Analysis of VH gene rearrangement and somatic hypermutation in Sjogren's syndrome and IgG4-related sclerosing sialadenitis.

IgG4-related sclerosing sialadenitis is currently considered as an autoimmune disease distinct from Sjogren's syndrome (SS) and responds extremely well to steroid therapy. To further elucidate the characteristics of IgG4-related sclerosing sialadenitis, we analysed VH fragments of IgH genes and their somatic hypermutation in SS (n = 3) and IgG4-related sclerosing sialadenitis (n = 3), using sialolithiasis (n = 3) as a non-autoimmune control. DNA was extracted from the affected inflammatory lesions. After PCR amplification of rearranged IgH genes, at least 50 clones per case (more than 500 clones in total) were sequenced for VH fragments. Monoclonal IgH rearrangement was not detected in any cases examined. When compared with sialolithiasis, there was no VH family or VH fragment specific to SS or IgG4-related sclerosing sialadenitis. However, rates of unmutated VH fragments in SS (30%) and IgG4-related sclerosing sialadenitis (39%) were higher than that in sialolithiasis (14%) with statistical significance (P = 0.0005 and P < 0.0001, respectively). This finding suggests that some autoantibodies encoded by germline or less mutated VH genes may fail to be eliminated and could play a role in the development of SS and IgG4-related sclerosing sialadenitis.

Standard steroid treatment for autoimmune pancreatitis.

OBJECTIVE: To establish an appropriate steroid treatment regimen for autoimmune pancreatitis (AIP). METHODS: A retrospective survey of AIP treatment was conducted in 17 centres in Japan. The main outcome measures were rate of remission and relapse. RESULTS: Of 563 patients with AIP, 459 (82%) received steroid treatment. The remission rate of steroid-treated AIP was 98%, which was significantly higher than that of patients without steroid treatment (74%, 77/104; p<0.001). Steroid treatment was given for obstructive jaundice (60%), abdominal pain (11%), associated extrapancreatic lesions except the biliary duct (11%), and diffuse enlargement of the pancreas (10%). There was no relationship between the period necessary to achieve remission and the initial dose (30 mg/day vs 40 mg/day) of prednisolone. Maintenance steroid treatment was given in 377 (82%) of 459 steroid-treated patients, and steroid treatment was stopped in 104 patients. The relapse rate of patients with AIP on maintenance treatment was 23% (63/273), which was significantly lower than that of patients who stopped maintenance treatment (34%, 35/104; p = 0.048). From the start of steroid treatment, 56% (55/99) relapsed within 1 year and 92% (91/99) relapsed within 3 years. Of the 89 relapsed patients, 83 (93%) received steroid re-treatment, and steroid re-treatment was effective in 97% of them. CONCLUSIONS: The major indication for steroid treatment in AIP is the presence of symptoms. An initial prednisolone dose of 0.6 mg/kg/day, is recommend, which is then reduced to a maintenance dose over a period of 3-6 months. Maintenance treatment with low-dose steroid reduces but dose not eliminate relapses.

Neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD) as a cause of liver disease in infants in the UK.

Citrin deficiency is a disorder with two phenotypes: neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD), and adult-onset type II citrullinaemia (CTLN2). NICCD presents in the first few weeks of life with prolonged cholestasis and metabolic abnormalities including aminoacidaemia (notably citrulline, tyrosine, threonine, arginine and methionine) and galactosuria. Symptoms resolve within the first year of life, thus making a diagnosis difficult after this time. Although patients subsequently remain generally healthy, some may develop more severe symptoms of CTLN2, characterized by neurological changes, one or more decades later. To date more than 400 cases have been reported, almost all from East Asia (mainly Japan). Here we describe the first two cases of NICCD in infants from the UK, one of caucasian origin and one of Pakistani origin. Both showed typical clinical and biochemical changes with a diagnosis confirmed by the presence of previously unreported mutations in the SLC25A13 gene. The presence of citrin deficiency in other ethnic groups means that NICCD needs to be considered in the diagnosis of any neonate with an unexplained cholestasis. We discuss both the difficulties in diagnosing these patients in populations where very few DNA mutations have been identified and the problems faced in the management of these patients. These findings also raise the possibility of adults with CTLN2 in whom a diagnosis has yet to be made.

An L-dopaergic relay from the posterior hypothalamic nucleus to the rostral ventrolateral medulla and its cardiovascular function in anesthetized rats.

