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The resting ventilation of awake rats, developing metabolic alkalosis as a result of sustained dietary potassium (K) restriction, was compared to that of age-matched controls. Extending the measurements over 17 weeks and using adult rats indicated, as soon as the third week, a significant progressive fall in the minute ventilation of low K rats, which previous studies limited to a single time determination did not consistently ascertain. The ventilatory adaptation observed in all groups, as well as the superimposed respiratory compensation to metabolic alkalosis in low K rats, resulted only from frequency changes. In both groups, the duration of inspiration was inversely correlated with the age of the animals. The duration of expiration was stable in controls but increased significantly with time in low K rats. According to these data, the respiratory compensation to K-depletion alkalosis in the rat is achieved only through an adjustment in the timing component of the control of breathing.

Respiratory frequency (f), tidal volume (VT) and minute ventilation (VE) were measured in restrained awake rats using a volumetric body plethysmograph excluding the head. An arterial catheter was then implanted and ventilatory measurements performed again two or three days later. Arterial blood gases and acid-base status were measured before entry in the plethysmograph (control values) and after, accompanying each ventilatory measurement. The pattern of ventilation (VT and VE) was significantly correlated with the respiratory status, particularly with PaCO2 (P less than 0.001). A ventilatory (VE, VT, f) and respiratory (PaO2, PaCO2, pH) steady state was obtained from the fifteenth minute to the end of the observation period. The present preparation is a stable experimental model providing respiratory and ventilatory data in the awake rat.

We studied the time course of the respiratory events in awake guinea-pigs catheterized with a chronic arterial cannula, exposed to 100% O2 during 48 hr and after air return breathing. 2. The oxygen toxicity has a pulmonary and respiratory expression: clinical, histological and biochemical data show that death is related to the asphyxia generated by acute pulmonary edema. 3. The O2 toxicity respiratory effects show striking differences in rats and guinea-pigs; the differences belong to a specific and particular lymphatic system in the rat. 4. Rat and guinea pig offer two different models of pulmonary edema, (the first is characterized by absence of arterial hypoxemia) and in consequence two different models of lung oxygen toxicity.

We compared left lateral thoracotomy and sternotomy in rats which were mechanically ventilated for at least 1 h in order to perfect the technique and the surveillance of thoracic opening. Lateral thoracotomy proved to be superior to sternotomy as it was associated with a lower mortality within the first 24 h (20% compared with 50%; p less than 0.05). Lateral thoracotomy causes a smaller reduction in mean blood pressure (104 +/- 11 vs. 71 +/- 7 mm Hg; mean +/- SD; p less than 0.05). Furthermore, following lateral thoracotomy, the rats had a higher postoperative PaO2 (77 +/- 16 vs. 72 +/- 7 Torr) and a lower PaCO2 (29.5 +/- 1.5 vs. 35 +/- 4.3 Torr), although these differences were not statistically significant.

1. 288 arterial blood samples were obtained at successive times, through indwelling catheters, from conscious rats subjected to selective dietary potassium restriction for up to 5 weeks. 2. In control rats with unrestricted access to potassium [HCO-3]a = 25.4 mmol/l, pHa = 7.47, PaCO2 = 34 mmHg, PaO2 = 94 mmHg and [K+]a = 4.3 mmol/l were steady and within the range of values reported in conscious rats. Five weeks of isolated potassium restriction resulted in significant hypokalaemia ([K+]a = 2.15 mmol/l) and metabolic alkalosis ([HCO-3]a = 34.1 mmol/1, pH 7.57). This alkalosis, due mostly to H+ transfer into cells, was accompanied by a significant increase in PaCO2 to 36.4 mmHg and decrease in PaO2 to 88 mmHg, contrary to previous reports in man and dog. The administration of neutral sodium phosphate in addition to potassium restriction enhanced both the alkalosis ([HCO-3]a = 42.3 mmol/l, pH 7.61) and its respiratory compensation (PaCO2 = 40.8, PaO2 = 82 mmHg), without altering the PaCO2: [HCO-3]a relationship. 3. The opposite variations of PaCO2 and PaO2 were significantly correlated to the increase in plasma bicarbonate concentration and described best by crossed sigmoid curves. The equations of both curves were calculated; their point of inflection occurred at the same bicarbonate concentration (36 mmol/l). The maximum intensity of respiratory compensation (0.62 mmHg PaCO2 for each mmol [HCO-3]a/l) observed at this point fell within the range of values yielded by previous estimations.

Pneumocystis carinii (P.c.) pneumonia was induced in 40 rats by a prolonged corticosteroid treatment (group 1); 40 healthy rats of equal weight constituted the control group (group 2); 9 rats received the same corticosteroid treatment as group 1, together with trimethoprim-sulfamethoxazole (TMP-SFZ) in order to prevent P.c. multiplication (group 3). We could distinguish the respiratory effects induced by corticosteroids from those caused by P.c. pneumonia (group 3 vs group 1). For six weeks the blood leukocyte count, the weight of the spleen and the thymus and the pulmonary status were monitored. Blood gases and acid-base status were measured in conscious rats. There was no pulmonary oedema. The infected P.c. rats had a low PaCO2 and a slight disturbance of blood oxygenation, exemplified by A-aDO2 of 30 mmHg, compared with 17.5 mmHg in control rats and 17 mmHg in TMP-SFZ treated rats. P.c. infected rats had a lymphocyte depletion induced by corticosteroids. They did not exhibit respiratory distress. P.c. pneumonia alone in rats did not cause frank hypoxemia.