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It is known that an optimal dose of intrathecal morphine for analgesia after total hip arthroplasty in older patients is 0.1 mg. On the other hand, minidose intrathecal morphine (0.05 mg) is useful for analgesia after the transurethral resection of the prostate in elderly patients. We evaluated the postoperative analgesic effect of minidose intrathecal morphine after bipolar hip prosthesis in seniors (age 85 years or more) undergoing spinal anesthesia. Twenty seniors undergoing bipolar hip prosthesis under spinal anesthesia were randomly allocated to one of two groups. Group A (n = 10) received intrathecal injection of 0.5% isobaric bupivacaine, 2.8 ml, and group B (n = 10) received intrathecal injection of 0.5% isobaric bupivacaine, 2.8 ml, plus morphine, 0.05 mg. Pain, nausea, and itching were evaluated using a numerical rating scale, ranging from 0 to 10, at 0, 4, 8, 12, and 24 h after the operation. The values on the numerical rating scale for pain in group B were significantly lower than those in group A at 4, 8, and 12 h after the operation. There were no significant differences between the groups in the values on the numerical rating scale for nausea or itching throughout the time course of the study. No patient in either group showed hypoxemia or respiratory depression throughout the time course. The results show that minidose intrathecal morphine provides a good analgesic effect without side effects, and it would be an effective and safe procedure for bipolar hip prosthesis in seniors.

The change of oxygen consumption after withdrawal of sedation is controversial. We evaluated the changes of sedation depth, oxygen consumption and hemodynamics after withdrawal of midazolam sedation in the patients undergoing major abdominal surgery.We evaluated 18 patients after major abdominal surgery. Midazolam was used for intravenous sedation after admission to the ICU. Midazolam was administered at a bolus dose of 0.1 mg kg(-1), followed by continuous infusion at 0.04 mg kg(-1) hr(-1), which was adjusted every 2 hrs to achieve a desired level of sedation of 4 on Ramsay sedation scale (RSS). After about 14 hours of sedation, we stopped the infusion of midazolam. From that time, we measured systolic and mean arterial pressure, heart rate, minute volume and oxygen consumption, and evaluated RSS every 5 minutes for 1 hour. We evaluated RSS as sedation depth, oxygen consumption index (V(O2)I) and rate pressure product (RPP=systolic arterial pressure x heart rate) as hemodynamic parameters.RSS significantly decreased gradually, but the other parameters including V(O2)I and RPP were unchanged.After withdrawal of midazolam sedation in the patients undergoing major abdominal surgery, the sedation depth became lighter, but V(O2)I and RPP were unchanged.

Adequate volume therapy is essential for stable hemodynamics and sufficient urinary output perioperatively. Hydroxyethyl starch (HES) has been reported to attenuate the microvascular hyperpermeability which occasionally occurs in surgical patients. This study was carried out to evaluate the effect of low-molecular-weight HES on the urinary microalbumin/creatinine ratio (MACR), a marker of microvascular permeability, in surgical patients.In a prospective, controlled, and randomized clinical trial, 21 patients undergoing abdominal surgery were divided into two groups. Group HES (n = 10) received HES at 2 ml x kg(-1) x h(-1) during surgery and at 1 ml x kg(-1) x h(-1) after surgery, and additionally they received acetated Ringer's solution (AR) at a rate to keep central venous pressure (CVP) 5 mm Hg. Group AR (n = 11) received AR at a rate to keep CVP at 3-5 mmHg. MACR, soluble intercellular adhesion molecule-1 (sICAM-1), and urinary output were measured intermittently in the perioperative period.MACR was significantly increased during surgery in both groups. There was no significant difference in MACR between the two groups throughout the study period. The serum concentration of sICAM-1 decreased during surgery in both groups, and that in group HES was significantly lower than that in group AR at the end of surgery. Postoperative urinary output in group HES was greater than that in group AR. The intensive care unit (ICU) stay in group HES was shorter than that in group AR.Although low-molecular-weight HES does not improve microvascular hyperpermeability, the expansion of the intravascular volume by HES results in higher urinary output in the postoperative period than that seen with crystalloid solution. The lower concentration of sICAM-1 after surgery may be due to hemodilution.