We have proposed that L-3,4-dihydroxyphenylalanine (L-DOPA) is a neurotransmitter in the central nervous system [Misu Y. et al. (1996) Prog. Neurobiol. 49, 415-454]. Herein, we attempt to clarify whether lesions in the posterior hypothalamic nucleus decrease the tissue content of L-DOPA in the rostral ventrolateral medulla. We also attempt to clarify whether or not endogenous L-DOPA is evoked by electrical stimulation of the posterior hypothalamic nucleus. It is possible that evoked L-DOPA functions as a transmitter candidate to activate pressor sites of the rostral ventrolateral medulla in anesthetized rats. Electrolytic lesions were made in the bilateral posterior hypothalamic nucleus by a monopolar direct current of 2 mA for 10 s, 10 days before measurements. The effect of the lesions was to selectively decrease the tissue content of L-DOPA by one-half in the right rostral ventrolateral medulla. Decreases in the amounts of dopamine, noradrenaline or adrenaline were not observed. Decreases were also not evident in the right caudal ventrolateral medulla. During microdialysis of the right rostral ventrolateral medulla, extracellular basal levels of L-DOPA and three types of catecholamine were consistently detectable by high-performance liquid chromatography with electrochemical detection. Tetrodotoxin (1 microM) perfused into the right rostral ventrolateral medulla gradually decreased basal levels of L-DOPA by 25%; it decreased basal levels of noradrenaline and adrenaline by 25-30% and dopamine levels by 40%. Intensive electrical stimulation of the ipsilateral posterior hypothalamic nucleus (50 Hz, 0.3 mA, 0.1 ms duration, twice for 5 min at an interval of 5 min) selectively caused the release of L-DOPA in a repetitive and constant manner. The stimulation was accompanied by hypertension and tachycardia. However, catecholamines were not released. Tetrodotoxin suppressed the release of L-DOPA, but partially inhibited hypertension with only a slight inhibition of tachycardia evoked by stimulation of the posterior hypothalamic nucleus. L-DOPA methyl ester, a competitive L-DOPA antagonist, was bilaterally microinjected into pressor sites of the rostral ventrolateral medulla at 1.5 microg x 2 and 3 microg x 2. The antagonist dose-dependently and consistently antagonized pressor and tachycardiac responses to mild transient stimulation of the unilateral posterior hypothalamic nucleus (33 Hz, 0.2 mA, 0.1 ms duration, for 10 s). In addition, the antagonist alone (3 microg x 2) elicited hypotension and bradycardia. These results show that an L-DOPAergic relay may project from the posterior hypothalamic nucleus directly to pressor sites of the rostral ventrolateral medulla and/or indirectly to certain neurons near pressor sites in microcircuits of the same region. When released, L-DOPA appears to function tonically to activate pressor sites; it also appears to be involved in the maintenance and regulation of blood pressure and heart rate.

Involvement of barium-sensitive K+ channels in endothelium-dependent vasodilation produced by hypercapnia in rat mesenteric vascular beds.

1. We examined the vasodilatory effect of hypercapnia in the rat isolated mesenteric vascular bed. The preparation was perfused constantly (5 ml min(-1) with oxygenated Krebs-Ringer solution, and the perfusion pressure was measured. In order to keep the extracellular pH (pHe) constant (around 7.35) against a change in CO2, adequate amounts of NaHCO3 were added to Krebs-Ringer solution. 2. In the endothelium intact preparations, an increase in CO2 from 2.5% to 10% in increments of 2.5% decreased the 10 microM phenylephrine (PE)-produced increase in the perfusion pressure in a concentration-dependent manner. Denudation of the endothelium by CHAPS (3-[(3-cholamidopropyl)-dimethylammonio]-1-propanesulphonate) (5 mg l(-1), 90 s perfusion) abolished the vasodilatory effect of hypercapnia. 3. An increase in CO2 from 5% to 10% reduced the increases in the perfusion pressure produced by 10 microM PE and 400 nM U-46619 by 48% and 44%, respectively. NG-monomethyl-L-arginine (100 microM) and indomethacin (10 microM) did not affect the vasodilatory effect of hypercapnia, whereas the vasodilatory response of the preparation to hypercapnia disappeared when the preparation was contracted by 60 mM K+ instead of PE or U-46619. 4. The vasodilatory effect of hypercapnia observed in the PE- or U-46619-precontracted preparation was affected by neither tetraethylammonium (1 mM), apamin (500 microM), glibenclamide (10 microM), nor 4-aminopyridine (1.5 mM). On the other hand, pretreatment with Ba2+ at a concentration of 0.3 mM abolished the hypercapnia-produced vasodilation. 5. An increase in the concentration of K+ in Krebs-Ringer solution from 4.5 mM to 12.5 mM in increments of 2 mM reduced the PE-produced increase in the perfusion pressure in a concentration-dependent manner. Pretreatment of the preparations with not only Ba2+ (0.3 mM) but also CHAPS abolished the vasodilatory effect of K+. 6. The results suggest that an increase in CO2 produces vasodilation by an endothelium-dependent mechanism in the rat mesenteric vascular bed. The membrane hyperpolarization of the endothelial cell by an activation of the inward rectifier K+ channel seems to be the mechanism underlying the hypercapnia-produced vasodilation. Neither nitric oxide nor prostaglandins are involved in this response.

