Clonidine produces a dose-dependent impairment of baroreflex-mediated thermoregulatory responses to positive end-expiratory pressure in anaesthetized humans.

BACKGROUND: Perioperative hypothermia is common and results from anaesthesia-induced inhibition of thermoregulatory control. Hypothermia is blunted by baroreceptor unloading caused by positive end-expiratory pressure (PEEP), and is mediated by an increase in the vasoconstriction threshold. Premedication with clonidine impairs normal thermoregulatory control. We therefore determined the effect of clonidine on PEEP-induced hypothermia protection. METHODS: Core temperature was evaluated in patients undergoing combined general and epidural anaesthesia for lower abdominal surgery. They were assigned to an end-expiratory pressure of zero (ZEEP) or 10 cm H(2)O PEEP. The PEEP group was divided into three blinded subgroups that received placebo (Cl-0), clonidine 150 microg (Cl-150) and clonidine 300 microg (Cl-300) respectively. Placebo or clonidine was given orally 30 min before surgery. We evaluated core temperature and thermoregulatory vasoconstriction. We also determined plasma epinephrine, norepinephrine, angiotensin II concentrations and plasma renin activity. RESULTS: Core temperature after 180 min of anaesthesia was 35.1 (0.4) degrees C in the ZEEP group. PEEP significantly increased final core temperature to 35.8 (0.5) degrees C (Cl-0 group). Clonidine produced a linear, dose-dependent impairment of PEEP-induced hypothermia protection: final core temperatures were 35.4 (0.3) degrees C in the Cl-150 group and 35.0 (0.6) degrees C in the Cl-300 group. Similarly, clonidine produced a linear and dose-dependent reduction in vasoconstriction threshold: Cl-0, 36.4 (0.3) degrees C; Cl-150, 35.8 (0.3) degrees C; Cl-300, 35.4 (0.6) degrees C. Plasma norepinephrine, angiotensin II concentrations and renin activity were consistent with the thermoregulatory responses. CONCLUSION: Baroreceptor unloading by PEEP normally moderates perioperative hypothermia. However, clonidine premedication produces a linear, dose-dependent reduction in this benefit.

Effect of preoperative amino acid infusion on thermoregulatory response during spinal anaesthesia.

BACKGROUND: Intravenous amino acid infusion during general anaesthesia prevents decreases in core temperature resulting from increased energy expenditure and heat accumulation. METHODS: We investigated whether such stimulation also occurs during spinal anaesthesia, which blocks sympathetic nervous activity. We examined the effect of i.v. amino acid infusion on changes in core temperature during spinal anaesthesia. Thirty-five patients were divided into two groups: an i.v. amino acid infusion group (4 kJ kg(-1) h(-1) starting 2 h before surgery); and a saline infusion group. Tympanic membrane core temperature, forearm-fingertip temperature gradient (an index of peripheral vasoconstriction) and mean skin temperature were measured for 90 min after the onset of spinal anaesthesia. RESULTS: Changes in mean arterial pressure and heart rate did not differ significantly between the groups during the study period. Mean final core temperature 90 min after induction of spinal anaesthesia was 35.8 (SEM 0.1) degrees C in the saline group and 36.6 (0.1) degrees C in the amino acid group (P<0.05). The increased level of oxygen consumption in the amino acid group compared with the saline group was preserved even after the onset of spinal anaesthesia. The thermal vasoconstriction threshold, defined as the tympanic membrane temperature that triggered a rapid increase in forearm-fingertip temperature gradient, was increased in the amino acid group [36.8 (0.1) degrees C] compared with the saline group [36.5 (0.1) degrees C] (P<0.05). CONCLUSIONS: Preoperative infusion of amino acids effectively prevents spinal anaesthesia-induced hypothermia by maintaining a higher metabolic rate and increasing the threshold core temperature for thermal vasoconstriction.

[Intraoperative transient incomplete left bundle branch block in a patient with left axis deviation in pre-anesthetic electrocardiogram].

