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At least 19 recordsLinked to original sources
PubMed1975

Occlusion pressure as a measure of respiratory center output in conscious man.

The output of the "respiratory centers" has been estimated by measuring ventilation, inspiratory muscle power, EMG of the diaphragm, and by various other means, each of which has serious disadvantages. The static pressure generated by the inspiratory muscles at FRC against an obstructed airway is here suggested as a useful alternative. Ten conscious, normal, sitting human subjects were subjected to CO2 rebreathing (Read, 1967) and their airways were occluded at end-expiration at intervals without the subjects being aware in advance. The inspiratory pressure waves so generated were found to be distorted by conscious or unconscious responses to the occlusion which had a minimum latency of 0.15 sec. The pressure generated at 0.1 sec after the onset of inspiration (P0.1) was nevertheless easy to measure and was reproducible in each subject. The CO2 response obtained by plotting P0.1 against PCO2, was curvilinear, the P0.1 increasing more rapidly at high PCO2. The P0.1 is independent of pulmonary mechanics. Since it measures the rate of rise of inspiratory activity and not the peak activity it is also independent of mechanisms that alter the respiratory pattern by affecting inspiratory duration, in particular the vagal volume-related inspiratory-inhibitory reflex. It is concluded that measurements of P0.1 represent a useful index of the output of the respiratory centers.

Airway Obstruction↗
PubMed1979

[The rate of isometric inspiratory pressure change as a measure for the CO2 sensitivity of the respiratory center in patients with obstructive lung disease].

In healthy persons with and without loaded breathing, in asthmatics, and in patients with chronic obstructive lung disease (COLD) the rate of isometric inspiratory pressure development ([dp/dt]max) has been measured in order to assess the clinical significance of (dp/dt)max as an index of the motor output of the respiratory center in response to increased levels of carbon dioxide. During unloaded breathing normal subjects showed an excellent correlation between the ventilatory and the (dp/dt)max responses to CO2. Normal persons breathing through an external expiratory flow resistance, the asthmatics, and the patients with COLD had not only a blunted ventilatory response, but also a reduced (dp/dt)max response. The parallel changes observed in both variables indicate that under conditions of mechanical loading the (dp/dt)max does not exclusively reflect the motor output of the respiratory center, but is influenced by other factors such as the work of breathing and the mechanical efficiency of the respiratory pump. Accordingly, measurements of (dp/dt)max are of little help in deciding whether the development of CO2 retention in patients with obstructive airway disease is primarily due to increased mechanical load or to decreased sensitivity of the respiratory center.

Adult↗
PubMed1992

[Muscarinic receptor subtypes in respiratory center and their functions].

Radioreceptor binding assays using [3H]quinuclidinyl benzilate and [3H]pirenzepine were performed on the pons and medulla oblongata (MeOb) of rat brain. The M1 cholinergic receptor (M1-R) was found to account for approximately 30-40% of the total muscarinic receptors (M-R) in the pons and MeOb, and the M2 accounted for about 60-70%. The receptor binding capacities of scopolamine and atropine were compared with those of pirenzepine (Pir) and AF-DX 116 on the 2 parts of the brain. The affinity values (pKi) suggest that the selectivity of scopolamine for M1-R is greater than for M2-R, and that of atropine for M2 is greater than for M1. In conscious rabbits, the respiratory frequency (FR), tidal volume (TV), and minute ventilation volume (MVV) were determined. Arterial blood samples were taken intermittently and analyzed for pO2, pCO2, and pH. When pilocarpine (a M1-R subtype selective agonist) was given, excitatory effects on respiration were seen through FR, TV, MVV, and the pO2, pCO2, and pH. When 6 beta-acetoxy nortropane (6 beta-AN, a novel M2-R subtype selective agonist) was given, the effects were inhibitory. These results were reversed after administration of Pir, scopolamine, AF-DX 116, and atropine. Thus, it shows that Pir and scopolamine inhibit respiration by blocking the M1-R subtype of the respiratory center, while the excitatory effects of AF-DX 116 and atropine are brought about by blocking the M2-R subtype of the respiratory center.

Animals↗
PubMed1975

A new method of evaluating the chemosensitivity of the respiratory center in children.