Malignant hyperthermia (MH) is an autosomal dominant disorder of skeletal muscle calcium regulation, and the rate of calcium-induced calcium release (CICR), determined by using skinned fibers of skeletal muscle, has been employed as a diagnostic test for MH susceptibility in Japan. The ryanodine receptor (RYR1), encoding the major calcium-release channel in skeletal muscle sarcoplasmic reticulum, has been shown to be mutated in a number of MH pedigrees. We experienced the detection of accelerated CICR and/or an RYR1 mutation in a patient with an MH episode and his family. Accelerated CICR and an RYR1 mutation (c.14512C>G, p.L4838V) were found in the patient and his father. The MH-causative mutation (c.14512C>G, p.L4838V) was also found in his brother and his son (resulting in the diagnosis of MH without the CICR test), but the mutation was not found in his mother or two daughters. With the detection of the family-specific mutation in other family members, the diagnosis of MH was made without the invasive CICR test.

A 50-year-old male patient developed diabetic ketoacidosis with shock, acute renal failure treated with continuous hemodiafiltration (CHDF) and high serum CPK levels. Because of acute onset of ketoacidosis accompanied with an elevation of serum amylase, and negative findings of antibodies associated with autoimmune type 1 diabetes mellitus, he was diagnosed as a fulminant type 1 diabetes mellitus, which is a newly established subtype of type 1 diabetes mellitus. We managed to keep blood glucose concentrations within 150-200 mg x dl(-1) with continuous insulin intravenous infusion, and controlled circulation with dopamine. Since the blood glucose on admission was extremely high (1,870 mg x dl(-1)), the severe dehydration due to extreme hyperglycemia might have caused acute renal failure (ARF) and rhabdomyolysis. He was treated with CHDF for them. In a case of fulminant type 1 diabetes mellitus complicated with ARF early intensive support including CHDF for ARF must be considered in addition to intensive insulin therapy.

We investigated the clinical usefulness of the Fick method using central venous oxygen saturation ScvO2 and cardiac output (CO) measured by pulse dye densitometry (PDD) for monitoring oxygen consumption VO2. This prospective clinical study was performed in 28 mechanically ventilated postoperative patients after major abdominal surgery. VO2 was determined by two methods, i.e., the Fick method and indirect calorimetry. The Fick method was employed using CO measured by PDD and VO2 obtained from a central venous catheter (CVC). VO2 measured by indirect calorimetry was averaged for 15 min. Fifty-six sets of measurements were performed. VO2 values determined by the Fick method were significantly lower than those measured by indirect calorimetry (110 +/- 29 vs 148 +/- 28 ml x min(-1) x m(-2); P < 0.01). Bland and Altma analysis showed that the mean bias and precision were 33 ml x min(-1) x m(-2) and 32 ml x min(-1) x m(-2), respectively. The correlation between the two measurements of VO2 was weak (r (2) = 0.145; P = 0.0038), indicating that the Fick method using PDD and ScvO2 is not clinically acceptable for the monitoring of VO2.

Acute respiratory distress syndrome (ARDS) is the most severe lung injury caused by many pathologic states. We treated a patient who suffered from ARDS caused by splenic infarction. A 75-year-old patient had a gastric cancer with multiple lung and liver metastasis. During anti-cancer therapy, she developed a high fever (above 39 degrees C) and a chest and an abdominal CT scan revealed splenic infarction. Hypoxia progressed gradually and she was transferred to ICU with tracheal intubation. Mechanical ventilation was performed according to open lung strategy, but she did not recover. On ICU day 3, the bilateral infiltration shadow on her chest X-ray was pointed out, and she had a low central venous pressure. We diagnosed her ARDS. The administration of methylprednisolone was started according to Meduri's report. Hypoxia was improved gradually and on ICU day 7, she was weaned from mechanical ventilation, and extubated. On ICU day 8, she was returned to her ward without ventilatory support.

The purpose of this study was to clarify whether prostaglandin E1 (PGE(1)) or corticosteroid could increase blood flow in the nerve root because neurologic symptoms in spinal stenosis may be based on the vascular insufficiency in the nerve root. Fifty-seven patients undergoing lumbar diskectomy were randomly assigned to one of three groups. Each group received one of three protocols for intravenous injection: 10 mL of saline solution, group A (n = 19); 10 mL of PGE(1) (20 microg) solution, group B (n = 19); and 10 mL of dexamethasone (8 mg) solution, group C (n = 19). After lumbar diskectomy, a probe for laser Doppler flowmetry was placed directly on the lumbar nerve root. Nerve root blood flow (RBF) velocity and mean arterial pressure (MAP) were measured before injection (T0), 5 minutes after the start of injection (T1), 10 minutes after the start of injection (T2), and 10 minutes after the end of injection (T3). In groups A and C, these did not change throughout the time course. In group B, MAP decreased significantly at T1 (92%; P

