The volume of N2O absorbed by the lung can be measured during inspiration before the gas is taken up in significant amounts by the capillary blood flow by a plethysmographic technique. If the alveolar fraction of N2O and its solubility coefficient are known, the combined pulmonary tissue and capillary blood volume (Vt+c) can be calculated. Vt+c averaged 517 ml, sd 61 ml, in nine adult males, values in good agreement with those obtained by other methods. The pulmonary tissue volume alone, Vt, in six of these subjects was 438 ml, sd 58 ml. A modification of the technique, using CO2 as the test gas, permitted calculation of the CO2 dissociation slope of the lung tissue. In five subjects, the CO2 dissociation slope of the lung, without the buffering effect of pulmonary capillary blood, over a range of PaCOCO2 from 31 to 55 mm Hg, averaged 0.30 ml CO2 STPD/100 ml lung tissue per mm Hg, or including physically dissolved CO2, 0.38 ml CO2 STPD/100 ml lung tissue per mm Hg. Because Vt is about four times larger than Vc, the lung tissue is of greater importance than the pulmonary capillary blood in buffering fluctuations in alveolar carbon dioxide during respiration. pulmonary tissue volume; pulmonary tissue space for N2O Submitted on August 26, 1963

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Pulmonary function was examined in 19 young asthmatic patients at rest and during two levels of exercise. Findings at rest included decreased flow rates, increased residual volume, normal minute (VE) and alveolar (VA) ventilation, increased ratio of physiological dead space to tidal volume (VD/VT), increased alveolar-arterial oxygen tension difference (A-a Po2), and mild arterial hypoxaemia and desaturation. On exercise there was a normal increase in VE and VA, the VD/VT and the A-a Po2 decreased towards normal, and arterial oxygen tension improved, approaching normal levels. Significant acidosis did not develop.

We have previously shown that the injection of sodium bicarbonate into the pulmonary artery of a dog enclosed in a body plethysmograph results in the evolution of gas in the alveoli which is measurable as an increase in the pressure in the plethysmograph (1). By comparing the time elapsed between injection and gas evolution following injection of a bicarbonate solution with the analogous time interval following injection of an inert gas, ether (2), a value for the over-all rate of the reactions leading to CO2 liberation in the lung can be obtained. Relatively small doses (5 mg per kg) of a carbonic anhydrase inhibitor, acetazolamide, given intravenously, markedly suppressed the evolution of CO2 after bicarbonate injection. This observation suggested to us a method for carrying out experiments to investigate the relationship between the time available and the time required for CO2 equilibration in the lungs. These experiments form the basis of the present report. METHODSFour dogs weighing 16 to 20 kg were used in these experiments. They were anesthetized with pentobarbital sodium in an initial dose of 25 mg per kg; this was usually supplemented by 100 mg about one hour later. A tracheal tube was inserted. A shortened no. 9 cardiac catheter (capacity 0.9 ml) was introduced via the external jugular vein into the pulmonary artery. The dog was then enclosed in a body plethysmograph, and just before the start of the actual experimental period, spontaneous breathing was arrested with appropriate doses of succinylcholine chloride and ventilation was maintained by a Starling pump. The pulmonary artery pres-* Supported by Contract DA-CML-18-108-G-46 with the Army Chemical Corps.tResearch Fellow of the American College of Physicians, 1961-1964. t This work was done during the tenure of an Established Investigatorship of the American Heart Association. sure 1 and the plethysmograph pressure 2 were recorded by using strain gauges and a direct-writing oscillograph.3 The electrocardiogram was monitored continuously. The details of the calibrating and the recording procedure are reported elsewhere (2).After checking the plethysmograph for air tightness and calibrating it, an injection of 0.5 ml of 1: 4 ether in alcohol was made into the pulmonary artery to determine the circulation time from the pulmonary artery to the site of gas exchange (2). This was followed by the injection, in the same manner, of 3 ml of a saturated solution of sodium bicarbonate (approximately 1.2 M at room temperature 200 C). At least duplicate control injections of both ether and bicarbonate were made. An injection of 10 or 20 mg of sodium acetazolamide (Diamox sodium) was then made into the pulmonary artery, and 10 to 12 minutes later duplicate ether and bicarbonate injection records were obtained. The process was then repeated using 10-to 20-mg increments of sodium acetazolamide until a total dose had been reached which markedly suppressed gas evolution.Analysis of records. All the records obtained were analyzed by determining the time taken for ha...

The effects of graded doses of norepinephrine on pulse rate, mean blood pressure, forearm blood flow and vascular resistance were studied in normal human subjects before, during, and after chronic administration of chlorothiazide. This drug prevented the negative chronotropic response normally induced by norepinephrine without altering the pressor response. Before giving and after discontinuing chlorothiazide, increasing doses of norepinephrine were associated with progressive decreases in blood flow. After 1 week of chlorothiazide administration, increasing doses of norepinephrine were associated with increases in flow. The results indicate that chlorothiazide decreases the responsiveness of the forearm vessels of normal subjects to the vasoconstrictor effect of norepinephrine. They suggest that chlorothiazide also may modify the effect of norepinephrine on cardiac output. Submitted on December 9, 1960