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R L Johnson

Publications and source records attributed to R L Johnson.

At least 415 records · Page 23Linked to original sources
PubMed1973

Vertical distributions of pulmonary diffusing capacity and capillary blood flow in man.

In six normal upright subjects, a 100 mol bolus-composed of equal parts of neon, carbon monoxide, and acetylene (Ne, CO, and C(2)H(2))-was inspired from either residual volume (RV) or functional residual capacity (FRC) during a slow inspiration from RV to total lung capacity (TLC). After breath holding and subsequent collection of the exhalate, diffusing capacity and pulmonary capillary blood flow per liter of lung volume (D(L)/V(A) and Q(C)/V(A)) were calculated from the rates of CO and C(2)H(2) disappearances relative to Ne. The means: D(L)/V(A) = 5.26 ml/min x mm Hg per liter (bolus at RV), 6.54 ml/min x mm Hg per liter (at FRC); Q(C)/V(A) 0.537 liters/minute per liter (bolus at RV), 0.992 liters/minute per liter (at FRC). Similar maneuvers using Xenon-133 confirmed that, during inspiration, more of the bolus goes to the upper zone if introduced at RV and more to the lower, if at FRC. A lung model has been constructed which describes how D(L)/V(A) and Q(C)/V(A) must be distributed to satisfy the experimental data. According to this model, there is a steep gradient of Q(C)/V(A), increasing from apex to base, similar to that previously determined by other techniques-and also a gradient in the same direction, although not as steep, for D(L)/V(A). This more uniform distribution of D(L)/V(A) compared with Q(C)/V(A) indicates a vertical unevenness of diffusing capacity with respect to blood flow (D(L)/Q(C)). However, the relative degree of vertical unevenness of D(L)/V(A) compared with Q(C)/V(A) can account only in part for previous observations attributed to the inhomogeneity of D(L)/V(A) and Q(C)/V(A). Thus, a more generalized unevennes of these ratios must exist throughout the lung, independent of gravitation.

Acetylene↗
PubMed1973

Health care myths.

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Ambulatory Care↗
PubMed1972

Lymphotoxin formation by lymphocytes and muscle in polymyositis.

Muscle pieces from 11 patients with dermatomyositis or polymyositis were incubated with autologous peripheral blood lymphocytes and the supernates examined for the production of lymphotoxin, a mediator of delayed hypersensitivity, using human fetal muscle monolayers as the target cell. In the case of all 10 active patients, production of lymphotoxin was demonstrated. This mediator was also demonstrated when muscle alone was incubated from two patients with extensive cellular infiltration. Lymphotoxic activity was not found in supernates obtained by incubation of muscle from nine control subjects with their autologous peripheral blood lymphocytes. Addition of methyl prednisolone to active cultures inhibited the action of lymphotoxin on the muscle monolayers. Lymphotoxin was not demonstrated when breast tumor tissue from a patient with dermatomyositis was incubated with autologous lymphocytes. The lymphotoxic agent in the active supernates had similar chromatographic properties to those of a sample of purified lymphotoxin. These findings suggest that muscle injury in polymyositis is a result of a cellular immune response to an antigen present in involved muscle tissue.

Adolescent↗