Prostaglandin E1 potentiation of the spontaneous phasic contraction of rat isolated portal vein by a cyclopiazonic acid-sensitive mechanism.

1. The effect of prostaglandin E1 (PGE1) on the spontaneous phasic contraction of the rat isolated portal vein was studied. 2. The isolated portal vein exhibited spontaneous phasic contractions. Removal of Ca2+ from Krebs-Ringer solution or application of nifedipine abolished the spontaneous contraction, indicating that the contraction depends exclusively on Ca2+ influx through L-type Ca2+ channels. On the other hand, cyclopiazonic acid (CPA), a specific inhibitor of Ca(2+)-ATPase of sarcoplasmic reticulum (SR) increased the amplitude of the contractions, suggesting that the SR regulates the spontaneous contractions negatively by sequestration of Ca2+ entering through L-type Ca2+ channels and buffering the rise in cytosolic Ca2+. 3. PGE1 increased the amplitude of the spontaneous contraction in a concentration-dependent manner without affecting the resting tension. The effect was completely abolished by nifedipine. Bay K 8644 and phenylephrine (PE) also increased the amplitude of the contraction in a concentration-dependent manner. PGE1 at a concentration of 1 microM. Bay K 8644 at 100 nM and PE at 30 nM doubled the amplitude, respectively. 4. Pretreatment with 1 microM CPA abolished the effect of PGE1, but the effects of Bay K 8644 and PE were not inhibited by pretreatment with CPA. In contrast, 10 microM ryanodine attenuated the effect of PE without affecting the contractile effect of PGE1. 5. When the SR was depleted of Ca2+ by repeated applications of caffeine in a nominally Ca(2+)-free Krebs-Ringer solution, it took about 120 s to restore the spontaneous contraction after addition of Ca2+ into the solution. In CPA-treated veins, the time taken to restore the contraction was shortened significantly. Pretreatment with 1 microM PGE1 shortened the time to the same extent as pretreatment with CPA did. 6. These results suggest that PGE1 increases the amplitude of the spontaneous phasic contraction by a different mechanism from those by which PE and Bay K 8644 increase it. Inhibition of Ca(2+)-ATPase of the SR might be involved in the vasoactive effect of PGE1.

Continuous negative extrathoracic pressure ventilation, lung water volume, and central blood volume. Studies in dogs with pulmonary edema induced by oleic acid.

The effect of continuous positive-pressure ventilation (CPPV) on extravascular lung water volume has been investigated, but there is only one report which studied the effect of continuous negative extrathoracic pressure ventilation (CNETPV). The effect of CNETPV on central blood volume (CBV) has not been studied. Changes in intrathoracic pressure by CNETPV may alter lung water volume and CBV. In this study the effects of CNETPV on lung water volume and CBV were compared with those of intermittent positive-pressure ventilation (IPPV) and CPPV in dogs with pulmonary edema induced by oleic acid. Nine mongrel dogs were anesthetized and given oleic acid at 0.06 ml/kg intravenously to induce pulmonary edema; CNETPV was applied with a cuirass and a negative thoracic pressure ventilator (Kimura OKT-100) for 1 h. Extravascular lung water volume (as extravascular thermal volume [EVTV]) and CBV were estimated with the double-indicator dilution method using thermal-sodium; PEEP and continuous negative extrathoracic pressure were matched to produce the same increments in FRC. The EVTV increased during CNETPV but did not change during CPPV. The CBV decreased during CPPV but did not change during CNETPV. An increase of transmural pulmonary microvascular pressure was thought to be one of the reasons for the increase in EVTV with CNETPV.

Effects of continuous negative extrathoracic pressure ventilation on renal function and alpha-atrial natriuretic peptide in normal individuals.

