Physical training augments plasma catecholamines and natural killer cell activity.

To elucidate the effects of a 10-week exercise training period on physical fitness and plasma catecholamine concentration at rest, and on natural killer cell activity in young healthy untrained females, subjects (20-22 years old. N = 16) carried out physical training by a protocol which consisted of treadmill jogging at a work-intensity of 50% of their VO2max, two hours a day three times a week for ten weeks. VO2max was increased significantly from 33.1 +/- 3.4 ml/kg/min to 38.3 +/- 6.6 ml/kg/min by the ten weeks of physical training (P < 0.005), and natural killer cell activity was also increased significantly from 31.9 +/- 14.3% to 46.4 +/- 18.4% (P < 0.05). The concentrations of epinephrine and norepinephrine before and after physical training were 18.3 +/- 8.7 pg/ml and 20.4 +/- 8.9 pg/ml, and 134.1 +/- 52.2 pg/ml and 248.1 +/- 106.8 pg/ml (P < 0.005), respectively. Changes in norepinephrine and epinephrine correlated with the change in VO2max (r = 0.780, P < 0.005; r = 0.556, P < 0.05). While the change in natural killer cell activity correlated with the change in epinephrine (r = 0.623, P < 0.01), the correlation of the change in natural killer cell activity with change in norepinephrine did not reach statistical significance (r = 0.497, P = 0.0503). From these results we concluded that physical training augments plasma catecholamine levels and natural killer cell activity at rest in young healthy females.

[Autonomic nerve function expressed by the baroreflex sensitivity (BRS) in elderly adults].

We examined 24 hour heart rate variability (HRV) components and baroreflex sensitivity (BRS) in elderly adults. Forty-eight subjects, aged 65-69 years old (24 men, 24 women) were examined in this study. BRS was measured in the morning (8:00-9:00) using noninvasive cross spectral analysis. There were significant correlations between BRS and low-frequency (LF) power (r = 0.593, p < 0.001) of HRV, and between BRS and high-frequency (HF) power (r = 0.402, p < 0.005). BRS values were lower in women compared with men (p < 0.01), and LF/HF was significantly lower in women than in men (p < 0.05).

[A case of systemic lupus erythematosus with various central and peripheral neurological disorders presenting with motor paralytic bladder as a major manifestation].

Myelopathy is a rare central nervous system manifestation in systemic lupus erythematosus (SLE). We present a case of SLE, who developed motor paralytic bladder and various other neurological abnormalities. A 29-year-old female with SLE was admitted to our hospital because of complete dysuria without any troubles on defecation. Accelerated hypertension had been noticed 2 weeks before the admission. Physical examinations revealed that she had muscle weakness in right brachial biceps, bilateral carpal extensor and flexor, and flexor muscles of bilateral lower extremities. Slight sensory disturbance was present on her soles. Bilateral Chaddok and Babinski's signs were positive. Electromyographic studies including nerve conduction velocities of her limbs were normal, however, neurogenic discharges were observed in anal sphincter muscles. Cystometry demonstrated atonic bladder, but any pathological findings such as lupus cystitis and interstitial cystitis were not observed in the biopsied specimens from her bladder. Antibodies to single-stranded DNA, U1 RNP, Sm and SS-A/Ro were positive in her serum, and lupus anticoagulant and anticardiolipin antibodies (IgG) were also detected. In her cerebral spinal fluid (CSF), elevated protein level and albuminocytologic dissociation were recognized, while glucose level was low. Magnetic resonance imaging (MRI) study detected high signal intensities in the inner part of medulla oblongata and in the spinal cord at second lumbar spine level. After two courses of methyl-prednisolone pulse therapy, the patient's neurological symptoms including dysuria had completely recovered and abnormal findings previously observed on MRI had also disappeared. After 7 months of the episode, she became normotensive. The proteins and glucose levels in her CSF had gradually returned to normal. Among patients with SLE, correlations of antiphospholipid antibodies with myelitis/myelopathy or accelerated hypertension have been reported. Therefore, possible roles of antiphospholipid antibodies were considered in the pathogenesis of neurologic abnormalities observed in our patient. In addition, low glucose level in CSF might be a good indicator for the diagnosis of lupus-associated myelopathy.

Combined treatment of probucol with diltiazem regresses atherosclerosis induced by 196 cholesterol diet in rabbit aorta.

To clarify whether probucol, an antioxidant, or diltiazem, a Ca2+ antagonist, favorably affect the regression of established atherosclerosis, rabbits were fed a 1% cholesterol diet for 10 weeks, then a standard diet for an additional 25 weeks (regression period). During the regression period, rabbits were grouped into a saline (S) group (n=8, 1 ml saline/d), a probucol (P) group (n=8, 1000 mg/d probucol), or a probucol and diltiazem (P+D) group (n=8, probucol 1000 mg/d in diet and diltiazem 30 mg/d). We measured cholesterol in serum, lipoprotein fractions, and serum triglyceride or phospholipid concentration and found no significant differences among the three groups at 10, 15, or 35 weeks. After 10 weeks of the atherogenic diet, the ratio of macroscopic atherosclerotic lesions in aortic intima rose to 36.6 + or - 5.6%. After the regression period, the S group developed more atherosclerotic lesions (48.6 + or - 6.4%). The P+D and P groups, however, had decreased scores of 24.3 + or - 5.5% (p<0.05 vs. S) and 32.3 + or - 5.6%, respectively. Moreover, these decreased scores were well correlated with the decrease in aortic tissue lipid compositions, but not the parameters for extracellular matrices. We concluded that P+D or P therapy might be effective in regressing established atherosclerosis by removing lipid contents but not extracellular matrices.

[A case of heterozygous familial hypercholesterolemia showing the regression of coronary atherosclerosis by LDL-apheresis].

A case showing the regression of coronary atherosclerosis by the treatment with LDL-apheresis, was reported. The patient was a 67-year old female with heterozygous familial hypercholesterolemia. She had noticed the xanthelasma or left cubital xanthoma at the age of 50 years old. She was informed about her high serum cholesterol level (greater than 350 mg/dl), and the abnormal thickness of her bilateral achilles tendon at the age of 61 years. As her serum cholesterol level did not decrease sufficiently with several lipid-lowering drugs, she was referred to our hospital in order to obtain treatment for it by LDL-apheresis at the age of 66 years. LDL-apheresis was performed once every two weeks with drugs such as probucol, cholestyramine and pravastatin. Her coronary angiogram after two and half years of LDL-apheresis showed a decrease of the coronary narrowing in segment 1 and segment 13 (from 96.8% to 74.6% in segment 1, and from 81.5% to 61.7% in segment 13, respectively). The thickness of her bilateral achilles tendons had also decreased from 18 mm in the right and 19 mm in the left to 14 mm in both, after receiving LDL-apheresis for two and half years. It is suggested from the result of this case that the regression of coronary atherosclerosis could be expected after treatment with LDL-apheresis in hypercholesterolemic patients.