Decreased ventilatory response to carbon dioxide is often present in lung disease. This can be due to a reduction in the output of the respiratory center or an inability of the respiratory pump to respond to a normal output because of the size or impedence of the pump. To separate these mechanisms we have measured the isometric force developed by the respiratory muscle during brief airway occlusion, by measuring the pressure generated at 100 msec (Pm100). We studied 43 subjects ranging in age from 6 to 50 years, and nine neonates. We found a linear rise of Pm100 with rising PAco2 during carbon dioxide rebreathing maneuvers. Our results also show that although there are wide variations in slopes of Pm100 to carbon dioxide tension (SPm100/PAco2) between individuals, in a given subject this slope remains constant even following repeated studies. It also remains constant for age and size, indicating that the neuromechanical output of the respiratory apparatus does not change with growth. In contrast the ventilatory response either assessed as Ve/PAco2 or Vt/PAco2 depended on age and lung size. The results suggest that throughout growth, comparison of Pm100/PAco2 and Ve/PAco2 can distinguish between abnormalities of neuromuscular output from other causes of ventilatory impairment.

Adolescent↗
PubMed1975

Modification of respiratory center output in the unanesthetized fetal sheep "in utero".

Diaphragmatic electromyographic activity, tracheal and amniotic fluid pressures, lung liquid flow, and carotid and jugular venous pressures were measured on eight fetal lambs who survived for periods of 9-43 days postoperatively. The fetal gestational age ranged from 98 to 113 days at operation. Respiratory center output of the fetus as indicated by electromyographic activity was modified by the following stimuli. It was suppressed by anesthesia and fetal hypoxia (Pao2 = 12 mmHg), tonically reduced by lung inflation, and stimulated by cyanide injections (150-600 mug) into the fetal jugular vein. Neuromuscular transmission to the diaphragm was blocked with d-tubocurarine (0.2-0.6 mg). These experiments indicate that central and motor pathways to the diaphragm are sufficiently mature by 101 days in the fetal sheep to permit their output to be modified by chemical and mechanical stimuli.

Amniotic Fluid↗
PubMedDate not supplied

[Muscarin-sensitive cholinoreactive systems in the respiratory center].

Muscarinic cholinergic drugs (arecoline, oxotremorine) which can easily overcome the blood-brain barrier inhibit the action potentials of the phrenic nerve in anesthetized or decerebrate curarized cats after a selective blockade of peripheral muscarinic cholinoreceptors with quaternary anticholinergic drugs (oxyphenonium, benzilycholine). These inhibitory effects are abolished by drugs blocking the central muscarinic cholinoreceptors (atropine, scopolamine, benactyzine). This suggests the existence of muscarinic cholinoreceptive neurons in the respiratory center of the cerebral ponto-bulbar region, the said neurons inhibiting the activity of the inspiratory motonerons.

Animals↗
PubMed1975

[Combined effects of hypoxia and hypercapnia on the functional state of the respiratory center].

Experiments were conducted on cats under nembutal anesthesia; a study was made of pulse activity of bulbar respiratory neurons, electrical activity of the diaphragm and of the intercostal muscles; pO2, pCO2, pH, arterial blood oxygen saturation were determined in combined action of hypoxia and hypercapnia. When hypoxic gaseous mixture was given for respiration the developing hypocapnia disturbed the discharge rhythmic activity of the respiratory neurons, the respiration acquiring a pathological character of the Cheyne--Stokes type. After addition to the hypoxic gaseous mixture of 2% CO2 the gaseous composition of the arterial blood approached the initial values; this addition prevented the development of hypercapnia and disturbances of rhythmic discharge activity of the respiratory neurons. Addition of 5% CO2 to the hypoxic gaseous mixture produced a negative effect: at first it intensified and then depressed the pulse activity of the respiratory neurons, caused metabolic and respiratory acidosis, and promoted asphyxia.

Animals↗
PubMedDate not supplied

The sensitivity of the respiratory center and some circulatory and subjective responses after nalorphine and naloxone injections.

In five volunteers the sensitivity of the respiratory centre to carbon dioxide after naloxone and nalorphine injections was studied using "double blind" method and increments of doses. Alterations in the respiratory centre sensitivity were reflected by changes in respiratory minute volume, which was measured before and after drug injections, as well as after carbon dioxide stimulation. Comparison of results and their statistical verification showed that nalorphine alone causes respiratory depression and carbon dioxide stimulation is, beside the weak initial action, almost ineffective. Naloxone causes very small, if at all, respiratory depression and the respiratory centre answers efficiently to carbon dioxide stimulation.

Carbon Dioxide↗