A ROLE FOR GLIA IN CENTRAL CHEMORECEPTION?

Glia control the ion concentrations and pH of brain extracellular fluid. The function of glia in chemosensitive brain stem regions may be of particular importance. Erlichman et al. (p. 1599) have used a diffusion-pipette system to administer a glial toxin, fluorocitrate, in the retrotrapezoid nucleus, a known site of central respiratory chemoreception. Administration of the toxin caused prompt tissue acidification and concomitant increases in respiratory output, both of which were reversed when the administration ceased. Morphological examination revealed small cells stained with a marker of increased cell permeability. The results indicate that a reversible disruption of glial function in the retrotrapezoid nucleus causes local acidification and, via central chemoreception, an increase in respiratory output. The paper is discussed in an Invited Editorial by Forster (p. 1597).

	MECHANICAL DISTENSION OF CUTANEOUS BLOOD VESSELS SPEEDS HEAT UPTAKE

Peripheral vasoconstriction decreases thermal conductance. Grahn et al. (p. 1643) hypothesized that an increase in blood flow to the skin of a hypothermic individual would enhance transfer of exogenous heat to the core, thereby increasing the rate of rewarming. Outer ear canal temperature was monitored in hypothermic subjects during recovery from general anesthesia. Heat was applied to a single forearm and hand placed at subatmospheric pressure (30 to 40 mmHg) to distend the blood vessels. Heat alone was applied to controls. The application of subatmospheric pressure increased the rate of rewarming 10-fold.

	INTEGRATED RESPONSES TO ENDOTHELIN-1 INFUSION AND CYCLOOXYGENASE INHIBITION

Endothelin-1 (ET-1) is a vasoconstrictor peptide of endothelial origin. Its effects in vivo appear to be blunted by the action of prostacyclin, a vasodilator produced in the endothelium by the action of cyclooxygenase (COx). Ahlborg and Lundberg (p. 1661) have examined the effects of COx inhibition on hemodynamic variables and their responses to ET-1 infusion in healthy human subjects. ET-1 infusion alone decreased cardiac output and splanchnic and renal blood flows and produced a moderate increase in arterial pressure. COx inhibition had similar effects and potentiated the decrease in renal blood flow induced by subsequent ET-1 infusion. The authors conclude that COx inhibition causes renal and splanchnic vasoconstriction and selectively increases the sensitivity of the renal vascular bed to ET-1.

	O2 MAX AND ACE GENOTYPES

Several angiotensin-converting enzyme (ACE) genotypes have been identified in human subjects and correlated with various cardiovascular functions and outcomes. Hagberg et al. (p. 1842) examined ACE genotype and maximal oxygen consumption (O_{2 max}) in postmenopausal women with a wide range of habitual physical activity levels. Age, body composition, and habitual activity did not differ among ACE genotype groups. After statistical adjustment for the influence of habitual activity, ACE genotype appeared to account for 12% of the variation in O_{2 max} among subjects. This influence was entirely attributable to variation in maximal arteriovenous oxygen content difference: ACE genotype did not affect maximal cardiac output. The findings suggest that the effects of ACE genotype on cardiovascular disease risk may be linked to its influence on O_{2 max}.

	DEVELOPMENT OF MUSCLE CAPILLARIES IN HIGH-ALTITUDE BIRDS

Hepple et al. (p. 1871) have investigated leg muscle capillarization in the high-altitude finch. As previously reported for pectoralis flight muscle, the researchers found that the less aerobic thigh muscle also had an increased capillary-to-fiber ratio, which had increased in proportion to a greater mitochondrial volume per unit fiber length in high-altitude compared to sea-level birds. How does hypoxia stimulate muscle capillary proliferation? The authors suggest that the major stimulus is the proportion of the available muscle aerobic capacity utilized, rather than the absolute energy expenditure, and that the capillary-to-fiber ratio is reorganized in hypoxia to match the muscle fiber mitochondrial volume.

	COCAINE AND THE SPLEEN

Cocaine, a potent vasoconstrictor, has been shown to alter the hemoglobin concentration, hematocrit, and red blood cell count in humans and animals. Kaufman et al. (p. 1877) have examined the question of whether cocaine administration induces splenic contraction in humans and, if so, whether changes in spleen volume correlate temporally with hematologic changes. Five healthy men reporting occasional cocaine use were studied. Spleen volume was assessed with magnetic resonance imaging at baseline and after intravenous cocaine administration. Spleen volume decreased by 20% 10 min after cocaine administration and returned to baseline within 35 min. Cocaine increased hemoglobin concentration, hematocrit, and red blood cell count but did not alter white blood cell or platelet count. The findings are consistent with the hypothesis that cocaine induces splenic contraction and consequent "endogenous transfusion" of splenic erythrocytes into the general circulation.

	PERIODIC BREATHING INDUCED BY VENTILATORY ASSISTANCE

Periodic breathing occurs during rapid-eye-movement sleep and conditions of ambient hypoxia, when feedback from peripheral chemoreceptors causes intermittent hypocapnia and central apnea. Meza et al. (p. 1929) used pressure support and ventilatory assistance in normal subjects during sleep to test the hypothesis that increases in the gain of the control system will produce periodic breathing. Pressure support ventilation produced periodic breathing in 11 of 12 subjects, with apneic thresholds 1.5-5.8 Torr below eupneic values. Proportional assist ventilation caused periodic breathing in 5 of 12 subjects. The results show that increases in gain of the respiratory control system by mechanical ventilatory assist produce periodic breathing when an apneic threshhold is reached, but the inherent susceptibility to such instability varies considerably among normal individuals.

	CARDIOVASCULAR REGULATION IN HYPERGRAVITY AND MICROGRAVITY

Schlegel et al. (p. 1957) investigated the cardiovascular responses of humans to the acute gravitational changes of parabolic flight. Measurements were done while the subjects were seated at rest and while they performed Valsalva maneuvers. Mean arterial pressure responses to Valsalva phases II_l, III, and IV were accentuated in hypergravity relative to microgravity, but the accentuations differed qualitatively and quantitatively from those induced by a supine to seated postural change at 1 G. These results suggest that arterial baroreflex control of vascular resistance may be altered by input from receptors in the cardiopulmonary region as well as by those in the vestibular apparatus.