Adjustment of anaesthesia depth using bispectral index prolongs seizure duration in electroconvulsive therapy.

Electroconvulsive therapy (ECT) under propofol anaesthesia induces relatively shorter seizures compared to barbiturate anaesthesia. Since significant correlation between seizure duration and bispectral index (BIS) value immediately before electrical stimulus has been reported among patients, adjustment of anaesthesia depth as determined by BIS may be effective in obtaining a longer seizure length. In the present study, we examined this hypothesis in those patients whose muscular seizure duration was less than 40s. ECT was prescribed to 20 patients suffering from endogenous depression. General anaesthesia was induced with propofol 1 mg/kg. Succinylcholine chloride 1 mg/kg was then given. The efficacy of electrical stimulation was determined using a tourniquet technique, electromyogram, and electroencephalography. When a patient had a seizure less than 40s in their second ECT treatment, the subsequent treatment was modified such that the electrical stimulus was given after waiting for a higher BIS value (+10-20). Intensity of electrical stimulus and anaesthesia conditions were identical in the two treatments. All 20 patients had longer seizures as determined by the electromyogram and/or electroencephalography when the stimulus was delivered at the higher BIS value. Seizure duration measured by muscle movement was 31+/-5 s when the stimulus was delivered without waiting and 46+/-10 s when delivered after waiting. There was a significant difference in seizure duration between the two treatments (P<0.01). Waiting for a recovery in BIS value before electrical stimulation can prolong seizure duration.

Alterations in autonomic nervous control of heart rate among tourists at 2700 and 3700 m above sea level.

OBJECTIVES: Many travelers who are not specially trained for activities at high altitude are at risk of physical problems, including cardiovascular disorders, when exposed to high-altitude environments. In the present study, we investigated how actual acute exposure to altitudes of 2700 and 3700 m affected the autonomic nervous control of heart rate in untrained office workers. METHODS: Physiological parameters (heart rate, respiratory rate, arterial blood oxygen saturation, and end-expiratory carbon dioxide tension) were measured at sea level, 2700 m, and 3700 m. The power of heart rate variability was quantified by determining the areas of the spectrum in 2 component widths: low frequency (LF; 0.04-0.15 Hz) and high frequency (HF; 0.15-0.5 Hz). The ratio of LF power to HF power (LF:HF), which is considered to be an index of cardiac sympathetic tone, was also assessed. RESULTS: Both HF and LF heart rate variability decreased according to the elevation of altitude. High- and low-frequency powers at 3700 m were significantly lower than those at sea level (P < .01 for HF, P < .05 for LF). The LF:HF ratio at 2700 m was not significantly different from that at sea level. However, it was significantly increased at 3700 m (P < .01). CONCLUSIONS: At 2700 and 3700 m, the activity of the autonomic nervous system measured by heart rate variability was decreased in untrained office workers. The sympathetic nervous system was dominant to the parasympathetic at 3700 m. These alterations in the autonomic nervous system might play some role in physical fitness at high altitudes.

Exercise-induced cerebral deoxygenation among untrained trekkers at moderate altitudes.

The pathophysiology of altitude-related disorders in untrained trekkers has not been clarified. In the present study, the effects of workload on cardiovascular parameters and regional cerebral oxygenation were studied in untrained trekkers at altitudes of 2700 m and 3700 m above sea level. We studied 6 males and 4 females at each altitude, and their average ages were 31.3+/-7.1 y at 2700 m and 31.2+/-6.8 y at 3700 m, respectively. The resting values of heart rate and mean blood pressure were not significantly different at 2700 m and 3700 m than at sea level. However, increases in these values after exercise were more prominent at high altitudes (heart rate increase = 51.6% at 2700 m and 70.4% at 3700 m; mean blood pressure increase: 19.0% at 2700 m and 17.2% at 3700 m). In addition, post-exercise blood lactate concentration was significantly higher at 3700 m than at sea level or at 2700 m (i.e., 7.6 mM at 3700 m, 3.8 mM at 2700 m, and 4.17 mM at 0 m, respectively). Exercise induced an acute reduction in the arterial oxygen saturation value (SpO2) at 2700 m and 3700 m (i.e., 11.2% reduction at 2700 m and 9.4% at 3700 m), whereas no changes were observed at sea level. The resting values of regional oxygen saturation (rSO2)--measured by a near infra-red spectrophotometer at sea level, 2700 m, and 3700 m-were nearly identical. Exercise at sea level did not reduce this value. In contrast, we observed a decrease in rSO2 after subjects exercised at 2700 m and 3700 m (i.e., 26.9% at 2700 m and 48.1% at 3700 m, respectively). The rSO2 measured 2 min and 3 min after exercise at 3700 m was significantly higher than the preexercise value. From these observations, we concluded that alterations in cardiovascular parameters were apparent only after an exercise load occurred at approximately 3000 m altitude. Acute reduction in cerebral regional oxygen saturation might be a primary cause of headache and acute mountain sickness among unacclimatized trekkers.

Rate pressure product and oxygen saturation in tourists at approximately 3000 m above sea level.

