Bronchiectasis may be more common in patients with alpha 1-antitrypsin deficiency than has been previously recognized. The diagnosis of alpha 1-antitrypsin deficiency should be considered in patients with emphysema and diffuse cystic bronchiectasis.

The present investigation was designed to determine the rate of development of tolerance during initiation of therapy with oral ISDN and the rate of tolerance reversal after withdrawal of this drug. MethodsStudy population. Ten patients, nine men and one woman, ranging in age from 37 to 77 years (mean 56), with stable, exercise-induced angina pectoris were studied. Patients who had had previous exposure to ISDN or other oral or cutaneous nitrate preparations were not included. These patients had been taking nitroglycerin, but this was not used in the 24 hr before study and was not required in any patient during this period of investigation. Other exclusion characteristics included the presence of cardiomegaly, cardiac failure, cerebral vascular disease, hepatic disease, renal dysfunction, or the administration of fl-blocking agents or vasodilators. Patients were also excluded if they had a history of severe headaches or symptoms of postural hypotension after nitroglycerin administration.Study design Day 1. After an overnight fast, control measurements were made of heart rate and blood pressure with patients in the supine and standing positions, and a 5 ml sample of venous CIRCULATION Downloaded from http://ahajournals.org by on

Reasons for an increase in maximal O2 consumption (VO2max) following blood reinfusion remain unclear; thus the present investigation was undertaken to examine the arterial and femoral venous blood gases during submaximal and maximal exercise. Four untrained males (22-25 yr) performed modified Balke work capacity tests under control conditions (Hct = 42.4 +/- 0.8%; Hb = 14.7 +/- 0.5 g X 100 ml-1) and following autologous blood reinfusion (Hct = 46.2 +/- 1.3%; Hb = 16.4 +/- 0.9 g X 100 ml-1). VO2 was determined by open-circuit spirometry and cardiac output by the N2O method; radial arterial and deep femoral venous blood were sampled at each work load throughout the incremental work tests. Following blood reinfusion, subjects' VO2max increased (P less than 0.05) from 4.0 (in control) to 4.5 1 X min-1. Throughout submaximal exercise arterial PO2 remained relatively constant (between 80.1 +/- 4.4 and 89.1 +/- 5.0 Torr) and cardiac output unchanged, comparing the two experimental conditions. Femoral venous PO2 values were almost identical throughout the work capacity tests, declining at exhaustion to 15.7 +/- 1.5 Torr in control and to 13.8 +/- 3.3 Torr postreinfusion. It appeared that the subjects' increase in VO2max postreinfusion was due to an increased O2 supplied to the tissue [i.e., cardiac output (Q) X arterial O2 content (CaO2)] by the central circulation. This resulted from a small (10%) increase in Q and a constant elevation in CaO2 of 1.7-2.2 ml X 100 ml-1, since virtually no changes were observed in the femoral venous blood postreinfusion and the acid-base status and temperature, important determinant of O2 dissociation, were (almost) identical, comparing the two experimental conditions.

Adenosine increases heart rate and sympathetic nerve activity reflexively in conscious humans through several mechanisms. The purpose of this study was to assess the relative contributions of arterial baroreceptor unloading, carotid chemoreceptor stimulation, and other adenosine-sensitive afferent nerves to these responses. In 12 healthy men, the effect on blood pressure, heart rate (HR), and muscle sympathetic nerve activity (MSNA; peroneal nerve) of lower body negative pressure (LBNP; -15 mmHg (1 mmHg =133.3 Pa)) was compared with the effect of intravenous adenosine (35, 70, and 140 |ag*kg"1*min_1). In eight subjects, the highest dose was reinfused during 100% oxygen to suppress arterial chemoreceptors. Blood pressure reductions during LBNP and adenosine (140 jxg-kg'^min"1) were similar. HR did not change significantly during LBNP (+2 ± 2 beats/min; mean ± SE) but increased at the highest adenosine dose (+25 ± 3 beats/min; p < 0.05). MSNA increased significantly (p < 0.05) during both interventions (+255 ± 82 and +247 ± 5 8 units/100 beats for adenosine and LBNP, respectively), and there was no difference in the MSNA response to these two stimuli (p > 0.1). Oxygen inhibited adenosine-induced increases in HR and MSNA (from +305 ± 99 to +198 ± 75 units/100 beats and from +26 ± 4 to +18 ± 3 beats/min;p < 0.05 for both comparisons). The MSNA response to these combined stimuli was similar to that observed during LBNP. In contrast, the residual HR response (+18 ± 3 beats/min) was significantly greater than the response to LBNP (+2 ± 2 beats/min; p < 0.05). These data indicate that arterial baroreceptor unloading cannot account for the marked adenosine-induced increase in HR, but may be sufficient to explain its effect on MSNA. The effect of 100% oxygen confirms that stimulation of carotid chemoreceptors accounts for approximately one-third of the HR and MSNA response to adenosine. However, other mechanisms, such as stimulation of adenosine-sensitive afferent nerves in other vascular beds, are involved in the HR and possibly the MSNA response.Key words: adenosine, human, heart rate, sympathetic nervous system, baroreflex.Résumé : L 'adénosine augmente la fréquence cardiaque et l'activité nerveuse sympathique de manière réflexe chez les humains conscients et ce, par 1*intermédiaire de divers mécanismes. Le but de la présente étude a été d'évaluer l'influence sur ces réponses d'une décharge des barorécepteurs artériels, d'une stimulation des chémorécepteurs carotidiens, ainsi que d'autres nerfs afférents sensibles à Padénosine. Chez 12 hommes sains, on a comparé l'effet d 'une pression négative des membres inférieurs (PNMI; -15 mmHg (1 mmHg = 133,3 Pa)) avec celui de Padénosine intraveineuse (35, 70 et 140 jig-kg^-m ür1) sur la pression artérielle, la fréquence cardiaque (FC) et l'activité nerveuse sympathique musculaire (ANSM; nerf périonnier). Chez huit sujets, on a réinjecté la plus forte dose d'adénosine en présence de 100% d'oxygène afin de supprimer les chémorécepteurs artériels. Les réductions de press...

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