[Anesthetic management of a patient with Saber-sheath trachea].

A 65-year-old man was scheduled for total gastrectomy. Preoperative chest radiograph showed significant narrowing of the trachea. On chest CT scan the trachea was U-shaped (tracheal index = 36%) and was diagnosed as saber-sheath trachea. During general anesthesia we took care to reduce the irritation by the endotracheal tube, particularly during intubation, and to avoid excessively high airway pressure. The trachea was watched carefully by bronchoscopy after intubation and during extubation not to neglect any complication. There was no complication after the operation.

[Body temperature changes during combined inhalational and epidural anesthesia].

We investigated the effects of combined inhalational and lumbar epidural anesthesia on body temperature in 8 women for long-lasting lower abdominal surgery. Probes for forehead deep temperature and skin-surface temperatures were placed on the forehead, forearm, fingertip and toe tip on patients' arrival at the operating room. Tympanic membrane temperature was also measured. Lumbar epidural block was established with 2% lidocaine 10 ml. Twenty minutes later, general anesthesia was induced and maintained with nitrous oxide-oxygen-isoflurane. Epidural anesthesia was maintained with intermittent dose of 1% mepivacaine. Before the end of surgery, isoflurane concentration was increased from about 0.5% to 2% and was maintained at this level for 20 minutes, after which it was reduced. With the establishment of epidural blockade, toe tip temperature increased and fingertip temperature decreased, while core temperature remained unchanged. After induction of general anesthesia, fingertip temperature increased, while core temperature decreased. The core temperature drop during the anesthetic induction was significantly affected by the increase in toe tip temperature. Before the end of surgery, core temperature remained at a reduced but constant level, while fingertip temperature continued to decrease. With the application of 2% isoflurane, fingertip temperature increased, while core temperature decreased. The core temperature drop was significantly affected by the increase in fingertip temperature. After the reduction of isoflurane concentration, these temperature changes were reversed fully. At the end of surgery, fingertip temperature decreased, while core temperature increased. During mild hypothermia, isoflurane depressed thermoregulatory vasoconstriction dose-dependently until its concentration reached 0.6-0.7%. In conclusion, anesthetics-induced redistribution of body heat significantly affects the core temperature throughout anesthesia. Peripheral hypothermia results in core temperature drop when the redistribution is induced by anesthetics. Thermoregulatory vasoconstriction may not only suppress heat loss but also increase core temperature through centralization of body heat.

The high prevalence of diabetes mellitus and hyperinsulinemia among the Japanese-Americans living in Hawaii and Los Angeles.

A comparative epidemiologic investigations was conducted among Japanese immigrants and their offspring living in Hawaii and the Los Angeles area, and among Japanese living in Hiroshima. All subjects received an oral glucose tolerance test and the diagnosis of diabetes was made on the basis of WHO criteria. In the subjects aged 40 years or older, the age, sex, and obesity-specific prevalence of diabetes was 2-3 times higher among Japanese living in America than those in Hiroshima. The fasting and post-glucose load serum immunoreactive insulin concentrations were higher in the Japanese-Americans compared to the Hiroshima inhabitants with the same degree of obesity and glucose tolerance. We suggest that a westernized lifestyle induces peripheral insulin resistance and promotes the development of diabetes among Japanese.

Sympathetic nervous activity to brown adipose tissue increases in cold-tolerant mice.

Brown adipose tissue (BAT) is thought to be responsible for increased heat production in cold-acclimated rodents. We measured sympathetic nerve activity (SNA) in interscapular BAT (IBAT) during cold stimulation in cold-acclimated C57BL/6J mice (ACCLI). Cold acclimation was achieved (cold tolerance was increased) by repeated exposure to cold stress every other week for 3 weeks. We compared SNA in these animals with SNA in mice that had no previous cold stress experience (naive). During the test, mice were anesthetized by urethane and isoflurane and were paralyzed with vecuronium bromide. Sympathetic nerve activity was recorded directly from one of the fine nerves to IBAT. The animal's body caudal to the pelvic area was covered with a plastic bag containing a slurry of ice water to decrease colonic temperature 7 degrees C below control level, which took approximately 20 min. Interscapular BAT-SNA increased during cold stress in both groups, but ACCLI mice had higher IBAT-SNA during cold stress than naive mice. These findings confirmed the hypothesis that during the acute cold exposure, cold-acclimated mice have greater sympathetic outflow to BAT adipocytes.