OBJECTIVES: Using modern transportation technology, many travelers easily access moderate altitudes of approximately 3000 m above sea level. In the present study the effects of this altitude on cardiovascular parameters were studied among office workers dwelling at sea level. METHODS: Heart rate, blood pressure, arterial oxygen saturation (SpO2), and electrocardiography were monitored before and after Master's double-step exercise at 2700 and 3700 m. The test consisted of stepping onto and off of two 23-cm steps for 3 min at a predefined rate. RESULTS: The resting values recorded for the heart rate and mean blood pressure at 2700 and 3700 m did not statistically significantly differ from those noted at sea level. However, the increases in these values after exercise were significantly greater at high altitude. The rate pressure product more than doubled after exercise at 3700 m. Electrocardiographic abnormalities were observed in some cases. The postexercise blood lactate concentration was significantly higher at 3700 m than at sea level or at 2700 m, suggesting that the oxygen supply-demand relationship was not balanced at this altitude. Furthermore, exercise provoked an acute reduction in SpO2 at 2700 and 3700 m but showed no effect at sea level. CONCLUSION: These observations suggest that the oxygenation status of the heart might be at risk in many travelers and workers during and after exercise load at an altitude of approximately 3000 m.

NaCl and/or urea infusion fails to increase renal inner medullary myo-inositol in protein-deprived rats.

As we recently demonstrated that in potassium depletion a decrease in inner medullary organic osmolytes might precede and cause a renal concentrating defect, we hypothesized that in the protein deprivation the same mechanism may occur. To clarify the relationship between renal medullary organic osmolytes and urine concentration defects during protein deprivation, we examined the effect of protein malnutrition on organic osmolyte content after water deprivation or sodium and/or urea infusion. Water deprivation did not restore urine urea and osmolality or tissue sodium and urea in protein-deprived rats to control levels. NaCl infusion only increased urinary and medullary Na. Urea infusion increased medullary urea but not urine urea. NaCl plus urea infusion increased only urinary sodium and urea. Regardless of the protocols of hyperosmolality used, protein deprivation significantly decreased the medullary contents of myo-inositol and taurine and the level of sodium-dependent myo-inositol transporter mRNA. We conclude that factors other than NaCl and urea but associated with protein feeding are responsible for the decreased accumulation of organic osmolytes.

The cerebral hemodynamic response to electrically induced seizures in man.

The hemodynamic response to seizure has long been a topic for discussion in association with the neuronal damage resulting from convulsion. Electroconvulsive therapy (ECT) is an appropriate clinical model for the investigation of the cerebral physiology of seizure. In this study, we monitored the oxygenation state of brain tissue using near infrared (NIR) spectrophotometry, and flow velocity at the middle cerebral artery (MCA) using transcranial Doppler ultrasonography (tc-Doppler) in ninety cases where flow velocity at the middle cerebral artery (MCA) using transcranial Doppler ultrasonography (tc-Doppler) in ninety cases where ECT was prescribed to patients suffering from endogenous depression. Under general anesthesia with thiopental and succinyl choline, an electrical current was applied bilaterally at the minimal energy level. Throughout the therapy, end-tidal CO2 tension was maintained at 30-35 mmHg, and the SpO2 value was maintained above 98% by manual ventilation assistance. The total- and oxy-hemoglobin contents in the brain were reduced during the electrical shock, and then recovered to the pre-shock value (total-hemoglobin; 44.13 +/- 12.88 s after the shock, oxy-hemoglobin; 88.62 +/- 11.69 s after the shock). Subsequently, these values further increased beyond the preshock value. On the other hand, the deoxy-hemoglobin content increased for 90.73 +/- 15.88 s during and after the electrical shock, and decreased afterward. Reduction of cytochrome aa3 began 3.04 +/- 0.51 s after the electrical shock, and this was reoxygenated at 171.88 +/- 12.95 s after the shock.(ABSTRACT TRUNCATED AT 250 WORDS)

Elevated serum pepsinogens in chronic renal failure patients.

Human pepsinogens, the precursors of pepsin, originating from the stomach mucosa, are classified into two biochemically distinct groups, namely pepsinogen I (PG I) and pepsinogen II (PG II). We studied the serum levels of PG I and II in 51 normal volunteers, 23 chronic glomerulonephritis patients, 21 continuous ambulatory peritoneal dialysis (CAPD) patients and 40 hemodialysis patients. Serum pepsinogen levels were measured with a competitive binding double antibody radioimmunoassay. In the group of chronic glomerulonephritis patients, a positive correlation between the serum creatinine and the pepsinogen levels were found. The serum pepsinogen levels were remarkably elevated in CAPD and hemodialysis patients. The median levels of post-hemodialysis PG I (265.4 +/- 165.2 ng/ml) and PG II (41.7 +/- 38.0 ng/ml) were significantly higher than prehemodialysis values (PG I 207.4 +/- 127.5 ng/ml, PG II 29.0 +/- 16.6 ng/ml). Pepsinogen release by isolated gastric glands of guinea pigs was suppressed by guanidinosuccinic acid and was facilitated by calcium. The data suggest that both removal of guanidinosuccinic acid and infusion of calcium during hemodialysis contribute to the raised serum levels of these pepsinogens after hemodialysis.