A MODEL OF ABSORPTION ATELECTASIS

Reduction in lung volume and alveolar collapse are still of major concern during general anesthesia. Collapse impairs gas exchange and, if it persists, it will cause hypoxemia through shunting. Mechanisms include gas absorption, gas compression, and loss of surfactant activity. Joyce and Williams (p. 1116) have modeled this problem mathematically and found that prior denitrogenation of the lungs by O₂ breathing is the most important factor contributing to the rate of atelectasis development. On the other hand, which inert gas (N₂, very insoluble; N₂O, moderately soluble) is used with O₂ to constitute the breathing mixture during anesthesia has little effect on the rate of alveolar collapse. The effects of prior O₂ breathing are consistent with the well-known role of N₂ retarding collapse because of its very low solubility; the lack of influence of N₂O reflects equilibrium between gas and blood in the collapsing region, such that its high solubility becomes unimportant. This paper is discussed in an Invited Editorial by Hedenstierna (p. 1114).

	NICOTINE AND ENDOTHELIUM-DEPENDENT ARTERIOLAR RESPONSES

The effects of chronic exposure to nicotine on endothelium-dependent arteriolar dilatation of cutaneous tissues was examined by Mayhan and Sharpe (p. 1126). Endothelium-dependent arteriolar dilatation, signaled by acetylcholine and ADP, was found to be decreased by 50% in hamsters treated with nicotine (2 µg · kg¹ · day¹ ip for 2-3 wk). The decreased arteriolar dilatation was not due to changes in the vascular smooth muscle of the arterioles, since responses to nitroglycerine were not altered by chronic nicotine treatment. Superfusion of the cheek pouch with superoxide dismutase restored impaired endothelium-dependent responses in nicotine-treated hamsters. These results suggest that the effects of nicotine on endothelium-dependent function are the result of synthesis/release of oxygen-derived free radicals. The authors suggest that chronic use of tobacco products containing nicotine may contribute to the development of cardiovascular diseases via impairment of endothelium-dependent vascular reactivity due to oxygen radical-mediated mechanisms.

	MIMICKING RESTRICTIVE PULMONARY DISEASE CAUSES DYSPNEA

Harty and colleagues (p. 1142) used extrinsic elastic restriction of the thorax as a model of human restrictive pulmonary disease. Consistent with restrictive disease in patients, the authors report a reduction in lung volume subdivisions and in forced expiratory volume in 1 s. Furthermore, during moderate exercise, this model of thoracic restriction caused a tachypneic alveolar hyperventilation and markedly increased dyspneic sensations. The authors suggest that this model does, indeed, mimic the essential features of restrictive pulmonary disease and may enhance dyspneic sensations because of atelectasis, increased work/effort of breathing, and/or a decrease in volume-related feedback from the lung.

	PULMONARY VASODILATION BY COMBINED NITRIC OXIDE AND PROSTACYCLIN

Vasodilator therapy for pulmonary hypertension has been frustrated by the fact that most effective pulmonary vasodilators delivered intravenously also cause systemic hypotension, limiting their usefulness. One attempt to improve pulmonary vascular targeting has been delivery of vasodilator drugs by inhalation. Prostacyclin (PGI₂) can be delivered as an aerosol for this purpose. Inhaled nitric oxide (NO) has the advantage that its effects are not transmitted to the systemic circulation, because the NO is rapidly inactivated when it reaches the blood. Hill and Pearl (p. 1160) examined the possibility that, since PGI₂ and NO cause vasodilation by different intracellular pathways, their combined effects may be greater than the maximum response produced by either one alone. Using monocrotaline-treated rats as the model of pulmonary hypertension, they found that, indeed, the combined therapy with PGI₂ and NO produced a pulmonary-selective vasodilator effect that was greater than that obtained with either one alone.

	NO EFFECT OF ACUTE EXERCISE ON HIV RNA

Exercise training is a candidate for treatment of patients with human immunodeficiency virus (HIV) because a complication of protease inhibitor treatment is an increase in visceral fat blood lipids. To evaluate the effect of an acute exercise bout on HIV replication in patients with a high viral load, Roubenoff et al. (p. 1197) measured HIV RNA in plasma of 25 patients before, and 5 and 7 days after, a 15-min bout of stepping exercise. No rise in RNA was detected, and the authors concluded that exercise training is safe in people with HIV infection.

	FAT BURNING IN MUSCLES OF DIVING PINNIPEDS

Kanatous and associates (p. 1247) took biopsies from swimming and nonswimming muscles of sedated and anesthetized Steller sea lions, Northern fur seals, and harbor seals. Samples were preserved for electron microscopy and assays of mitochondrial enzymes. Swimming muscles of pinnipeds had relatively high mitochondrial volume densities (6.2-9.7%) that compare to those in athletic terrestrial mammals. However, the citrate synthase and -hydroxyacyl-CoA dehydrogenase activities and the -hydroxyacyl-CoA dehydrogenase-to-citrate synthase ratio per unit mitochondrial volume density were very high. The authors conclude that these adaptations support intramuscular lipid oxidation in swimming muscles during diving.

	SODIUM CYANATE AND MAXIMAL O2 TRANSPORT

There has long been debate on how shifts of the hemoglobin dissociation curve affect exercise. This has been fueled in part by the always opposite effects of such shifts on pulmonary O₂ loading and venous O₂ unloading. Thus increased O₂ affinity, e.g., by cyanate, is well known to increase arterial and venous O₂ saturation due to better loading and worse unloading. McCanse et al. (p. 1257) elegantly show that the net result of this push-pull effect depends on where the organism is positioned on its dissociation curve. When arterial PO₂ is high, on the flat part of the curve, cyanate cannot greatly increase arterial O₂ saturation, so impaired tissue unloading dominates and maximal exercise is compromised. However, when severe hypoxemia is superimposed, the capacity to increase arterial saturation with cyanate is much greater and more than offsets the impairment in unloading, so that maximal exercise is facilitated.

	MATERNAL ETHANOL AND FETAL BREATHING MOVEMENTS

Maternal ethanol ingestion is well known to inhibit fetal breathing movements. PGE₂ has been implicated as a mediator of this response in fetal sheep of >130-day gestation. Watson et al. (p. 1410) examined potential mediators in cortical dialysate samples from slightly younger fetuses (123 days). Dialysate PGE₂ decreased and adenosine increased after ethanol infusion. The increase in adenosine was coincident with decreased fetal breathing movements. The results suggest a role for adenosine, but not for PGE₂, in the ethanol-induced inhibition of fetal breathing movements and low-voltage electrocortical activity in fetal sheep of <130-day gestation.

	ACTIVITY LEVEL, FITNESS, AND BODY FAT IN CHILDREN

Rowlands et al. (p. 1428) examined the relationships among activity level, aerobic fitness, heart rate, and body fat in a group of normal 8- to 10-yr-old children. Activity was determined by a Tritrac-R3D activity monitor or a pedometer worn during a 6-day period. Activity level correlated positively with fitness and negatively with fatness. In contrast, heart rate did not correlate consistently with fitness or fatness and thus has little utility as a measure of activity in this age group.