Aged C57BL/6J mice respond to cold with increased sympathetic nervous activity in interscapular brown adipose tissue.

Aged, male C57BL/6J mice produce less heat than adults during cold, which may lead to a reduced ability to maintain core temperature, but the underlying mechanisms of the decreased heat production in aged mice are still unclear. We measured sympathetic nervous activity (SNA) to interscapular brown adipose tissue (IBAT) in aged mice and compared this activity with that of adults. Mice were anesthetized by urethane and isoflurane, and SNA was recorded from one of the fine nerves to IBAT. The animal's body caudal to the pelvic area was covered with a plastic bag containing iced-water to decrease colonic temperature 7 degrees C below control over 20 minutes. SNA to IBAT (IBAT-SNA) increased during cold in both groups, but aged mice had higher IBAT-SNA before and during cold. These findings indicate that neither the ability of aged mice to detect cold nor their ability to generate sympathetic outflow to BAT is deficient.

Overnight increases in haematocrit: additional evidence for a nocturnal fall in plasma volume.

Our previously published studies with monkeys describe a characteristic nocturnal haemodynamic pattern consisting of a monotonic decline in cardiac output and central venous pressure, and a concomitant rise in total peripheral resistance. These findings led us to hypothesize that there is a reduction in total plasma volume during the night. Since a fall in plasma volume should cause an increase in haemoglobin and plasma protein concentration, we designed this experiment to test the hypothesis that haematocrit levels would be significantly greater in the morning than in the evening. In a study of five monkeys, the levels of haematocrit were measured at 1700 h and at 0900 h the next morning for 14 days. The average morning haematocrit levels were 6.5% higher than the average evening values. Lower plasma volume and possibly greater blood viscosity could contribute to the pathophysiology of the morning increase in the incidence of 'silent' ischaemia and catastrophic vascular events such as sudden cardiac death, myocardial infarctions and strokes in man.

Zinc metabolism in thyroid disease.

This study was designed to evaluate the zinc metabolism in adults of both sexes with thyroid disease. Plasma and erythrocyte zinc concentration and urinary zinc excretion were investigated. The mean concentration of plasma zinc in hypothyroid patients and in euthyroid patients, previously either hyperthyroid or hypothyroid, was lower than that of control subjects, whereas no statistically significant differences were observed in plasma zinc values between hyperthyroid patients and control subjects. The average erythrocyte zinc level in patients with thyroid disease was significantly lower than that in control subjects. Erythrocyte zinc concentration was significantly decreased in hyperthyroidism compared with hypothyroidism, or patients previously either hyperthyroid or hypothyroid but now euthyroid. Increased urinary zinc excretion in hyperthyroidism was noticed compared to euthyroid and hypothyroid patients and to control subjects. Increased urinary zinc concentrations may result from increased tissue catabolism such as muscle. The results of this study suggest that abnormal zinc metabolism occurs commonly in patients with thyroid disease.

Metabolism, 45Ca uptake and insulin releasing capacities of glucose and mannose.

A detailed dose-response study relating mannose and glucose oxidation with the induction of 45Ca uptake and insulin release was performed using in vitro incubation of collagenase digested rat islets of Langerhans. The threshold value for 14C-U-D-glucose oxidation, glucose-stimulation of 45Ca uptake, and insulin release was about 5.5 mM. The half maximal response for these 3 parameters occurred at 13.4 mM, 11.6 mM, and 12.2 mM, respectively. Their maximal responses were obtained at approximately 20 mM. The threshold level for mannose oxidation, induction of 45Ca uptake and insulin release was about 11.0 mM, with half maximal responses obtained at 24.6 mM, 20.5 mM, and 22.2 mM, respectively. The maximum response of the 3 parameters to mannose was obtained at 38.8 mM and appeared to reach the same level obtained for glucose. These results suggest that hexose degradation has a significant role in controlling Ca uptake and subsequent insulin release. A lower rate of mannose oxidation appeared to account for its weaker stimulating efficacy for Ca uptake and insulin release.

Effect of somatostatin on glucose-induced 45Ca uptake in the pancreatic islets.