Objective To analyze quantitatively the relationship between sedation and resting energy expenditure or oxygen consumption in postoperative patients. Design A prospective, clinical study. Setting An eight-bed intensive care unit at a university hospital. Patients Thirty-two postoperative patients undergoing either esophagectomy or surgery of malignant tumors of the head and neck who required mechanical ventilation and sedation for > or = 2 days postoperatively. Interventions None. Measurements and main results A total of 133 metabolic measurements were performed. Ramsay sedation scale (RSS), body temperature, and the dose of midazolam were evaluated at the time of the metabolic cart study. All patients received analgesia with buprenorphine at a fixed dose of 0.625 microg x kg(-1) x hr(-1) continuously. Midazolam was used for induction and maintenance of intravenous sedation after admission to the intensive care unit. The initial dose was 0.04 mg x kg(-1) x hr(-1) and was adjusted to achieve a desired depth of sedation at 3, 4, or 5 on the RSS every 4 hrs. The degree of sedation was classified into three states: light sedation (RSS 2-3; n = 49), moderate sedation (RSS 4; n = 39), and heavy sedation (RSS 5-6; n = 45). Results With increasing the depth of sedation, oxygen consumption index (mL x min(-1) x m(-2)), resting energy expenditure index (REEI; kcal x day(-1) x m(-2)), and REE/basal energy expenditure (BEE) decreased significantly. Oxygen consumption index (mean +/- SD), REEI, and REE/BEE were 151 +/- 18, 1032 +/- 120, and 1.29 +/- 0.17 in the light sedation, 139 +/- 22, 947 +/- 143, and 1.20 +/- 0.16 in the moderate sedation, and 125 +/- 16, 865 +/- 105, and 1.13 +/- 0.12 in the heavy sedation, respectively. Conclusion An increase in the depth of sedation progressively decreases in oxygen consumption index and REEI in postoperative patients.

Acute withdrawal syndromes, including agitation and a long weaning time, are common adverse effects after long-term sedation with midazolam. We performed this study to determine whether the sequential use of midazolam and propofol could reduce adverse effects as compared with midazolam alone. We studied 26 patients receiving mechanical ventilation for three or more days after surgery. Patients were randomly assigned to two groups. In Group M, patients were sedated with midazolam alone. In Group M-P, midazolam was switched to propofol approximately 24 h before the expected stopping of sedation. The level of sedation was maintained at 4 or 5 on the Ramsay sedation scale. The sedation agitation scale was evaluated for 24 h after extubation. The recovery time from stopping of sedation to extubation was significantly shorter in Group M-P (1.3 +/- 0.4 h) compared with Group M (4.0 +/- 2.4 h). The incidence of agitation in Group M-P (8%) was significantly less frequent than that in Group M (54%). The results indicate that sequential use of midazolam and propofol for long-term sedation could reduce the incidence of agitation compared with midazolam alone.Our study indicates that sequential use of midazolam and propofol could reduce the incidence of agitation compared with midazolam alone.

UNLABELLED We sought to determine the hemodynamic and cardioprotective effects of sevoflurane in canine stunned myocardium. Forty-nine dogs were allocated to one of seven groups (n = 7 for each). In six separate groups, dogs received vehicle, glibenclamide (a nonselective adenosine triphosphate-dependent potassium [K(ATP)] channel antagonist) (0.3 mg/kg IV) or 5-hydroxydecanoic acid (a mitochondrial K(ATP) channel antagonist) (5 mg/kg IV) in the presence or absence of 1 minimum alveolar concentration (1 MAC) sevoflurane. In an additional group, dogs received 1 MAC sevoflurane with hemodynamic correction. Regional myocardial contractility was evaluated with segment shortening. Measurements were made before and during 15-min ischemia and 90-min reperfusion. Recovery of segment shortening 90 min after reperfusion was significantly improved in the dogs anesthetized with sevoflurane either with or without hemodynamic correction (70.1 +/- 4.2 and 75.9 +/- 3.1% of baseline, respectively), whereas the recovery was poor in control and glibenclamide or 5-hydroxydecanoic acid pretreated dogs (33.3 +/- 4.3, 33.8 +/- 6.8, and 45.0 +/- 5.5% of baseline, respectively). Regional myocardial perfusion showed no significant difference among groups. The results indicate that sevoflurane has a cardioprotective effect mediated through activation of mitochondrial K(ATP) channels and independent of coronary blood flow or reduction in cardiac work. IMPLICATIONS Sevoflurane exerts a cardioprotective effect that is mediated via activation of adenosine triphosphate-sensitive potassium channels in ischemic canine hearts.

