The effects of intravenous infusion of solutions with different colloid osmotic pressures on rat mesenteric lymph pressure.

The effects of intravenous infusion of solutions of varied colloid osmotic pressure on mesenteric lymph pressure were measured by a glass micropipette. The lymph pressure was 4.0 +/- 1.6 cm H2O between the second and third valve of rat mesenteric lymphatic vessels with diameter of 101 +/- 25 micron (mean +/- SD). Intravenous infusion of 1 ml/100g body weight (B.W.) of isotonic saline, 5% glucose solution, and 20% glucose solution increased the lymph pressure by 1.6 +/- 0.5 cm H2O, 1.5 +/- 0.3 cm H2O and 2.0 +/- 1.0 cm H2O, respectively. Infusion of 2 ml/100g B.W. of the same solutions increased the lymph pressure by 3.3 +/- 1.3 cm H2O, 3.3 +/- 1.6 cm H2O and 3.7 +/- 0.8 cm H2O, respectively. Infusion of hydroxyethyl starch solution, with colloid osmotic pressure of 25 mmHg, minimally altered the lymph pressure. One ml/100g B.W. infusion of low molecular weight dextran solution, with colloid osmotic pressure of 162 mmHg, decreased the lymph pressure by 1.3 +/- 0.9 cm H2O, and 2 ml/100g B.W. infusion of this solution decreased the lymph pressure by 2.0 +/- 1.0 cm H2O. The different effects on lymph pressure derive from the differences in colloid osmotic pressure of these solutions in conformity with the Starling hypothesis.

Propofol relaxes extrapulmonary artery but not intrapulmonary artery through nitric oxide pathway.

The object of this study was to compare vasorelaxing responses to propofol by the intrapulmonary artery (IPA) and the extrapulmonary artery (EPA), and to identify the mechanisms of action. Rat pulmonary arterial rings were isolated and suspended in organ chambers where isometric tension development was measured under optimal resting tension. All pulmonary arterial rings were pre-contracted with phenylephrine. Propofol (Diprivan) and the vehicle (10% Intralipid) were administered cumulatively in the presence or absence of N(omega)-nitro-L-arginine methyl ester (L-NAME). Sodium nitroprusside (SNP), a nitric oxide donor, was administered cumulatively. Propofol relaxed both EPA and IPA in a dose dependent manner (p<0.05), while the vehicle alone showed no effect. The vasorelaxing responses to propofol were significantly higher in EPA than IPA at higher concentrations (10(-4) M and 10(-4.5) M) (p<0.05), and were decreased by L-NAME in EPA (p<0.05), though it had no effect in IPA. The concentration for SNP causing 50% relaxation was not significantly different between the two arteries. We concluded that the response of smooth muscle to nitric oxide was the same between EPA and IPA; however, the vasorelaxing mechanisms of propofol seemed to be different between them at higher doses, suggesting that a mechanism exists and operates through the nitric oxide pathway.

Buckling of transesophageal echocardiography probe: a pitfall at insertion in an anesthetized patient.

Buckling of the transesophageal echocardiography probe was encountered in 6 of 23 patients (26.1%), although no complication occurred. When buckling occurred, acquisition of images and manipulation of the probe became difficult, resistance was felt when withdrawal of the probe was attempted, and the probe was fixed in the extreme ante- or dorsiflexion. In this situation, the probe was carefully advanced into the stomach, in which the buckled probe was unfolded, and then withdrawn to the esophagus. Buckling of the probe tip is not uncommon at insertion of the probe, especially when using a flaccid probe in an anesthetized patient. A TEE operator should be aware of the possibility of buckling. Unusual resistance associated with buldging of the submandibular region is a sign of a folded-up probe tip. Use of laryngoscopy is recommended in order to avoid inserting the buckled probe into the esophagus.

The volume limit in fluid resuscitation to prevent respiratory failure in massively burned children without inhalation injury.

We evaluated the accurate fluid requirement to prevent respiratory failure during the postresuscitation period in the resuscitation of massively burned children without inhalation injury. Forty-nine children were treated by similar fluid resuscitation and physiologic support protocols. Using a retrospective chart review, the children were divided into three groups as follows: Group N (no lung injury, n = 33, 41.4+/-18.7%TBSA burned), Group M (mild-to-moderate lung injury, n = 11, 73.7+/-17.1%TBSA burned) and Group S (severe lung injury, n = 5, 67.2+/-16.6%TBSA burned). Information about fluid resuscitation during the first 24 hr post-injury was collected and compared among the three groups. There was no significant difference in the hourly urine output and the resuscitation volume estimated by body weight and burn size among the groups. The volumes estimated by ml/kg/%TBSA burned were 7.0 ml/kg/%TBSA burned, 8.0 ml/kg/%TBSA burned, and 9.4 ml/kg/%TBSA burned in Groups N, M, and S, respectively. According to the fluid volume estimated by the burn index (BI; 1/2 of % second-degree burns plus % third-degree burns), the volumes were 13.8+/-4.0 ml/kg/BI, 14.4+/-4.4 ml/kg/BI, 18.8+/-3.7ml/kg/BI in Groups N, M, and S, respectively (Group N < Group S, p < 0.05). There was a significant positive correlation between the maximum respiratory index (AaDO2/PaO2) during the first week and the initial total volume administered (ml/kg/BI). These findings indicated that the fluid requirements to prevent postresuscitation respiratory failure in massively burned children might be estimated according to the depth of burned area in addition to body weight and burn size.

Characteristic magnetic resonance imaging for neurological assessment in HELLP syndrome with eclampsia: a case report.

