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Ten healthy unanaesthetized full-term lambs, aged 4-12 days, were studied during moderate radiant heat stress, and 21 full-term newborn infants were studied during moderate convective heat stress. The rate of breathing and the breathing pattern were recorded, using strain gauges made of mercury-filled rubber tubing placed around the thorax and abdomen. In both the lambs and the infants the respiratory rate increased during heat stress. When this increase began, both the lambs and infants had short periods of very rapid breathing followed by short apnoeas. The concentrations of carbon dioxide and water in a flow-through system collecting expired air increased during the short periods of rapid breathing and then decreased again during the subsequent short apnoeic period.

The temperature of inspired air influences respiratory water loss (RWL) in young lambs. Water loss from the airways, oxygen consumption and carbon dioxide production were measured using an open flow-through system with a mass spectrometer, specially equipped with a water channel, for gas analysis. Measurements were made in 9 newborn lambs at 3 different inspired air temperatures keeping all other environmental factors stable, including the ambient air temperature. The water content of the inspired air was also kept constant. RWL was found to be 9.9 +/- 3.9 (SD) mg/kg/min when the temperature of the inspired air was 30 degrees C and its humidity 30%. At 40 degrees C this loss increased to 11.5 +/- 3.6 mg/kg/min, and at about 60 degrees C it increased further to 26.0 +/- 8.2 mg/kg/min. The oxygen consumption was 10.0 +/- 0.8 (SD) ml/kg/min at 30 degrees C and 10.4 +/- 2.0 ml/kg/min at 60 degrees C, a change which is not significant. Thus RWL is influenced by the temperature of the inspired air, with greater loss at higher temperatures.

A study was made to determine whether adenosine is involved in the regulation of breathing and whether the respiratory response to injections of adenosine and its analogue L-PIA (phenylisopropyl adenosine) is modified by moderate hypoxemia or by heat stress. Unanesthetized lambs with chronically implanted catheters were used for the investigation. Intravenous injections of adenosine caused an increase in the rate of breathing lasting for 5-30 s, except during heat stress, when the rate of breathing decreased. Injection of L-PIA also increased the rate of breathing, but the effects lasted longer than after injection of adenosine. During heat stress the response to injection of L-PIA varied. Both the arterial blood pressure and heart rate decreased transiently after intravenous injection of adenosine or L-PIA, while the central venous pressure increased. Adenosine might thus be part of a positive feedback system that stimulates breathing under normal environmental conditions with or without moderate hypoxemia. The respiratory responses to injection of adenosine during heat stress are different, which might indicate that under this condition the effects of adenosine on breathing are modified by its influence on temperature control.

To investigate how continuous positive airway pressure (CPAP) changes the vagal nerve activity and whether CPAP alters the efferent phrenic nerve activity or the breathing pattern similarly before and after vagotomy, a study was made of vagal and phrenic nerve activity in chloralose-anaesthetized cats. In the vagal nerve, CPAP increased the mean impulse frequency during expiratory rest. The breath-related impulse frequency also increased with CPAP. With higher CPAP (greater than or equal to 0.5 kPa), the peak of breath-induced activity in the vagal nerve lasted longer than inspiration. In the phrenic nerve, the impulse frequency in the bursts increased almost linearly with CPAP irrespective of whether the vagal nerves were intact or not. The duration of the phrenic nerve bursts decreased with increasing CPAP when the vagal nerves were intact. When the vagal nerves were cut, the burst duration did not change. The rate of breathing was almost unchanged by CPAP regardless of whether the vagal nerves were cut or not. The inspiration/expiration ratio decreased with increasing CPAP when the vagal nerves were intact, but not when they were cut.

A study was made to determine whether the ventilatory pattern, in terms of ventilatory frequency, insufflation period and end-expiratory pressure, influences the arterial blood gas level at which central inspiratory activity is inhibited, and whether further expansion of the lung changes this activity. This was accomplished by measuring arterial pH and blood gases, and intratracheal, intrapleural and transpulmonary pressures, at the setting of positive-pressure ventilation causing inhibition of phrenic nerve activity in chloralose-anaesthetized cats. Spontaneous breathing movements were prevented by muscle relaxation. Ventilatory frequencies of 15-120 breaths per minute (b.p.m.) were studied at at least two different insufflation times. A volume-controlled ventilator with a large compressible volume was used in the frequency range 15-45 b.p.m. and a constant flow respirator with a low-compressible volume in the range 45-120 b.p.m. A much lower PCO2 was needed for phrenic nerve activity to be inhibited at a ventilatory frequency of 15 b.p.m. than at higher frequencies. At ventilatory frequencies between 30 and 120 b.p.m. inhibition could be achieved at a higher PCO2, within the normal range. The inhibition of phrenic nerve activity tended to be less stable when PEEP was added during ventilation with a long insufflation period, but PEEP did not influence the arterial blood gas level at which inhibition occurred. In the lower frequency range of 15-30 b.p.m., inspiratory activity was observed with bursts at the same rate as the insufflations given by the ventilator. The intratracheal peak pressures at ventilation causing inhibition of phrenic nerve activity decreased with increasing ventilatory frequencies.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of intra-arterial and intravenous injections of adenosine and hypoxanthine were investigated with special reference to respiratory variables in anesthetized young cats. Studies were made of the effects on inspiratory activity (phrenic nerve activity), heart rate, blood pressure and central venous pressure. To assess the risk of accumulation of adenosine degeneration products after several injections measurements were also made of hypoxanthine, xanthine and urate in plasma at intervals after the injections. It was found that intra-arterial and intravenous injections of adenosine increased central inspiratory activity during the first few breaths after the injection. The blood pressure and heart rate decreased slightly and central venous pressure increased slightly after the injection. Degradation of adenosine and its metabolites takes place rapidly and it is therefore unlikely that metabolites influence the results. It is concluded that adenosine causes brief stimulation of inspiratory activity.