Perfusion index derived from a pulse oximeter can predict the incidence of hypotension during spinal anaesthesia for Caesarean delivery.

BACKGROUND: Hypotension during spinal anaesthesia for Caesarean delivery is a result of decreased vascular resistance due to sympathetic blockade and decreased cardiac output due to blood pooling in blocked areas of the body. Change in baseline peripheral vascular tone due to pregnancy may affect the degree of such hypotension. The perfusion index (PI) derived from a pulse oximeter has been used for assessing peripheral perfusion dynamics due to changes in peripheral vascular tone. The aim of this study was to examine whether baseline PI could predict the incidence of spinal anaesthesia-induced hypotension during Caesarean delivery. METHODS: Parturients undergoing elective Caesarean delivery under spinal anaesthesia with hyperbaric bupivacaine 10 mg and fentanyl 20 µg were enrolled in this prospective study. The correlation between baseline PI and the degree of hypotension during spinal anaesthesia and also the predictability of spinal anaesthesia-induced hypotension during Caesarean delivery by PI were investigated. RESULTS: Baseline PI correlated with the degree of decreases in systolic and mean arterial pressure (r=0.664, P<0.0001 and r=0.491, P=0.0029, respectively). The cut-off PI value of 3.5 identified parturients at risk for spinal anaesthesia-induced hypotension with a sensitivity of 81% and a specificity of 86% (P<0.001). The change of PI in parturients with baseline PI ≤ 3.5 was not significant during the observational period, while PI in parturients with baseline PI>3.5 demonstrated marked decreases after spinal injection. CONCLUSIONS: We demonstrated that higher baseline PI was associated with profound hypotension and that baseline PI could predict the incidence of spinal anaesthesia-induced hypotension during Caesarean delivery.

Massive macroglossia developing fast and immediately after endotracheal extubation.

We report an unusual case of massive macroglossia that developed very rapidly after neurosurgery in the park bench position with neck flexion. A few minutes after endotracheal extubation, massive macroglossia was noticed with marked protrusion of the tongue from the oral cavity. The patient's hospital stay was prolonged due to difficulty in speaking and eating. Macroglossia is a rare complication; however, it may cause life-threatening airway obstruction. It is important to be prepared for managing post-operative macroglossia and keep in mind that it may develop rapidly, especially after prolonged surgery performed with sustained neck flexion. The patient should be informed of the risk of macroglossia and the associated problems prior to the operation.

Histologic evaluation of preventive measures for scald injury on the peritoneo-serosal surface due to intraoperative hyperthermic chemoperfusion for patients with gastric cancer and peritoneal metastasis.

To histologically assess the preventive efficacy of cimetidine against scald injury on the peritoneo-serosal surface during intraperitoneal hyperthermic chemoperfusion (IHCP) for advanced gastric cancer, a randomized histologic study using cimetidine, a histamine H2-receptor antagonist, was performed for 20 patients with advanced or recurrent gastric cancer and peritoneal metastasis. Cimetidine 50 mg/kg was administered intravenously to 10 patients just prior to the IHCP (cimetidine group), and the remaining 10 patients underwent the IHCP without cimetidine (control group). The background factors and IHCP treatments of these two groups were nearly the same. Although the antitumour efficacy of the IHCP was not histologically different between the two groups, the histological analysis revealed that the peritoneo-serosal surface in the cimetidine group was protected against scald injury, compared with the control group. This finding suggests that pre-IHCP cimetidine is of great benefit for protecting the peritoneo-serosal surface from scald injury due to IHCP.

High-dose fentanyl does not suppress interleukin-1 beta-induced increases in plasma ACTH and corticosterone in rats.

BACKGROUND: High-dose fentanyl anesthesia is reported to attenuate the metabolic and endocrinal responses to surgery. Interleukin-1 (IL-1) is one of the key mediators in the immunoneuroendocrine system, and may be involved in the stress responses to surgery. We studied whether high-dose fentanyl may influence the IL-1 beta-induced alterations in plasma ACTH and corticosterone in rats. METHODS: Plasma ACTH, corticosterone, blood pressure, heart rate and acid-base status were determined in either awake or fentanyl-anesthetized animals immediately before and after either phosphate buffered saline or IL-1 beta administration. Fentanyl anesthesia was induced by bolus intravenous injections of fentanyl at 50 micrograms/kg and pancuronium bromide at 0.2 mg/kg, and maintained by continuous administrations of fentanyl at 100 or 200 micrograms.kg-1.h-1 and pancuronium bromide at 0.4 microgram.kg-1.h-1. RESULTS: In awake rats, IL-1 beta at incremental doses of 0.25, 0.5 and 1 microgram/kg increased plasma ACTH in a dose-dependent manner, but heat-inactivated IL-1 beta at 4 micrograms/kg did not influence plasma ACTH. A noxious stimulus with tail clamping for 30 min did not significantly alter plasma ACTH in fentanyl-anesthetized rats. Fentanyl reduced the basal plasma corticosterone, but it did not modulate the increases in plasma ACTH and corticosterone after the administration of IL-1 beta at 1 microgram/kg. Fentanyl moderately increased the basal blood pressure and heart rate, but it moderately attenuated the IL-1 beta-induced elevations of blood pressure and heart rate. IL-1 beta moderately decreased PCO2 in awake animals. CONCLUSIONS: Fentanyl anesthesia, which is able to suppress the endocrine responses to noxious stimuli, does not attenuate the IL-1 beta-mediated activation of the pituitary-adrenal axis in rats.