To evaluate the effect of controlled hypotension combined with acute hypervolemic or normovolemic hemodilution on the splanchnic perfusion in the clinical setting.Randomized, prospective study.Inpatient surgery at Nagasaki Rosai Hospital.28 ASA physical status I and II patients scheduled for total hip arthroplasty.Patients were randomly divided into two groups. Group A (n = 14) received controlled hypotension with acute normovolemic hemodilution (ANH). Group B (n = 14) received controlled hypotension with acute hypervolemic hemodilution (HHD). ANH was produced by drawing approximately 1000 mL of blood and replacing it with the same amount of 6% hydroxyethyl starch solution (HES). HHD was produced by preoperative infusion of 1000 mL of 6% HES without removing blood. The final hematocrit values were 24+/-2% (mean +/- SD) in Group A and 25+/-3% in Group B. Controlled hypotension was induced with prostaglandin E1 (PGE1) to maintain mean arterial blood pressure at 55 mmHg for 80 minutes.Measurements included the gastric pH (pHi), the arterial blood pH (pHa), and plasma lactate. These indices were measured before hemodilution, after hemodilution, 80 minutes after starting hypotension, 60 minutes after recovery from hypotension, and on the first postoperative day. The value of pHi was measured by tonometric method.The pHa and lactate values showed no change in either group A or group B throughout the time course. Gastric pHi values in group A showed a significant decrease from 7.424+/-0.033 to 7.335+/-0.038 (p0.05) after hemodilution, whereas it showed no further decrease at 80 minutes after starting hypotension and 60 minutes after recovery from hypotension. The pHi values in group B showed no significant decrease after hemodilution and no further change at 80 minutes after starting hypotension.HHD does not impair splanchnic perfusion, whereas ANH might cause impairment. Controlled hypotension with prostaglandin E1 would not impair splanchnic perfusion in combination with either HHD or ANH.

UNLABELLED The combination of propofol and ketamine has been used for total IV anesthesia. This study was designed to clarify the effects of propofol-ketamine anesthesia on cerebral circulation by using transcranial Doppler ultrasonography. In Study 1, we examined the time course of time-mean middle cerebral artery blood flow velocity (Vmca) after ketamine (n = 10) or saline (n = 6) administration during propofol anesthesia. In Study 2, CO(2) responses were measured under the following conditions: awake (Group C, n = 7), propofol anesthesia (Group D, n = 7), and propofol-ketamine anesthesia (Group E, n = 8). Ketamine administration during propofol anesthesia administration did not affect Vmca, mean arterial pressure, or heart rate. Vmca under normocapnia in Groups D and E were 36 +/- 3 and 37 +/- 3 cm/s (mean +/- SE), respectively. The values were significantly lower than that of Group C (70 +/- 3 cm/s). The CO(2) response slopes of Groups D and E were significantly lower than that of Group C, although there was no significant difference between Groups D and E. These results suggest that ketamine does not influence Vmca or the cerebrovascular CO(2) response during propofol anesthesia administration, although the sample size in each group was small. IMPLICATIONS Our study suggests that ketamine does not influence middle cerebral artery blood flow velocity or the cerebrovascular CO(2) response assessed by transcranial Doppler ultrasonography during propofol anesthesia administration in patients without neurological complications.

