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The substituted benzylamin-derivative fominoben (PB 89 Noleptan) was intravenously administered to 12 patients with chronic obstructive lung disease in order to determine, whether an analeptic action on respiration, which had been found by others in animal studies and in healthy subjects, can also be demonstrated in patients with COLD. Time ventilation showed no statistically significant change. Respiratory rate was increased for a short time, alveolar ventilation showed a slight but significant increase 35 minutes after i.v. injection of fominoben, however no significant change in the first 10 minutes after injection.--Arterial pO2 was slightly but not significantly increased in the first 10 minutes after fominoben, while the same patients showed a significant decrease of pO2 after injection of placebo. As alveolar ventilation at this time had not significantly changed, the increase in pO2 can only be explained by an improvement of regional ventilation-perfusion ratio by fominoben. -In conclusion it can be stated, that a marked stimulative action on respiration by fominoben could not be demonstrated. There was, however, no depression of respiration as it is associated with most other caugh medications. As the drug has been shown to be an excellent caugh sedative, lack of respiratory depression can be considered as a considerable advantage.
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Three 3-year-old ewes with surgically exteriorized carotid loops were twice exposed to ambient temperatures (Ta) of 25, 30, 35 and 40 C (at constant 40% relative humidity) for 120 min in the presence (6.6 cm) and absence (less than 0.3 cm) of fleece. Thermoregulatory responses were evaluated during the last 30 min of each exposure by measurements of rectal (Tre), 6 skin surface temperatures (Ts), respiratory frequency (f), oxygen consumption (Vo2) and respiratory evaporative heat (Er); arterial blood samples were analyzed for pH, Pco2 and HCO-3 concentration. Both shorn and unshorn sheep exhibited a progressive increase in f, Er and Ts as Ta was elevated, with the unshorn group showing a higher Er than the shorn sheep at each Ta without a significant change in heat production. Er was found to be the principal avenue of heat loss, accounting for as much as 59% of the total in the shorn sheep compared to65% for the unshorn sheep. Increases in Er were accompanied by a decline in the arterial Pco2 which was linearly related to the Ta in both shorn and unshorn sheep. These data suggest that in defending against hyperthermia, sheep appear unable to increase Er without a concurrent elevation in Va at nearly allstages of acute heat stress.
We have previously shown in the anaesthetized rabbit that the ventilatory response to an increase in Paco2 is greater if that increase is produced by intravenous infusion of hypercapnic blood than by inhalation of CO2 (Linton et al., 1976). The present set of experiments was designed to investigate the reason for this. It was found that the difference in ventilatory response observed in the intact rabbit was abolished by cutting the carotid sinus nerves or by eliminating the pH/Paco2 oscillations in the carotid blood flow. It is concluded that the normally greater ventilatory response to intravenous infusion of hypercapnic blood compared with inhalation of CO2 is due to a respiratory signal derived from Paco2 oscillations and carried in the carotid sinus nerves.
The present study examines the influence of oxygen tension on the recurrent tidal volume changes caused by oscillations in arterial P(CO2). The oscillations have a period equal to two respiratory cycles, and are produced by giving alternately CO2 -enriched and CO2 -free gas mixtures. The results show alternation of the tidal volume with the same incidence (is greater than 50%) at low, normal and high oxygen tensions. However, the magnitudes of the breath-by-breath changes are significantly greater at low oxygen tension than at normal oxygen tension. Under high oxygen tension breath-by-breath tidal volume changes are indistinguishable from those at normal oxygen tension.
The effect of continuous positive airway pressure (C.P.A.P.) on the breathing pattern of ten newborn infants with respiratory-distress syndrome (R.D.S.) has been studied using an impedance pneumograph; arterial oxygenation improved and respiration, previously disorganized, became regular in both rate and depth. Grunting usually ceased within 15 minutes of the start of C.P.A.P., and there was also on average a 30 percent increase in the respiratory-rate. The rapidity with which the breathing pattern changed suggests a reflex mechanism. Sudden reductions in airway pressure were frequently followed by apnoea, regular breathing restarting with the reintroduction of C.P.A.P. These observations suggest that C.P.P.A. provides a respiratory drive in babies with R.D.S., possibly mediated through the Hering-Breuer inflation reflex.
Various amounts of carbon dioxide were removed through an extracorporeal membrane lung in spontaneously breathing lambs. The decrease in alveolar ventilation was proportional to the fraction of total carbon dioxide removed by the membrane lung. When extracorporeal CO2 removal approximated CO2 production (VCO2), alveolar ventilation almost ceased. Pulmonary ventilation can be controlled by extracorporeal carbon dioxide removal.
Recent studies demonstrated that epinephrine causes significant pulmonary A-V shunting. This study reports the effect of alpha and beta adrenergic blockade on this shunting. Sixty-three anesthetized mongrel dogs were ventilated with a mechanical respirator. Measurements of (1) the pulmonary shunt, (2) cardiac output, (3) mean pulmonary artery, pulmonary capillary wedge and systemic pressures, and (4) pulmonary and systemic vascular resistances were obtained at 5, 15 and 30 minute intervals during the first hour and hourly for 5 hours. Fifteen dogs received no treatment. All others received epinephrine hydrochloride, 2 mug/kg/min for 5 hours. Ten received epinephrine only. Ten were pretreated with propranolol hydrochloride, 250 mug/kg, 12 with phenoxybenzamine, 1 mg/kg, and 16 with phenoxybenzamine and propranolol. Propranolol significantly decreased the epinephrine induced pulmonary shunt at all times and was the most effective drug. Phenoxybenzamine decreased the early shunting, but less than propranolol, and did not decrease the late shunting. Blockade with propranolol and phenoxybenzamine was less effective than propranolol alone. Based on the observed hemodynamic changes it was suggested that beta blockade is effective in reducing epinephrine induced pulmonary insufficiency by favorably altering the flow and distribution of pulmonary blood flow which in turn decreases epinephrine induced ventilation-perfusion inequalities and capillary hypertension both of which result in shunting. Conversely phenoxybenzamine has an unfavorable effect on the pulmonary flow. These studies support previous work in animals and man which showed that beta adrenergic stimulation is important in the pathogenesis of pulmonary insufficiency. Because the amounts of epinephrine used produce blood levels observed in critical illness, these studies add support to a relationship between the increased catecholamine stimulation of critical illness and the associated and often unexplained pulmonary insufficiency.
The effect on the systemic and pulmonary circulation of unsupplemented nitrous oxide in about 30% oxygen, with and without IPPV, was investigated in five cardiac patients and compared with control periods at rest with air breathing. The results of this investigation show that nitrous oxide in conventional oxygen concentration does not cause any great haemodynamic changes. During tracheal intubation, however, significant increases in both systemic and pulmonary blood pressures were registered. However, these pressures reverted to the control values immediately after the tracheal intubation. The results of this study support many earlier clinicaly good experiences obtained when using this conventional nitrous oxide-oxygen mixture in cardiac patients.
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We describe a new form of mechanical pulmonary ventilation, low-frequency positive pressure ventilation with extracorporeal CO2 removal (LEPPV-ECCO2R). In a series of animal studies the rate of mechanical ventilation was 0.66, 1, 2, and 4 min-1 at a tidal volume of 3, 10, and 15 ml kg-1. We were able to maintain normal blood gases and normal lung volumes and lung mechanics even at the lowest ventilator rate with tidal volumes of 10 or 15 ml kg-1. Each experiment lasted 7 hours. Our data suggest a possible new dimension in the management of a difficult patient on mechanical pulmonary ventilation.
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