Beta H2 Research Articles

Effects of experimental rhinovirus 16 infection on airways and leukocyte function in normal subjects

We infected 7 normal volunteers with rhinovirus 16. In general, the symptoms and alterations in airways were minimal although all subjects had upper respiratory symptoms. Three subjects developed in addition lower respiratory and systemic symptoms accompanied by either an increase in the volume of isoflow or a positive methacholine response. Furthermore, these three had a decrease in beta adrenergic and Hz histamine receptor responses of their granulocytes. Since the peripheral airway obstruction and decreased beta adrenergic and H2 histamine responses occurred together, these two phenomenon may have a common cause. All seven subjects had a decrease in number of circulating E rosette forming lymphocytes, and in 6 of 7, there was a decrease in the antibody-dependent cellular cytotoxicity capacity of mononuclear cell preparations. It is not clear whether these changes reflect redistribution of mononuclear cells or alteration of their function.

Rate constants associated with changes in sodium conductance in axons perfused with sodium fluoride.

1. Membrane currents during step depolarizations were measured in axons which were perfused with 300 mM-NaF and placed in K-free artificial sea-water, -0.3-4 degrees C. The Na conductance was fitted by the modified Hodgkin-Huxley model, g(Na) = g(Na)m(3)(h(1) + h(2)). Changes in h(1) and h(2) were assumed to follow [Formula: see text] where x represents the inactive state.2. The rate constants and steady-state values for m were in agreement with the Hodgkin-Huxley equations except that the experimental relationship of m(infinity) (3) against V was shifted 10-15 mV in the negative direction. This discrepancy, which was not found in an experiment with choline sea-water, can be explained on the basis of a resistance in series with the membrane between the voltage measuring electrodes.3. At 0 degrees C the rate constants (in msec(-1)) associated with changes in h(1) and h(2) were fitted using the following equations: beta(h1) = 0.5/{exp [- (V + 32)/10] + D(1)exp (- V/V(1))}, alpha(h2) = pexp (V/V(2)), beta(h2) = pexp (V/V(2) - V/23.5) + pD(2), with the condition that at 0 mV, (alpha(h2) + beta(h2)) = p(D(2) + 2) = 0.55 msec(-1). The experiments gave average values D(1) = 3.6, V(1) = 240 mV, p = 0.08 msec(-1) and V(2) = 70 mV. The average value of g(Na) was 66 mmho/cm(2).4. At negative voltages where m(infinity) (3) against V is steep, the points for beta(h1) and alpha(h2)/beta(h2) from axons in Na sea-water were not fitted well by the above equations whereas data from an axon in choline sea-water were. These discrepancies can be explained on the basis of a series resistance.5. Measurements made at 16-17 degrees C indicated that g(Na) has a Q(10) of 1.6, tau(m) (-1) a Q(10) of 2.8 and beta(h1) a Q(10) of 3.5. The ratio alpha(h2)/beta(h2) was decreased relative to the value at 0 degrees C and could be fitted by using Q(10) = 0.6.6. Measurements made with 250 mM-NaF + 50 mM-KF inside gave rate constants which were very similar to those obtained with 300 mM-NaF. Perfusion with 300 mM-KF appeared to double the value of beta(h1), relative to that obtained with 300 mM-NaF, and to reduce alpha(h2)/beta(h2) by about half.7. The voltage dependence of alpha(h2) makes it likely that following depolarization recovery from the inactive state x occurs via x --> h(1) rather than x --> h(2) --> h(1).