Continuous negative extrathoracic pressure ventilation (CNETPV) may induce atrial distention by augmenting venous return, resulting in the increased secretion of atrial natriuretic peptide (ANP) and natriuresis. To clarify this hypothesis, we investigated the effect of CNETPV on renal function and plasma ANP level. Nine male healthy volunteers were studied during three successive 60-minute periods under (1) spontaneous breathing, (2) CNETPV with continuous negative extrathoracic pressure of -10 cm H2O, and (3) spontaneous breathing again. Continuous negative extrathoracic pressure ventilation induced a transient increase in plasma ANP level, but changes in plasma ANP level were not statistically significant. Although there was no significant difference in urine volume and urinary sodium excretion among three successive periods, a slight but significant increase in creatinine clearance was noticed during CNETPV. These results indicate that CNETPV with continuous negative extrathoracic pressure of -10 cm H2O does not induce the major change in ANP secretion and renal function in normal subjects.

L-DOPA inhibits spontaneous acetylcholine release from the striatum of experimental Parkinson's model rats.

Acetylcholine (ACh) release was measured by microdialysis. Addition of 10 nM L-DOPA to the perfusate significantly decreased ACh release, from the striatum of rats lesioned with 6-hydroxydopamine (6-OHDA), but not sham-operated rats. The L-DOPA-induced decrease was not affected by (-)-sulpiride which completely blocked D2- and D3-agonist-induced decrease in ACh release in lesioned rats. Neither 10 nM D-DOPA nor 100 nM dopamine caused by any change in ACh release. These findings suggest that L-DOPA-sensitive mechanisms are supersensitized in Parkinson's disease model rats.

6-OHDA-induced lesion of the nigrostriatal dopaminergic neurons potentiates the inhibitory effect of 7-OHDPAT, a selective D3 agonist, on acetylcholine release during striatal microdialysis in conscious rats.

Using striatal microdialysis, we attempted to clarify whether or not locally infused 7-hydroxy-N,N-di-n-propyl-2-aminotetralin (7-OHDPAT), a selective D3 agonist, modulates the basal acetylcholine (ACh) release in conscious rats sham-operated and lesioned with 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. In the sham-operated rats, 7-OHDPAT at 1 microM decreased ACh release by 19% of control. In the 6-OHDA-lesioned rats, 7-OHDPAT (0.1-10 microM) decreased ACh release in a concentration-dependent manner. The decrease of 37% of control was seen at 1 microM 2 weeks after the lesion. The 7-OHDPAT (1 microM)-induced decrease was completely antagonized by 1 microM (-)-sulpiride, a D2 and D3 antagonist, while (-)-sulpiride at 1 microM alone failed to alter ACh release. There may exist intrastriatal D3 receptors to inhibit ACh release, and supersensitization is evident in a 6-OHDA-lesioned rat Parkinson's model.

Involvement of angiotensin II in development of spontaneous nephrosis in Dahl salt-sensitive rats.

We investigated the effect of angiotensin-converting enzyme inhibition on spontaneous nephrosis in Dahl salt-sensitive (Dahl/S) rats. Dahl/S rats fed on a normal sodium diet spontaneously developed nephrosis and mild hypertension from a young age. In young Dahl/S rats, an angiotensin-converting enzyme inhibitor, imidapril, attenuated the development of proteinuria accompanied by a decrease in blood pressure. Methylprednisolone, a potent therapeutic agent for proteinuria, did not affect the development of nephrosis. An angiotensin AT1 receptor antagonist, losartan, but not a Ca2+ channel blocker, verapamil, inhibited the development of nephrosis while both agents decreased blood pressure to a similar extent as imidapril. In mature Dahl/S rats, imidapril suppressed not only the development of proteinuria but also the glomerular lesions. It is concluded that the development of spontaneous nephrosis in Dahl/S rats is mediated by angiotensin II.

Supersensitization of intrastriatal dopamine receptors involved in opposite regulation of acetylcholine release in Parkinson's model rats.

Using striatal microdialysis, we studied effects of SKF 38393, a D1 agonist, and quinpirole, a D2 agonist, on the acetylcholine (ACh) release from the striatum of 6-hydroxydopamine (6-OHDA)-lesioned rats by local infusion into the striatum. The present experiments clearly demonstrated evidence for the existence of intrastriatal D1 and D2 receptors regulating ACh release and for supersensitization of the striatal stimulatory D1 and inhibitory D2 receptor mechanisms in 6-OHDA lesioned rats.

An L-DOPA-like depressor action of L-threo-dihydroxyphenyl-serine in the rat caudal ventrolateral medulla.