This study was designed in an attempt to elucidate a mechanism of somatostatin inhibition of glucose-induced Ca+ uptake by rat pancreatic islets. Rat pancreatic islets were perifused with Krebs-Ringer bicarbonate (KRB) buffer containing 16.7 mM of glucose with somatostatin (2 micrograms/ml) or/and diltiazem HCl (2 x 10(-5) M). Somatostatin inhibited preferentially the early phase of glucose-induced insulin release, whereas diltiazem HCl inhibited the late one. And the concomitant presence of the submaximal concentration of somatostatin (2 micrograms/ml) and diltiazem HCl (2 x 10(-5 M) provided the completely additive inhibition of glucose-induced insulin release. Rat pancreatic islets were incubated with KRB buffer supplemented with 16.7 mM of glucose and 45CaCl2 (10 muCi/ml) for 5--60 min and the biphasic 45Ca uptake by pancreatic islets was obtained. Somatostatin (500 ng/ml-4 micrograms/ml) gave the suppressive effect on the early phase of glucose-induced 45Ca uptake, but the higher concentration (2 micrograms/ml) of somatostatin did not impair the late phase of 45Ca uptake by pancreatic islets. On the other hand, diltiazem HCl did suppress the late phase of glucose-induced 45Ca uptake dose-dependently, but did not suppress the early phase (2 x 10(-5) M). These data indicate that somatostatin suppresses the early phase of glucose-induced Ca2+ uptake preferentially to the late one and has a different action mechanism from Ca antagonist on glucose-induced insulin release.

Alloxan inhibits glucose oxidation in the pancreatic islets.

The effects of alloxan on glucose oxidation and the protection by anomers of D-glucose from alloxan inhibition of glucose oxidation in the pancreatic islets were investigated using in vitro incubation of rat isolated islets. The pretreatment by alloxan (5-30 mg/dl) for 6 minutes inhibits significantly 14CO2 formation from 14C-U-D-glucose (10 mM) and the addition of alpha-anomer of D-glucose (8.3 mM) to alloxan (20 mg/dl) completely reverses alloxan inhibition of glucose oxidation. These findings seem to be incompatible with the recent view that alloxan acts at the glucose receptor on the plasma membrane of pancreatic beta-cells without affecting glucose metabolism in the pancreatic islets.

Diabetes mellitus and its vascular complications in Japanese migrants on the Island of Hawaii.

Japanese migrants and their offspring on the island of Hawaii and Japanese living in Hiroshima were examined for diabetes mellitus and its vascular complications. the same methods and investigators were used in both locations. Death certificates of Japanese and Caucasians dying on the island during the past 26 yr were analyzed. Diabetes, defined as a venous serum glucose concentration of at least 200 mg/dl 2 h after a 50-g oral glucose load, was significantly more common in the Hawaiian Japanese than in the Hiroshima Japanese subjects. This suggests that diabetes is more prevalent in Japanese in Hawaii than in Japan, although lack of knowledge about the total population of Japanese migrants in Hawaii makes this generalization uncertain. The proportion of deaths attributed to diabetes was much higher in Japanese migrants and their offspring in Hawaii than in Japan. During the 1950s, the proportional death rate from diabetes was about half as large in Japanese Hawaiians as in Caucasian Hawaiians, but it increased to become 1.6 times the Caucasian rate during the 1970s. A nutritional study revealed that the total caloric intake was similar in Japanese in Hawaii and Hiroshima, although the estimated level of physical activity was less in the Hawaiian subjects. Consumption of animal fat and simple carbohydrates (sucrose and fructose) were at least twice as high in Hawaiian as in Hiroshima Japanese. Conversely, Hiroshima Japanese consumed about twice the amount of complex carbohydrate as the Hawaiian Japanese. These observations support the hypothesis that a high fat, high simple carbohydrate, low complex carbohydrate diet and/or reduced levels of physical activity increase risk of diabetes. The proportion of deaths attributed to ischemic heart disease was higher in both diabetic and nondiabetic Japanese Hawaiians than in diabetic subjects in Japan. The rates were similar for Japanese and Caucasians in Hawaii. There was no evidence of an environmental influence on the development of microangiopathy (retinopathy) in diabetes, as the prevalence of diabetic retinopathy (stratified for diabetes duration) was similar in Japanese subjects in Hawaii and in Japan, and it was similar to previous reports from England. On the other hand, diabetes alone did not appear to account for the greater prevalence of macroangiopathy in Hawaiian Japanese than in Hiroshima. Thus environmental factors, possibly including diet, appear to be involved in the development of macrovascular complications of diabetes.