Montmorillonite-aminocaproic acid complexes (monomer complexes) were prepared by the intercalation of 6-aminocaproic acid to various homoionic (Na+, Ca2+, Mg2+, Co2+, and Cu2+) montmorillonites. Infrared spectra of the monomer complexes indicated that the interaction between the exchangeable cations and the 6-aminocaproic acid increased in the following order: Na-, Ca-, and Mg- < Co- < Cu-montmorillonite-aminocaproic acid complex. Montmorillonite-nylon complexes (polymer complexes) were prepared by thermal treatment of the monomer complexes, which was confirmed by X-ray powder diffraction and infrared spectroscopy the results of which indicated the condensation of 6-aminocaproic acid in the interlayer space.

Thermal degradation of montmorillonite-nylon complexes was studied by thermogravimetry. It was found that the thermal stability of the polymer complexes increased in the following order: Cu- < Co- < Na- < Mg- < Ca-montmorillonite-nylon complex.

It was suggested that the difference in thermal stability depended upon the length of the polymer chain which might be influenced by the interaction between the exchangeable cations and the 6-aminocaproic acid. The activation energy for the thermal degradation of each montmorillonite-nylon complex was obtained, and the value for Cu-montmorillonite-nylon complex was smaller than that for the other cation-exchanged montmorillonite-nylon complexes.

Aminocaproic acid (ACA) and Premarin® (PRE) are used to treat exercise-induced pulmonary haemorrhage (EIPH) at the racetrack based upon their putative coagulation effects. We hypothesized that neither ACA nor PRE would reduce EIPH because the literature does not substantiate coagulation deficits being manifested in EIPH. Six Thoroughbreds were run from 4 m s− 1 until fatigue (1 m s− 1s × 1 min increments; 6° inclined treadmill) after being treated with placebo, PRE (25 mg) or ACA (5 g) at 2-week intervals in a randomized crossover design. Coagulation and exercise-related variables were measured at rest and maximal effort. EIPH and inflammation were quantified via bronchoalveolar lavage fluid (BALF) 30–60 min post-exercise. EIPH was not altered by either treatment (3.8 ± 1.7 (placebo), 4.6 ± 3.2 (ACA) and 2.4 ± 1.2 (PRE) × 106 RBC ml− 1 BALF; p = 0.12), nor was coagulation. However, inflammation was decreased (5.9 ± 0.9 (placebo), 4.4 ± 0.9 (ACA) and 4.2 ± 0.4 (PRE) × 105 WBC ml− 1 BALF; both p < 0.05). There was a trend for decreased time-to-fatigue (720 ± 27 (placebo), 709 ± 24 (ACA) and 726 ± 28 (PRE) s; p = 0.09 for placebo vs. ACA) and a reduction in plasma lactate (19.5 ± 3.0 (placebo), 14.7 ± 1.0 (ACA) and 17.6 ± 2.5 (PRE) mmol l− 1; p < 0.05 for placebo vs. ACA) following ACA administration. ACA and PRE were not effective in reducing EIPH, and ACA may be detrimental to performance. However, both may mitigate exercise-induced pulmonary inflammation.