We have proposed that L-3,4-dihydroxyphenylalanine (L-DOPA) is a neurotransmitter and/or neuromodulator in the central nervous system (1). In this study, we investigated whether or not L-threo-dihydroxyphenylserine (L-threo-DOPS), a synthetic amino acid structurally related to L-DOPA, microinjected into the caudal ventrolateral medulla (CVLM) and the rostral ventrolateral medulla (RVLM) shows cardiovascular actions similar to those of L-DOPA in anesthetized rats. When L-threo-DOPS was microinjected into CVLM, it produced dose-dependent (0.01-3 ng) depressor and bradycardic responses. D-threo-DOPS (3 ng) produced no effect. The responses to L-threo-DOPS (1 ng) were almost completely blocked by L-DOPA methyl ester (1 microg), a competitive antagonist for L-DOPA, supporting the existence of an L-threo-DOPS-sensitive recognition site for L-DOPA in CVLM. Microinjection of L-threo-DOPS into RVLM, however, showed no effect (0.001-100 ng), which contrasted with the cardiopressor action of L-DOPA applied in RVLM. In RVLM, there may exist an L-threo-DOPS-insensitive recognition site for L-DOPA.

Preoperative estimation of cerebral blood flow autoregulation curve for control of cerebral circulation after cerebral revascularization.

In this report, the anesthetic management for cerebral revascularization in 3 patients with ischemic cerebral vascular disease was presented. Arterial pressure was maintained above their ordinary level before revascularization. To prevent cerebral hemorrhage or edema due to the breakthrough phenomenon, the arterial pressure was reduced to the lower limit pressure of cerebral blood flow (CBF) autoregulation which was measured preoperatively. The patients did not show any new neurological deficit after the operations.

Supersensitization of neurochemical responses by L-DOPA and dopamine receptor agonists in the striatum of experimental Parkinson's disease model rats.

We studied the mechanisms of dopamine receptor agonist- and L-DOPA-mediated supersensitization in experimental Parkinson's disease model rats, by measuring in vivo acetylcholine (ACh) release, GTPase activities, and mRNA expression in the striatum of 6-hydroxydopamine-treated rats. D1 agonist (SKF38393) and D2/D3 agonists (bromocriptine and quinpirole) showed more potent stimulation or inhibitions on ACh release in the model rat than in the control. However, quinpirole-evoked stimulation of GTPase activity was enhance in the model rats, compared to the control, while there was no significant enhancement of the bromocriptine-evoked stimulation. On the other hand, L-DOPA at 0.3-10 pM showed a biphasic action including significant inhibition on the GTPase activity in the lesioned striatal membranes, but not in the control. In the RNAase protection assay, neither D1, D2, Gi1 alpha, GoA alpha nor Gs alpha mRNA expression in the model was significantly different from the control. These findings suggest that there is supersensitization of D1 and D2/D3 receptors in the experimental Parkinson's disease model, while the upregulation of their receptors or GTP-binding proteins (G-proteins) to be coupled to their receptors is unlikely involved in major parts of such mechanisms. In addition, the present report provides the first evidence that L-DOPA mediates neurochemical responses in the plasma membranes, possibly through its receptor.

Effects of strong pulsed magnetic fields on the cardiac activity of an open chest dog.

The heart of an open chest dog was stimulated by strong magnetic fields which were damped sinusoidal pulses with the one-cycle period of 1.47 ms. Stimulation effects were detected by electrocardiograph (ECG) and arterial blood pressure as a function of the strength of the field, the triggering point in the cardiac cycle, and the position of a stimulating coil. The threshold for arrhythmias was a minimum for the stimuli triggered at the apex of the T wave and on the P wave in the ECG. Premature ventricular and premature atrial contractions occurred according to whether the coil was placed over the ventricles or the atria. Ventricular defibrillation can not be attained by the magnetic stimulus with the flux density of 9.2 T which was the maximum field used.

Intraoperative management for removal of tumor thrombus in the inferior vena cava or the right atrium with multiplane transesophageal echocardiography.