We encountered a case of transient incomplete left bundle branch block (TILBBB) during standard mastectomy under general anesthesia. The patient was a 40 year-old female (70 kg, 164 cm) without any abnormalities on preanesthetic examinations except -61 degrees left axis deviation in exercise electrocardiogram. Adriamycin 20 mg was administered preoperatively. After the skin incision, heart rate increased from 104 min-1 to 130 min-1 and the cardiac axis gradually rotated leftward with increasing Q wave depth on leads I and aVL. We diagnosed this as blockade of the anterior branch in the left bundle branch. After the administration of fentanyl (0.2 mg) and sevoflurane (3%), the heart rate decreased to 105 min-1 and the electrocardiogram returned to the initial wave form. This anesthetic course indicated that adriamycin had slightly damaged the cardiac muscle and inadequate anesthesia had caused tachycardia and transient left bundle branch block. Left axis deviation on preoperative exercise electrocardiogram suggests that the left bundle branch can easily be blocked with an increasing heart rate. Adequate depth of anesthesia would have prevented the increase in heart rate and abnormality in the cardiac conduction process.

Elevated venous concentrations of vasoactive intestinal polypeptide in cord blood of infants with fetal distress.

Concentrations of vasoactive intestinal polypeptide (VIP) in cord plasma were determined in 70 neonates (birth weight, mean +/- SD, 3,213.5 +/- 50.9 g, gestation 39.5 +/- 0.2 weeks), 22 of whom had fetal distress. Arterial VIP levels in cord blood were not significantly different between infants with and without fetal distress. The mean venous VIP in cord blood of distressed infants (28.1 +/- 8.4 pg/ml, mean +/- SE) was significantly (p < 0.05) higher than that of normal neonates (12.6 +/- 3.4 pg/ml). The mean placental content of VIP was 5.1 +/- 0.3 ng/g wet tissue, although a correlation with the venous concentration in the cord was not demonstrated. Venous VIP levels were elevated 24 h after birth (34.6 +/- 13.7 pg/ml) and decreased on the 5th day of life to 12.9 +/- 3.8 pg/ml, which was not significantly different from the mean VIP level in childhood (14.7 +/- 3.1 pg/ml). These results demonstrate that, in the perinatal period, plasma VIP levels are elevated on two occasions: at delivery associated with fetal distress (cord vein), and at 24 h of age. VIP in the former seems to be of placental and/or maternal origin.

Prevalence of obesity, leanness and anorexia nervosa in Japanese boys and girls aged 12-14 years.

Body weight and height of Japanese boys and girls aged 12-14 years were measured to calculate the prevalence of obesity, leanness and anorexia nervosa. In boys, the prevalence of obesity as well as leanness was significantly higher in the areas where population density was lower and among the boys who attended schools with smaller numbers of pupils. In the girls, these findings were similar to the boys. On the other hand, anorexia nervosa was found in girls only more commonly in the areas with higher population density and in the larger schools. These results suggest that higher prevalence of obesity in certain subjects may be associated with increased numbers of leanness but not with anorexia nervosa.

Prolonged suppression of gonadotropin secretion after weight recovery in an anorectic patient with Turner's syndrome: reduced gonadal function in anorexia nervosa is independent in part on nutrition.

Two hypotheses have been postulated as to the pathogenesis of hypogonadotropinemia in anorexia nervosa; one is starvation and weight loss and the other is a psychological factor to influence gonadotropin secretion. Our patient suffered from very rare concurrence of Turner's syndrome and anorexia nervosa and a study of this experiment in nature provided important evidences concerning decreased secretion of gonadotropins in the eating disorder. The patient was diagnosed as Turner's syndrome when she was 6 years old. Her gonadotropin levels were elevated to the castrated ranges (LH 61.8 IU/l; FSH 175.8 IU/l) after 8 years of age. She was noticed to be anorectic at the age of 13 years. Serum levels of the pituitary gonadotropins were lowered (LH 2.9 IU/l; FSH 3.0 IU/l) and their responses to luteinizing hormone-releasing hormone were decreased beneath the normal prepubertal limits. After one year of the anorectic period, she recovered the weight though her gonadotropin levels remained in the very low ranges (LH 2.7 IU/l; FSH 2.5 IU/l). The results suggest that hypogonadism in anorexia nervosa is not solely caused by nutritional deficiency but rather by other factors such as psychological abnormalities.