We investigated the effects of controlled hypotension with haemodilution under isoflurane anaesthesia on splanchnic perfusion in elderly patients. We determined the intramucosal pH using gastric tonometry in 28 patients scheduled for hip surgery. Patients without cardiac disease were assigned to two groups according to age. Group A (adult patients, n = 14) included patients aged less than 60 years (range 29-58 years, 47 +/- 11 years, mean +/- SD) and group B (elderly patients, n = 14) more than 65 years (68-78 years, 72 +/- 5 years). Anaesthesia was maintained with N2O-O2-isoflurane. After induction of anaesthesia, haemodilution was produced by drawing 800-1000 mL of blood and replacing it with the same amount of hydroxyethyl starch. Final haematocrit values were 23-24% in all groups. Controlled hypotension was induced with prostaglandin E1 (PGE1) and mean blood pressure was maintained at approximately 60 mmHg for approximately 80 min. Measurements, including gastric intramucosal pH (pHi), arterial blood pH (pHa) and serum lactate were measured before haemodilution (T0), after haemodilution (T1), 80 min after starting hypotension (T2), 60 min after recovery from hypotension (T3) and on the 1st post-operative day (T4). The values of pHa and lactate showed no change in the groups throughout the time course. The gastric pHi values showed significant decreases from 7.418 +/- 0.035 to 7.334 +/- 0.024 (P < 0.05) in group A and from 7.428 +/- 0.029 to 7.320 +/- 0.039 (P < 0.05) in group B after haemodilution, while no further decreases were found at 80 min after starting the hypotension (7.329 +/- 0.038 in group A and 7.322 +/- 0.031 in group B) and 60 min after recovery from hypotension (7.331 +/- 0.029 in group A and 7.328 +/- 0.034 in group B). It can be concluded that moderate haemodilution under isoflurane anaesthesia might impair splanchnic perfusion in adult and elderly patients. The addition of controlled hypotension with PGE1 or an increase in age did not further impair splanchnic perfusion nor the splanchnic oxygen supply.

Study Objectives: To evaluate renal function during and after hypotensive anesthesia with sevoflurane compared with isoflurane in the clinical setting. Design: Randomized, prospective study. Setting: Inpatient surgery at Rosai Hospital. Patients: 26 ASA physical status I and II patients scheduled for orthopedic surgery. Interventions: Patients received isoflurane, nitrous oxide (N 2 O), and fentanyl (Group I=isoflurane group; n=13) or sevoflurane, N 2 O, and fentanyl (Group S=sevoflurane group; n=13). Controlled hypotension was induced with either isoflurane or sevoflurane to maintain mean arterial pressure at 60 mmHg for 120 minutes. Measurements and Main Results: Measurements included serum inorganic fluoride (previously speculated to influence renal function), creatinine clearance (CCr; to assess renal glomerular function), urinary N-acetyl-β-D-glucosaminidase (NAG; to assess renal tubular function), blood urea nitrogen (BUN), and serum creatinine (as clinical renal function indices). Serum fluoride, CCr, and NAG were measured before hypotension, 60 minutes, and 120 minutes after the start of hypotension, 30 minutes after recovery of normotension, and on the first postoperative day. BUN and serum creatinine were measured preoperatively and on the third and seventh postoperative days. Minimum alveolar concentration times hour was 3.6 ± 1.8 in Group I and 4.0 ± 0.7 in Group S. In both groups, BUN and serum creatinine did not change, and CCr significantly decreased after the start of hypotension. In Group I, serum fluoride and NAG did not change. In Group S, serum fluoride significantly increased after the start of hypotension compared with prehypotension values and compared with Group I values. In addition, NAG significantly increased at 120 minutes after the start of hypotension and at 30 minutes after recovery of normotension, but returned to prehypotension values on the first postoperative day. Conclusions: Two hours of hypotensive anesthesia with sevoflurane under 5 L/min total gas flow in patients having no preoperative renal dysfunction transiently increased NAG, which is consistent with a temporary, reversible disturbance of renal tubular function.

To evaluate the effect of controlled hypotension combined with hemodilution on gastric intramural pH in the clinical setting.Randomized, prospective study.Inpatient surgery at Nagasaki Rosai Hospital.30 ASA physical status I and II patients scheduled for total hip arthroplasty.Patients were randomly divided into two groups. Group A (n = 15) received controlled hypotension with mild hemodilution. Group B (n = 15) received controlled hypotension with moderate hemodilution. Hemodilution was carried out after induction of anesthesia. Drawn blood was replaced with 6% hydroxyethyl starch solution. Final hematocrit values were 32 +/- 2% (mean +/- SD) in Group A and 23 +/- 2% in Group B. Controlled hypotension was induced with prostaglandin E1 (PGE1) to maintain mean arterial blood pressure at 55 mmHg for 80 minutes.Measurements included gastric intramural pH (pHi), arterial blood pH (pHa), and plasma lactate. These indices were measured before hemodilution, after hemodilution, 80 minutes after starting hypotension, 60 minutes after recovery from hypotension, and on the first postoperative day. The value of pHi was measured by tonometry. The pHa and lactate values showed no change in either Group A or Group B throughout the time course. Gastric pHi values showed no change in Group A throughout the time course. The pHi value in Group B showed a significant decrease from 7.420 +/- 0.028 to 7.339 +/- 0.034 (p0.05) after hemodilution, while it showed no further decrease at 80 minutes after starting hypotension (7.331 +/- 0.039) and 60 minutes after recovery from hypotension (7.330 +/- 0.048).The results suggest that moderate hemodilution, such as 23% of hematocrit value, might impair oxygenation in gastrointestinal mucosa, whereas controlled hypotension induced by PGE1 combined with the hemodilution would not increase this impairment.

