The effects of acute exercise and increased atmospheric pressure on the hemostatic mechanism and plasma catecholamine levels.

The hemostatic response to acute exercise and increased atmospheric pressure was studied in 20 healthy male subjects (18-35 yr of age) exercised to volitional exhaustion on a cycle ergometer in a hyperbaric chamber at 3 atmospheres absolute (ATA). As a means of comparison, 6 of the 20 subjects were exercised in the same manner at 1 ATA. Similar increases in fibrinolytic activity (FA), Factor VIII activity (VIII:C), von Willebrand factor antigen (vWF:Ag) and plasma catecholamine levels were observed following acute exercise at 1 ATA and at 3 ATA. There were no changes in the levels of plasminogen, antithrombin III, Protein C or Fibrinopeptide A (FPA) with exercise either at 1 ATA or at 3 ATA. In addition, there were no changes in plasma catecholamine levels or any of the hemostatic variables measured when atmospheric pressure was increased from 1 ATA to 3ATA without exercise. These findings demonstrate that increasing atmospheric pressure from 1 ATA to 3 ATA does not alter the exercise-induced changes in hemostasis. Therefore, exercise or physical exertion at 3 ATA for a time period not to exceed 30 min does not perturb the hemostatic mechanism and increase the risk of bleeding or thrombosis.

Induction of minor alloantigen-specific T cell subsets in vivo: recognition of processed antigen by helper but not by cytotoxic T cell precursors.

Primary cytotoxic T lymphocyte (CTL) and helper T (Th) cell responses were generated from regional lymph nodes of heterozygous mice sensitized in the footpad with spleen cells of parental H-2 genotype but differing for multiple minor alloantigens of the B10 background. Cytotoxic and helper responses were read after a short in vitro culture period, which did not influence the restriction specificities of in vivo sensitized T cells. We show that under these conditions, Th cell responses appear unrestricted, whereas CTL responses are restricted to the immunizing parental H-2 genotype. Furthermore, we present evidence that these two functions are mediated by distinct T cell subsets and that the in vivo induction of Lyt-2- Th cells has the appearance of being unrestricted whereas that of Lyt-2+ CTL is restricted by H-2. These findings suggest that in a primary immune response, in vivo precursors of Th cells recognize processed antigen on F1 antigen-presenting cells (clones restricted to each parental H-2 genotype are cross-sensitized) under conditions in which those of CTL only respond directly to foreign minor alloantigens on the injected stimulator cells (clones restricted to parental H-2 genotypes are not cross-immunized). This dichotomy is taken to suggest the possibility that processing of cell membrane-bound antigens is controlled at their association step with products of the major histocompatibility complex.

Lymphocyte activation by Con A.

Con A can activate cytotoxic effector cells, helper cells and suppressor cells. In all cases Con A activates polyclonally and thus the entire T cell repertoir can be revealed by Con A activation. Nylon purified T cells cannot be activated by Con A. however, in the presence of helper cells, such as adherent cells, or in the presence of serum from several species, Con A activates purified T cells. The serum factors that are responsible for Con A activation of purified T cells are present in the albumin fraction. It is suggested that Ia molecules may be responsible for the ability of Con A to activate purified T cells and a general hypothesis for T cell activation is outlined.

Experimental conditions for obtaining suppressor and helper effects on the primary in vitro immune response by lymphocytes activated by polyclonal T-cell activators.

The effect of the polyclonal T-cell activators (PTA) Con A and PHA on the specific immune response to sheep red blood cells (SRC) was studied. Addition of PTA either enhanced or suppressed the anti-SRC response, and two variables were found to affect the results: time of addition of the PTA and the strength of the response in control cultures not given PTA. If the response was high, even suboptimal PTA concentrations induced suppressive effects, but if the control response was low, due to deficient batches of sera or because of the absence of serum, the addition of PTA increased the response or restored it to normal levels. Suppression could be obtained if the PTA were added before or at the same time as the antigen and required high (optimal) PTA concentrations. If addition was delayed for 12-24 h the suppressive effects disappeared and previously suppressive concentrations of the PTA now caused an enhanced response. Analogous results were obtained if preactivated lymphocytes were added to the cultures instead of soluble PTA. Neither Con A, PHA, or lymphocytes preactivated by these PTA suppressed the polyclonal response induced by LPS or PPD. Irrespective of the time of addition and the culture conditions, enhancement of the anti-SRC response occurred at lower PTA concentrations than suppression. It was concluded that suppressor T cells, if they exist, do not act on B cells, but rather on helper cells needed for induction of thymus-dependent responses. The findings in this system are not compatible with the existence of a specific subset of suppressor T cells, but rather with the notion that suppression is caused by too much help.