We have developed a method for quantitatively assessing respiratory control in a group of 10 full-term healthy babies, mean age at test 5 days, by measuring their ventilatory response to added external dead spaces. The dead spaces were equal to 0.5, 1, 2, and 3 anatomic dead spaces (2.2 ml/kg body weight), respectively. Tidal volumes were measured by a nasal mask and a 200-I rigid container. End-tidal CO2 was monitored via a tube in the nostril by a mass spectrometer. Baseline measurements were made during a 10-minute period, after which similar recordings were obtained with each of the dead space tubes. The system was calibrated against a 20-ml syringe. The mean baseline ventilation was 602 ml/minute. On the addition of 0.5, 1, 2, and 3 dead spaces, minute ventilations were increased by 37.5, 74.7, 150.7, and 273.6%, respectively. These increases were due to rises in tidal volume rather than respiratory rate. End-tidal CO2 rose by 1.8 and 4 mmHg on the addition of 2 and 3 dead spaces. When the results were compared with expected minute ventilations--based on the baseline recordings and corrected for the added dead spaces and for changes in anatomic dead space ventilation due to alterations in respiratory rate--the results were within 10% of expected values.

Carbon Dioxide↗

PubMedDate not supplied

Tubuloproteinuria in cancer chemotherapy.

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Albuminuria↗

PubMedDate not supplied

Hypophosphataemia and its consequences in patients following open heart surgery.

Plasma phosphate concentration (Pi), red cell 2,3-diphosphoglycerate (2,3-DPG) and adenosine triphosphate (ATP) concentrations were measured pre-operatively and at intervals after operation for 30 h in twelve patients (nine males and three females, 44--61 years of age), who underwent open heart surgery. All patients received intravenous injections of glucose, insulin and potassium at regular intervals. In all patients studied Pi decreased within hours following operation, remained low for about 6 h and pre-operative values were reached by 18 h. Pi decreased from 1.04 +/- 0.6 mmol/litre (mean +/- s.e. mean) to 0.32 +/- 0.06 mmol/litre. This fall in Pi was accompanied by a small but significant fall in 2,3-DPG (from 14.8 +/- 0.60 mumol/g Hb to 11.2 +/- 0.60 mumol/g Hb). ATP concentration did not change significantly. The calculated P50 (partial pressure of oxygen at which there was 50% saturation of haemoglobin) decreased by 1.2 mmHg. The regular fall in Pi which is probably due to the glucose-insulin-potassium injections was of short duration and had very little effect on red cell 2,3-DPG and ATP.

Adenosine Triphosphate↗

PubMedDate not supplied

Changes in body weight and body protein with intravenous nutrition.

Body weight, protein, fat and water were measured before and after intravenous nutrition in 20 surgical patients. The group included both young and old patients who were suffering from a wide variety of catabolic illnesses and the period of intravenous feeding ranged from 11 to 40 days. Eight of the patients were able to take small amounts of food orally. During the period of intravenous nutrition ten patients gained significant weight although only two of these gained significant protein. Most of the weight gain was due to an increase of water. There was also a gain of water in the patients who lost weight; this water gain occurred in small daily increments over the course of treatment. It is concluded that weight gain can occur without protein gain in patients who are being fed intravenously and that body weight is not a reliable guide to changes in body protein or fat in critically ill patients receiving intravenous nutrition.

Adult↗

PubMedDate not supplied

Increased urinary beta 2-microglobulin after cancer chemotherapy.

The serum and urinary concentrations of beta 2-microglobulin (beta 2-m) and creatinine and the urinary concentration of albumin and IgG were measured in 14 patients with hematologic malignancies before and during chemotherapy. There was a transient increase in urinary beta 2-m in nine of the 14 patients during chemotherapy. All of the nine patients but only one of the other five patients had had recent multiple chemotherapy. The urinary beta 2-m increased in 24 courses of chemotherapy given to these nine patients and was already abnormal before 13 of these courses. The increase in urinary beta 2-m was not associated with an increase in serum beta 2-m or a significant increase in urinary albumin or IgG excretion. These results suggest that chemotherapy causes a marked transient tubular proteinuria, particularly in patients who have had previous chemotherapy.

Adolescent↗