We investigated the effect of a new ultrashort-acting β-blocker, ONO-1101, on hemodynamic responses to isoflurane inhalation and tracheal intubation.Fifty-four ASA PS 1 or 2 patients were randomly allocated to receive either ONO-1101, 0.04 mg·kgSignificant increases in heart rate occurred in both groups in response to isoflurane inhalation and tracheal intubation, but the magnitude of the increase was significantly less in the ONO-1101 group. Blood pressure increased after tracheal intubation in the saline group but remained unchanged in the ONO-1101 group. Plasma concentrations of norepinephrine increased after induction and intubation in both groups, with no significant difference between the groups.ONO-1101 infusion is effective for the attenuation of hemodynamic responses to isoflurane inhalation and tracheal intubation.

Study Objective: To evaluate the catecholamine and renin-angiotensin response during controlled hypotension combined with hemodilution in the clinical setting. Design: Randomized, prospective study. Setting: Inpatient surgery at Nagasaki Rosai Hospital. Patients: 30 ASA physical status I and II female patients scheduled for total hip arthroplasty. Interventions: Patients were randomly divided into three groups. Group A (N = 10) received hemodilution alone. Group B (N = 10) received controlled hypotension alone. Group C (N = 10) received hemodilution plus controlled hypotension. Hemodilution was carried out after induction of anesthesia, in which drawn blood was replaced with 6 % hydroxyethyl starch, and the final hematocrit value was approximately 22%. Controlled hypotension was induced with prostaglandin E 1 (PGE 1 ) to maintain mean arterial blood pressure at 55 mmHg for 80 minutes. Measurements and Main Results: Measurements included plasma renin activity (RA) and plasma concentrations of angiotensin-II (AG-II), aldosterone (AS), norepinephrine (NE), and epinephrine (EP). These indices were measured before hemodilution, after hemodilution, 80 minutes after starting hypotension, and 60 minutes after recovery from hypotension. Hemodilution alone caused no significant change in the values throughout the time course. Controlled hypotension alone caused significant increases in plasma concentrations of NE (+295%) and EP (+203%) at 80 minutes after starting hypotension, whereas it caused no change in plasma RA and plasma concentrations of AG-II and AS. Hemodilution plus controlled hypotension caused significant increases in plasma RA(+271%) and plasma concentrations of AG-II (+188%), AS (+199%), NE (+279%), and EP (+184%) at 80 minutes after starting hypotension. Conclusion: The combination of hemodilution and PGE 1 induced controlled hypotension causes significant responses, especially in a renin-angiotensin-aldosterone system under isoflurane anesthesia.

This study was carried out to evaluate the effects of fentanyl on cardiovascular and catecholamine responses during rapid sequence induction (RSI) in hypertensive patients. Twenty-eight patients were allocated into one of 3 groups: group 1 (n=7) consisted of normotensive patients receiving no fentanyl, group 2 (n=10) consisted of normotensive patients receiving fentanyl, and group 3 (n=11) consisted of hypertensive patients receiving fentanyl. RSI was performed with thiamylal (4mg·kg−1) and succinylcholine (2mg·kg−1) for all groups. In groups 2 and 3, fentanyl (4 μg·kg−1) was given prior to induction. Measurements including systolic arterial pressure (SAP) and heart rate (HR) were made at preinduction (T1), preintubation (T2), 1 min after intubation (T3), and 3 min after intubation (T4). Simultaneously, plasma concentrations of epinephrine (E) and norepinephrine (NE) were measured at T1 and T3. Group 1 showed significant increases in SAP, HR, and NE at T3 as compared to T1. Group 2 showed a significant increase in HR at T3 but not in SAP or catecholamines. Group 3 showed no increase in SAP, HR, or catecholamines throughout the time course. The results suggest that fentanyl is useful to suppress sympathoadrenal and cardiovascular responses to RSI in hypertensive patients as well as normotensive patients.

