Adenosine is an endogenous nucleoside which stimulates respiration in man and other mammals. In animals adenosine appears to initiate respiratory stimulation within the carotid body, but whether this is the site of action in man is not known. We administered adenosine by intra-aortic infusion to 12 subjects undergoing cardiac catheterisation. When adenosine was infused at three sites proximal to the carotid circulation, minute ventilation was significantly higher than baseline values or those during adenosine infusion at a more distal site. These results support the hypothesis that adenosine-induced respiratory stimulation in man is mediated in the carotid body.

Ò) in the management of pulmonary haemorrhage secondary to Aspergillus infection in a patient with leukaemia and acquired FVII de®ciency. British Journal of Haematology, 106, 254± 255.

Rapid bacterial detection and viability measurements have been greatly enhanced by recent advances in the use of fluorescent stains in cytometry. It has previously been shown that four physiological states can be distinguished : reproductively viable, metabolically active, intact and permeabilized. Previous sorting experiments have shown that not all intact cells readily grow, but some intact cells can grow even when they fail to show metabolic activity, as determined by esterase turnover. To circumvent the limitations imposed by active dye extrusion or cell dormancy on viability measurements used to date (e.g. enzyme activity or cell polarization), a fast triple fluorochrome staining procedure has been developed that takes account of these problems. This allows further cellular characterization of intact cells by : active exclusion of ethidium bromide (EB) (metabolically active cells), uptake of EB but exclusion of bis‐oxonol (BOX) (de‐energized but with a polarized cell membrane) and uptake of both dyes (depolarized). Permeabilized cells were identified by propidium iodide (PI) uptake. The method was validated using an electronically programmable single cell sorter (EPICS Elite®) and aged Salmonella typhimurium cells. Reproductive viability was determined by sorting single cells to their staining pattern directly onto agar plates. Most polarized cells could be recovered as well as a significant fraction of the depolarized cells, demonstrating that depolarization is a sensitive measure of cell damage but a poor indicator of cell death.

To determine whether intense exercise training affects exercise-induced vasodilatation, six subjects underwent 4 weeks of handgrip training at 70% of maximal voluntary contraction. Exercise forearm vascular conductance (FVC) responses to an endothelium-dependent vasodilator (acetylcholine, ACH; 15, 30, 60 micrograms min-1) and an endothelium-independent vasodilator (sodium nitroprusside, SNP; 1.6, 3.2, 6.4 micrograms min-1) and FVC after 10 min of forearm ischaemia were determined before and after training. Training elicited significant (P < 0.001) increases in grip strength (43.4 +/- 2.3 vs. 64.1 +/- 3.5 kg, before vs. after, mean +/- SEM), forearm circumference (26.7 +/- 0.4 vs. 27.9 +/- 0.4 cm) and maximal FVC (0.4630 +/- 0.0387 vs. 0.6258 +/- 0.0389 units, P < 0.05). Resting FVC did not change significantly with training (0.0723 +/- 0.0162 vs. 0.0985 +/- 0.0171 units, P > 0.4), but exercise FVC increased (0.1330 +/- 0.0190 vs. 0.2534 +/- 0.0387 units, P < 0.05). Before and after the training, ACH increased exercise FVC above the control (no drug) exercise FVC, whereas SNP did not. Training increased (P < 0.05) the exercise FVC responses to ACH (0.3344 +/- 0.1208 vs. 0.4303 +/- 0.0858 units, before vs. after training, 60 micrograms min-1) and SNP (0.2066 +/- 0.0849 vs. 0.3172 +/- 0.0628 units, 6.4 micrograms min-1). However, these increases were due to the increase in control (no drug) exercise FVC, as the drug-associated increase in exercise FVC above control did not differ between trials (P > 0.6). These results suggest that exercise FVC is increased by both exercise training and stimulating the release of endothelium-dependent vasodilators. However, training does not affect the vascular response to these vasodilators.