyrosine) failed to alter it. We conclude that the long-lasting increase of respiratory activity following stimulation of carotid body afferents is due to activation of an endogenous central serotoninergic mechanism which facilitates respiration.

5,7-Dihydroxytryptamine↗
PubMed1980

Central respiratory effects of carbon dioxide, and carotid sinus nerve and muscle afferents.

1. In anaesthetized and paralysed cats, artificially ventilated and with the vagi and carotid sinus nerves cut, the effects of (a) changing end-tidal CO2, (b) stimulation of carotid sinus nerves, and (c) squeezing the calf muscles, on neural respiratory output have been studied. 2. The peak value of integrated phrenic activity, which is the neural equivalent of tidal volume (VTn), the rate of rise of integrated phrenic activity (Slope), inspiratory duration (TI), expiratory duration (TE), and total cycle length (Ttot) were measured. It was found that Slope-VTn, VTn-Ttot and VTn-TE relationships were similar whether respiration was stimulated by carotid sinus nerve stimulation or by increasing end-tidal CO2. However, when respiration was stimulated by squeezing the calf muscles, a given Slope was associated with a smaller VTn and a given VTn was associated with smaller Ttot and TE values than obtained with the other two inputs. 3. It is concluded that these results are compatible with the hypotheses that (1) inputs from central and peripheral chemoreceptors have similar actions at various sites in the respiratory centre complex, and (2) afferents activated by squeezing the limb muscles have additional facilitatory actions on mechanisms terminating inspiration and expiration.

Animals↗
PubMed1979

Naloxone enhances respiratory output in cats.

To investigate the physiological role of opiate receptors and opiatelike neurotransmitters, which are present in brain-stem respiratory centers, we administered naloxone to 10 cats by intravenous injection. These animals were vagotomized, paralyzed, and servo-ventilated to maintain constant end-tidal CO2; in addition, their carotid sinus nerves were sectioned bilaterally. Respiratory output was assessed by integration of phrenic nerve activity. Control saline infusions had no effect on respiratory output. However, administration of naloxone (0.4 mg/kg) caused phrenic minute output to increase significantly in each of five anesthetized cerebrate cats (control 7,272 +/- 1,615 U/min; 30 min postnaloxone 12,920 +/- 3,857 U/min; P less than 0.05) and five unanesthetized decerebrate cats (control 10,368 +/- 1,222 U/min; naloxone 14,648 +/- 3,225 U/min; P less than 0.05). In addition to the effect on phrenic minute output, naloxone infusion resulted in an increase of the inspiratory rate of rise of phrenic nerve activity in each cat. There was no change in the ratio of inspiratory duration to total respiratory period (TI/Ttot). Because naloxone is a specific opiate antagonist, we suggest that endogenous opiatelike neurotransmitters (endorphins) may modulate central inspiratory drive.

Action Potentials↗
PubMed1978

Servo control of end-tidal CO2 in paralyzed animals.

We are reporting an electronic circuit which uses the peak end-tidal CO2 signal from a rapid infrared CO2 analyzer to vary the motor rate of a fixed volume respirator. It contains variable gain and a lag compensation network which permits critical damping to prevent oscillation. The CO2 analyzer, circuitry, and respirator are connected in a closed-loop servo system that allows automatic control of the CO2 level. The system's gain and performance are such that it can accommodate large changes of CO2 return to the lungs with no more than +/- 0.5 Torr carbon dioxide pressure (PCO2) error signal. It has proved useful in experiments on neural respiratory control in paralyzed animals where it is desired to keep PCO2 constant despite changes in cardiac output and venous and CO2 return to the lungs, and to monitor the approximate magnitude of these changes.

Carbon Dioxide↗
PubMed1978

Lack of effect of vagal afferent input on central neural respiratory afterdischarge.

The effect of respiratory inhibition caused by vagal stimulation or lung inflation on the central neural mechanism that maintains respiration after cessation of a facilitatory stimulus was studied in anesthetized cats. Phrenic activity was increased by carotid sinus nerve stimulation or by squeezing or stretching calf muscle. On cessation of stimulation there was an immediate decrease in respiratory output followed by a slow decrease (afterdischarge) over a period of 5 min. Vagal stimulation or lung inflation, which caused marked inhibition of inspiration, had no effect on the development of the afterdischarge or on the course of the subsequent recovery process. The mechanism causing afterdischarge is probably a buildup of activity in a neural network in the medulla and pons. Since its activity is unaffected by vagal inhibition of respiration, it can be concluded that the network is separate from inspiratory output neurons and those involved in phase switching and that it is not dependent on increased central inspiratory neuron activity.

Afferent Pathways↗
PubMed1977

Relationship of thoracic volume and airway occlusion pressure: muscular effects.

The occluded airway pressure generated by contraction of inspiratory muscles was measured in spontaneously breathing, anesthetized, vagotomized cats at thoracic volumes below, at, and above true FRC (range, -8 to +28 ml/kg). A relatively constant neural drive at all volumes was shown by recordings of integrated phrenic nerve and external intercostal muscle activities. Peak occlusion pressure declined progressively with increasing thoracic volume and increased with occlusion volumes below FRC. Occlusion pressures measured early in inspiration (0.3 and 0.5 s) decreased similarly. Since occluded airway pressure was a satisfactory index of muscle force output of all inspiratory muscles, the study demonstrates that inspiratory muscle performance decreases with increasing thoracic volume throughout the range studied. Analysis of all occluded breaths shows that, quantitatively, the decline in muscle performance from that occurring at true FRC was -1.9% per ml/kg volume change from FRC. Zero effective muscle pressure generation occurred at 52 ml/kg above FRC, or 2.8 times FRC. These findings have important implications for the use of occlusion pressures and ventilatory responses in respiratory control system studies, since changes in FRC may affect muscle performance.

Airway Obstruction↗
PubMed1977

Sleep apnea syndrome due to upper airway obstruction: a review of 25 cases.

A sleep apnea syndrome due to upper airway obstruction was diagnosed in 25 adult men (25 to 65 years of age) using nocturnal polygraphic monitoring. Excessive daytime somnolence, hypnagogic hallucinations, and automatic behavior, personality changes with abnormal behavioral outbursts, impotence, morning headaches, abnormal motor activity during sleep, nocturnal enuresis, and high blood pressure should suggest this diagnosis when any of the symptoms are associated with loud snoring. Respiratory monitoring during sleep and nocturnal cardiovascular evaluation bring prognostic information and indications for therapy. Three types of therapeutic trials, namely, diet, medications with or without diet, and surgery have been performed. Only surgery has been beneficial in these cases.

Adult↗
PubMed1976

Two occult causes of insomnia and their therapeutic problems.

Insomnia may be associated with a sleep-induced apnea syndrome in nonobese patients who snore. The "central" type of apnea appears to be predominant in this population, in opposition to Pickwickian and nonobese hypersomniacs. An abnormal "swallowing reflex syndrome," also induced by sleep, may be a differential diagnosis. Sleeping pills that are central nervous system depressants should be cautiously prescribed for patients with such syndromes.

Adult↗