Study Objective: To evaluate the effects of hemodilution during controlled hypotension on the hepatic, renal, and pancreatic function in the clinical setting. Design: Randomized, prospective study. Setting: Inpatient surgery at Rosai Hospital. Patients: 20 ASA status I and II patients scheduled for total hip arthroplasty. Interventions: Hemodilution was carried out after induction of anesthesia, in which drawn blood was replaced with dextran solution to achieve final hematocrit (Hct) of 31% (Group A=mild hemodilution group, N=10) or 23% (Group B=moderate hemodilution group, N=10). In both groups, controlled hypotension was induced with prostaglandin E 1 (PGE 1 ) to maintain mean arterial blood pressure at 55 mmHg for 80 minutes. Measurements and Main Results: Measurements included arterial ketone body ratio (AKBR, aceto-acetate/3-hydroxybutyrate) for hepatic cellular function, pancreatic phospholipase A 2 (P-PLA 2 ) for pancreatic cellular function, and urine N-acetyl-β-dglucosaminidase (NAG index) for cellular function of the renal tubule. These indices were measured before hemodilution, after hemodilution, 80 minutes after starting hypotension, 60 minutes after recovery of normotension, and on the first postoperative day. Neither AKBR norP-PLA2 showed a significant change throughout the time course of the study in either group. Urine-NAG index showed a significant increase in moderate hemodilution group at 60 minutes after recovery of normotension (+136%) and on the first postoperative day (+149%) compared with prehemodilution value, whereas it showed no significant change in the mild hemodilution group. Blood urea nitrogen and serum creatinine measured postoperatively were within normal range. Conclusions: PGE 1 -induced hypotension combined with moderate hemodilution using dextran, such as 23 % of Hct value, maintains hepatic and pancreatic function but causes damage to the renal tubular cells.

The effects of the prolonged 3-hour and 6-hour controlled hypotension induced by prostaglandin E(1) (PGE(1)) on renal tubular function have been comparatively studied with trimethaphan (TMP; 3-hour hypotensive anesthesia) and enflurane deep anesthesia (6-hour hypotensive anesthesia), using the urine N-acetyl-Beta-D-glucosaminidase (NAG index) and the serum and urine Beta(2)-microglobulin (fractional clearance of Beta(2)-m; Fc-Beta(2)-m) as markers. During 3-hour and 6-hour controlled hypotension PGE(1), NAG index and Fc-Beta(2)-m and urine volume could be maintained without remarkable changes. In the group with TPM, NAG index and Fc-Beta(2)-m significantly increased. The increasing trend was also noted over time in deep anesthesia with enflurane. On 1st postoperative day, Fc-Beta(2)-m significantly increased in PGE(1) group in both 3-hour and 6-hour hypotensive anesthesia, whereas it restored to normal on 2nd postoperative day. Also, in TMP and enflurane deep anesthesia, Fc-Beta(2)-m significantly increased on 1st postoperative day. With the latter, significant increase was also observed on 2nd postoperative day. These results suggest that, in 3-hour and 6-hour controlled hypotension induced by PGE(1), renal tubular function is normally maintained and that it is useful for prolonged controlled hypotensive anesthesia. However, further study is necessary because tubular dysfunction might appear on 1st postoperative day.

ブロマゼパム坐剤の麻酔前投薬としての効果を客観的に評価するために, 血漿および尿中カテコラミン (CA) 濃度を測定し, 麻酔前投薬非投与群 (C群), ジアゼパム前投薬群 (D群) と比較検討した. ブロマゼパム前投薬群 (B群) は, 3mgを手術前夜に投与し, D群は, 麻酔導入約1時間前に10mgを筋注した. 血漿CA濃度は, エピネフリンのみD群, B群で有意な低下傾向にあり, その低下度は, D群よりB群のほうが大きかった. 尿中CA濃度もB群, D群は, C群に比べ優位に低下していた. 以上より, ブロマゼパム坐剤の手術前夜の投与は, ジアゼパム筋注と同程度かそれ以上に麻酔導入前の副腎-交感神経系緊張を抑制すると考えられた.