A single case report of healing through specific martial art therapy: comparison of MRI to clinical resolution in severe cervical stenosis: a case report.

OBJECTIVES: A 76-year-old patient with chronic and severe spinal cord compression secondary to cervical stenosis, a cervical osteophyte, and a herniated intervertebral cervical disk had lasting resolution of symptoms after completing a specific, martial art-based, physical therapy program. We wanted to determine if there were structural changes in the cervical spine that could account for the prompt resolution of symptoms. DESIGN: A 76-year-old female completed 8 weeks of a specific, martial art-based, physical therapy. The pretherapy and posttherapy cervical magnetic resonance images (MRIs) were compared. A follow-up evaluation was done at 1 year. RESULTS: The patient was symptom-free within 8 weeks of the start of therapy. She remained symptom-free at 1 year follow-up evaluation. There were no obvious structural differences in the pretherapy and posttherapy MRI studies. CONCLUSIONS: Resolution of symptoms was directly related to the specific martial art therapy. However, there were no changes in the pretherapy and posttherapy MRI studies, suggesting a significant adaptation to the spinal compression had occurred. These data suggest a viable option to surgery in elderly patients with chronic and severe cervical spinal stenosis.

Cadmium-induced attenuation of coronary blood flow in the perfused rat heart.

The present studies were undertaken to test the hypothesis that cadmium alters myocardial metabolism, producing effects on coronary blood flow. Hearts isolated from adult, male Sprague-Dawley rats were control-equilibrated and then treated with Cd (0.1-100 microM). Myocardial O2 consumption (MVO2), lactate production, contractile activity, and coronary flow were determined at regular intervals. Parallel experiments were also performed in hearts administered 0.5 mM KCN to compare the effects of cadmium on myocardial lactate release with that of a known inhibitor of mitochondrial respiration. Coronary flow decreased significantly in response to Cd. This effect was dose-related (ED50 = 0.4 microM Cd), achieving maximal levels within the initial 5 min of exposure and persisting thereafter. Cd treatment also significantly decreased myocardial contractile activity [ED50 = 2.4 microM Cd (+dP/dt)] and MVO2 in a dose-dependent manner. This latter effect was time-dependent with an ED50 value of 2.1 microM at 5 min, as compared to a value of 0.5 microM Cd at 30 min. Lactate levels measured in the coronary effluent were unaffected by Cd treatment, except at the highest dose. Collectively, the results of this study failed to support a metabolic mechanism as the basis for the observed changes in coronary flow in response to cadmium administration. Instead, these results suggest an alternative hypothesis that Cd disturbs coronary flow via a mechanism involving direct actions on the coronary vasculature.

Inhibition of rat heart mitochondrial respiration by cadmium chloride.

Mitochondria were isolated from hearts obtained from adult male Sprague-Dawley rats by two-part differential centrifugation of heart homogenates. Time-dependent (0-120 sec) and concentration-dependent (0-10 microM CdCl2) effects of cadmium on pyruvate-malate-supported state 3 and state 4 respiration were measured in a constant temperature reaction chamber at 37 degrees C, according to established procedures. The ID50 for cadmium chloride on state 3 respiration was determined to be 4.2 microM. The inhibition produced by cadmium chloride in heart mitochondria was compared, using identical procedures, to the effects induced by two compounds, sodium atractyloside and potassium cyanide, which are known to alter mitochondrial respiration at specific sites. The calculated ID50 values for these agents in heart mitochondria were 1.8 and 16 microM, respectively. The concentration-dependent inhibition of mitochondrial respiration induced by either cadmium chloride or potassium cyanide was maintained in the presence of 50 microM carbonyl cyanide m-chlorophenylhydrazone (CCCP), a known uncoupling agent. In contrast, sodium atractyloside did not block the uncoupling effect of 50 microM CCCP. In addition cadmium chloride was also shown to inhibit CCCP-uncoupled mitochondrial respiration. The cadmium-induced inhibition of mitochondrial respiration was reversed partially by cysteine and completely by 2,3-dimercaptopropanol. The results of the present study indicate that, at all concentrations, cadmium chloride acted solely as an inhibitor of rat heart pyruvate-malate-supported mitochondrial respiration. These findings suggest a possible mechanism for the reported disturbances in myocardial metabolism and function that occur in conjunction with acute and chronic cadmium exposure in humans and experimental animals.