Upper airway obstruction during midazolam sedation: modification by nasal CPAP.

We examined the depressant effect of midazolam on respiration in 21 healthy women undergoing lower abdominal surgery with spinal anaesthesia. Airway gas flow, airway pressure, and the sound of snoring were recorded together with arterial oxygen saturation (SpO2). After spinal anaesthesia was established, subjects were deeply sedated with pentazocine 15 mg followed by incremental doses of midazolam 1 mg i.v. up to 0.1 mg.kg-1. When SpO2 decreased to < 90% or snoring and/or apnoea was observed, continuous positive airway pressure applied through the nose (nasal CPAP) was increased until the respiratory deterioration was reversed. While one patient remained free of respiratory events, the other 20 patients were successfully treated with nasal CPAP restoring normal SpO2 (95.5 +/- 1.7%) without snoring. Stepwise reduction of nasal CPAP determined the minimally effective CPAP to prevent snoring to be 5.1 +/- 2.1 cm H2O. Further reduction of nasal CPAP induced snoring in 15 patients and obstructive apnoea in five patients with the latter accompanied by a severe reduction of SpO2 (87.4 +/- 6.1%). Patients with apnoea were older than those who snored (P < 0.05. We conclude that upper airway obstruction contributes considerably to decreases in SpO2 during midazolam sedation for spinal anaesthesia.

Modulation of protein kinase C alters hemodynamics and metabolism in the isolated liver in fed and fasted rats.

The activation of protein kinase C (PKC) has been implicated in the pathogenesis of gram-negative sepsis. The effects of PKC modulation on hepatic flow and metabolism were studied using isolated liver perfusion. The liver was isolated from well-fed or overnight-fasted, male Sprague-Dawley rats weighing 250-310 g, and perfused at a constant pressure of 12 cmH2O using a recirculating system. Phorbol 12-myristate 13-acetate (PMA), a potent activator of PKC, decreased hepatic flow and oxygen consumption, and increased net lactate production. It enhanced net glucose production in fed animals. Neither 4 alpha-phorbol didecanoate, an inactive phorbol ester for PKC nor 4 alpha-phorbol, an inactive phorbol had any significant effect. The effects of PMA were augmented by increasing calcium concentration in the medium. PMA at an initial concentration of 4 x 10(-8) M stimulated net lactate and/or glucose production more than a reduction of perfusion pressure from 12 to 6 cmH2O. Staurosporine, a potent PKC inhibitor, significantly attenuated the PMA-induced alterations of hepatic flow and oxygen consumption. These results indicate that modulation of PKC exerts significant effects on hepatic flow and metabolism, which are dependent on extracellular calcium concentrations and feeding conditions, and that the effect of PMA on carbohydrate metabolism is not merely attributed to decreases in hepatic flow and oxygen consumption. It is suggested that PKC activation may be involved in the alterations of hepatic flow and metabolism during severe sepsis.

Modification of hepatic protein kinase C with phorbol myristate acetate and staurosporine alters hemodynamics in the perfused rat liver.

Activation of protein kinase C (PKC) has been implicated in the pathogenesis of endotoxicosis and severe sepsis. Since hepatic blood flow and metabolism have been known to be altered in endotoxicosis and sepsis, we studied the hemodynamic effect of PKC modulation with phorbol 12-myristate 13-acetate (PMA) and staurosporine (St) on the perfused rat liver. The liver was isolated from overnight-fasted male Sprague-Dawley rats and placed in a recirculating perfusion apparatus. The liver was perfused with Krebs-Ringer-bicarbonate solution at a constant pressure of 12 cmH2O. Flow to the liver was continuously monitored with an electric magnetic flowmeter. PMA at an initial concentration of 2 x 10(-8) M significantly decreased hepatic flow. Staurosporine (St), a potent PKC inhibitor at 4 x 10(-7) M produced a small increase in hepatic flow. Pretreatment with St significantly attenuated the flow reduction by PMA. St significantly suppressed the flow reductions by 4 x 10(-6) M of prostaglandin E2 and D2. These results suggest that the PKC inside the liver may play an important role in the regulation of hepatic blood flow during endotoxicosis and sepsis.