BACKGROUND: To investigate the role and impact of multiplane transesophageal echocardiography during thrombectomy in the inferior vena cava or the right atrium. EXPERIMENTAL DESIGN: Retrospective. SETTING: A university hospital. PARTICIPANTS: Four patients who underwent removal of tumor thrombus in the inferior vena cava (IVC) or the right atrium. INTERVENTIONS: The medical records of 4 patients and videotapes of these intraoperative transesophageal echocardiography examinations were reviewed. RESULTS: Before thrombectomy, multiplane transesophageal echocardiography (MTEE) provided excellent IVC long axis view, which offered precise recognition of the cephalic extent of tumor, extent of caval occlusion, characterization of the tumor head. During surgery, MTEE could provide continuous monitoring of cardiac function, cardiac volume, and pulmonary embolism. Moreover, MTEE could provide the useful images of a cannula or the caval occlusion balloon catheter, which facilitated removal of neoplasm extending into the IVC. CONCLUSIONS: We presented four surgical cases, in which the removal of the tumor extended into the inferior vena cava or the right atrium using MTEE. MTEE could provide valuable information such as excellent images of the tumor, cardiac function, the position of a cannula or the caval occlusion balloon catheter. These findings could improve the anesthetic management of the patients, as well as the surgical approach and technical maneuvers, and facilitate removal of neoplasm into the IVC.

Retroperitoneal malignant fibrous histiocytoma causing variegated colonic lesions.

A 68-year-old man visited our hospital because of heartburn. A firm mass was palpated in the left upper abdominal quadrant. Ultrasonography and computed tomography revealed a large left sided retroperitoneal tumor. A barium enema examination showed shallow irregularly depressed or elevated lesions. Colonoscopy revealed an irregularly shaped ulcer and multiple submucosal masses suggesting invasion by an extrinsic malignant tumor. Although colonoscopic biopsy was negative, a resected tumor was histologically diagnosed as a malignant fibrous histiocytoma (MFH). When such varigated lesions are detected in the colon, MFH should be considered, and an attempt to sample the submucosal layer may be necessary.

[Minimal-flow xenon and semiclosed circuit anesthesia for computed tomographic measurement of local cerebral blood flow (LCBF)].

For the purpose of decreasing the volume of expensive xenon, anesthesia with minimal-flow xenon and semiclosed circuit were induced for computed tomographic LCBF measurement. Eighteen patients with ischemic cerebral disease were studied. Anesthesia was induced with minimum dose of thiopental, diazepam and fentanyl. Muscle relaxation was obtained by means of pancuronium bromide. Patients were intubated and ventilated mechanically with flows of 6 l/min. O2 for 20 to 30 minutes to eliminate nitrogen from the system. O2 concentrations in semiclosed circuit were monitored throughout the procedures using galvanic battery. Endtidal CO2 tension was also measured for maintaining normocarbia. Blood gas analyses were carried out before xenon inhalation, during xenon inhalation and immediately before stopping inhalation of xenon-oxygen mixture. Xenon inhalation programs were subdivided into three groups, each of them consisted of 6 patients. The formula for calculating fresh gas flow for low flow semiclosed circuit was introduced according to Shimoji's which was based on the original formula of Foldes. O2 concentration in circuit was predicted to be 25%. Mean xenon uptake for initial 20 minutes was predicted to be 125 ml/min. or 360 ml/min. (Formula: see text) (CRO2: O2% in semiclosed circuit. FO2: fresh O2 flow ml/min. FXe: fresh xenon flow ml/min. VO2: oxygen consumption ml/min. VXe: mean xenon uptake ml/min.) The first group started xenon inhalation during pure xenon inflow into semiclosed circuit for two minutes and followed by about 68% xenon in O2 inhalation for 23 minutes. FXe and VXe were fixed at 700 ml/min and 360 ml/min respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

[Anesthetic management of elderly patients in open heart surgery].

In the National Cardiovascular Center, 46 patients whose ages were above 70 underwent open heart surgery from 1977 to 1986. Twenty of them received AC bypass and 5 had repair of the rupture of ventricular septum or left ventricular aneurysm. Among them 2 had also insertion of left ventricular assist device because of acute myocardial infarction (MI). Eighteen underwent mitral and/or aortic valve replacement. The other 3 were operated on because of atrial myxoma etc. Preoperatively, in ischemic heart disease group, due to resultant heart failure, one third of the patients were given catecholamines. In valvular heart disease group, angina pectoris and old MI were also common. Beside arrhythmias, respiratory complications, renal dysfunction and diabetes mellitus, neurological complications such as brain infarction were prominent in both groups. Hospital mortality was 15% in AC bypass group, 40% in acute MI group and 11.1% in VHD group. In 36 patients who left hospital, mean NYHA class improved after operation. The mortality rate and symptomatic improvement demonstrate that cardiac surgery can be performed with acceptable risk in elderly patients. Anesthesiologists should manage them carefully, considering the problems stated above.