Prostaglandin E1 (PGE1) attenuates vasoconstriction induced by PGE2, PGD2 and phorbol myristate acetate in the perfused rat liver.

It has been shown that prostaglandins (PGs) produced by Kupffer and endothelial cells play an important role in mediating physiological responses to various immunological stimuli. We studied the effect of prostaglandin E1 (PGE1) on the hemodynamic and metabolic changes induced by prostaglandin E2 (PGE2), D2 (PGD2) and phorbol 12-myristate 13-acetate (PMA), a potent inducer of PGs in the isolated rat liver perfused with Krebs-Ringer-bicarbonate (KRB) solution at a constant pressure of 12 cmH2O. The liver was taken from overnight-fasted male Sprague-Dawley rats weighing 260 to 310 g. Both PGE2 and PGD2 significantly decreased hepatic flow when their initial concentration was elevated to micromolar range. Although 1 x 10(-6) M of PGE1 did not have a major effect on hepatic flow, it significantly attenuated the declines of hepatic flow produced by 4 x 10(-6) M of PGE2 and PGD2. However, none of PGs tested influenced glucose and lactate concentrations in the medium. Continuous infusion of PGE1 into the medium at a rate of 5 microg.min(-1) significantly diminished the decreases in hepatic flow and oxygen consumption induced by 2 x 10(-8) M of PMA. These results suggest that administration of PGE1 may preserve hepatic blood flow by modifying the intrahepatic regulatory mechanism involving the activation of Kupffer and endothelial cells.

K252a, a potent protein kinase inhibitor, improves endotoxic lethality and glucose dyshomeostasis.

To investigate whether the inhibition of protein kinases including protein kinase C can antagonize endotoxicosis, the in vivo effects of K252a, a potent inhibitor of protein kinases, on endotoxin-induced lethality and glucose dyshomeostasis were determined in conscious rats. Sprague-Dawley rats (260-340 g) were divided into the following four groups: Group DS, 2.5% dimethyl sulfoxide (DMSO), 6 ml/kg iv + 0.9% saline, 2 ml/kg iv; group KS, K252a in 2.5% DMSO, 4 mg/kg iv + 0.9% saline; group DE, 2.5% DMSO + endotoxin (E. coli), 15 mg/kg iv; and group KE, K252a in 2.5% DMSO + endotoxin. A quarter of DMSO or K252a solution was continuously infused over a 15 min period before a bolus injection of either saline or endotoxin. The remaining dose was administered over a 180 min period after saline or endotoxin. All animals in the DS and KS groups survived for 24 hrs. K252a significantly improved endotoxic lethality. It attenuated the initial hyperglycemia, and late hypoglycemia, hyperlactacidemia, and base deficit after endotoxin. However, K252a had no influence on the endotoxic alterations of blood pressure, PaCO2 or PaO2. These results suggest that the activations of protein kinases, particularly protein kinase C, are involved in the pathogenesis of lethal endotoxicosis and sepsis.

Free-space optical bus using cascaded vertical-to-surface transmission electrophotonic devices.

A free-space optical bus, which consists of cascaded optical switch devices, is proposed. The switch devices have multiple functions, such as data transmission, data detection, and data repetition. Basic interconnection characteristics were measured with vertical-to-surface transmission electrophotonic devices. Optical switching energy as low as 150 FJ and up to 4 MHz and a relatively high datatransmission rate, i.e., more than 20 MHz, were obtained. Connection cascadability and extendibility were confirmed.

[Inhalation anesthetic therapy of status asthmaticus].

Status asthmatics is characterized pathologically by bronchial smooth muscle spasm, and mucous plugging of the small airways. Clinically, it is characterized by the disturbance of gas exchange. In severe cases, unresponsive to standard therapy (including oxygen, epinephrine, aminophylline and steroids, artificial ventilation, tracheobronchial lavage and inhalation), anesthetic therapy should be started without delay. Inhalation anesthetics, halothane or ether, have potent bronchodilating properties which facilitate the removal of mucous plugging. We reported nine cases with status asthmatics treated by inhalation anesthetic therapy. Halothane (0.5-3.0%) was used in all cases, ether (1.5-3.0 ml/kg) was used in five cases. The duration of anesthesia was 0.5 to 13.5 hours. In three halothane anesthesia cases, blood pressure was reduced before there was improvement in wheezing, so we were forced to change halothane to ether. In all cases, the symptoms of status asthmatics were improved, but two patients died due to other complications. We recommended the following method, viz that halothane be administered at first, and be changed to ether in order to maintain circulatory movement.