HELLP syndrome is a complication of pregnancy characterized by hemolytic anemia, elevated liver enzymes, and low platelets. We describe a patient who suffered a generalized tonic seizure as a clinical onset. Magnetic resonance imaging (MRI) of the brain showed high intensity lesions on T2-weighted images and low- and iso- intensity on T1-weighed images. The patient fully recovered and on follow-up MRI the abnormal lesions were almost totally resolved. The sensitivity and specificity of MRI is useful in distinguishing this complication of pregnancy from cerebral apoplexy, brain tumor, epilepsy and other causes.

[Intraoperative coronary artery spasm--retrospective review of 10 cases].

Ten cases of intraoperative coronary artery spasm were reviewed retrospectively. Four cases were open heart surgeries, one was a surgery for aortic dissecting aneurysm, and the other five were abdominal ones. In the cases of open heart surgery under anesthesia with high dose fentanyl, coronary artery spasm occurred at weaning period from cardio-pulmonary bypass. In the cases of abdominal surgery, all under neuroleptanesthesia with continuous epidural block, coronary artery spasm occurred within one hour after the beginning or before the end of operation. In four of five abdominal surgeries, systolic blood pressure became less than 90 mmHg when coronary artery spasm occurred. Coronary artery spasm brought severe depression of myocardial contractility and life threatening arrhythmias by which weaning from cardiopulmonary bypass became difficult during open heart surgery. There was a case which required several hours before hemodynamics became stable also in abdominal surgery. It was suggested that general anesthesia with continuous epidural block could be a triggering factor of coronary artery spasm when hypotension and insufficient depth of general anesthesia are present simultaneously.

[Intraoperative management of emergency coronary artery bypass grafting].

Intraoperative hemodynamics during emergency coronary artery bypass grafting (CABG) for acute evolving myocardial infarction (26 cases) were measured and compared with those during elective CABG (39 cases). Before cardiopulmonary bypass period, it was strongly suggested that the cardiac function of emergency cases was worse than that of elective cases because of the following 5 factors; (1) hypotension, (2) tachycardia, (3) low stroke volume index, (4) pulmonary congestion and (5) metabolic acidosis. Proper usage of inotropic supports, vasodilators, anesthetic agents, and control of acidosis and hypoxemia seemed to be more important in emergency CABG. These prudent intraoperative hemodynamic managements have played important roles in the progress of the operative outcome of emergency CABG.

[Anesthesia for patients receiving hemodialysis--a report of 122 cases].

A hundred and twenty-two cases of anesthesia for patients receiving hemo-dialysis were reported and peri-operative management of them was analyzed, retrospectively. For the past ten years, most of the patients were anesthetized with neurolept-anesthesia and post-operative mechanical ventilation was continued until the patients regained stable hemodynamics and complete awareness. The procedures of pre-operative hemo-dialysis and intraoperative management were almost compatible with previous reports. In the cases of emergency operation, pre-operative control was not enough and intra-operative water intake was larger than that of scheduled cases. The detailed analysis of peri-operative management of water which affects the pathophysiological state of each patient will be the problem in future.

[Anesthesia in patients undergoing valvular replacement and coronary artery bypass grafting].

We investigated the intraoperative hemodynamic changes in patients who underwent combined valvular replacement (VR) and coronary artery bypass grafting (CABG). The data of 8 patients who under went VR + CABG were compared with those of 50 patients who underwent VR during the same period (1986). Heart rate before the institution of cardiopulmonary bypass (CPB) was not different between these two group, but blood pressure of VR + CABG cases was significantly higher than that of VR cases. This required a higher dosage of fentanyl in VR + CABG cases.

[Perioperative hemodynamic changes and management of hemodialysed patients].

Perioperative hemodynamic changes of hemodialysed patients were investigated and the changes of emergency cases (group E, n = 8) were compared with those of scheduled ones (group S, n = 13). By preoperative hemodialysis (HD), the values of blood urea nitrogen, serum creatinine, serum potassium, serum bicarbonate, and hematocrit were adjusted within normal range in group E, with no significant difference from those of group S. On the other hand, concerning the effect of preoperative removal of body water by HD, cardio-thoracic ratio (CTR, 53.6 +/- 3.1%) and pulmonary artery diastolic pressure (PADP, 11.6 +/- 5.0 mmHg) of group E were significantly higher than those of group S (CTR = 46.9 +/- 4.5%, PADP = 7.8 +/- 3.0 mmHg), indicating that the removal of body water by preoperative HD might be less in group E. However, group E patients required more administration of fluid and pressor agents in order to maintain their blood pressure and/or cardiac output during operation. Although with less water removal preoperatively and more fluid intraoperatively, postoperative PADP was significantly reduced (8.3 +/- 3.0 mmHg) in group E, suggesting that the requirement of perioperative water is more in group E. We conclude that the safe perioperative hemodynamic management for emergency surgery of hemodialysed patients requires following points; (1) The excessive removal of body water by preoperative HD should be avoided. (2) Intraoperative fluid infusion should be adequate so that they do not fall into hemodynamic collapse.

Vasodilation and mechanism of action of propofol in porcine coronary artery.

BACKGROUND: A decrease in myocardial perfusion pressure may reduce myocardial blood flow. However, it may not significantly affect myocardial perfusion when in presence of a concurrent coronary artery vasodilation. However, the effects of propofol in coronary arteries are not well determined. In this study, the effects of propofol on porcine coronary artery responses to vasoactive agents that operate through voltage- and receptor-mediated calcium mechanisms were investigated. METHODS: Hearts of adult pigs (n = 103) were obtained from a slaughter house, and the left anterior descending coronary arteries were dissected. The arteries were cut into vessel rings and prepared with and without the endothelium organ chambers filled with buffered salt solution. The effect of propofol (10(-7), 10(-6), 10(-5), and 10(-4) M) on vascular smooth muscle contraction caused by intracellular Ca(2+)-influx through voltage- and receptor-mediated mechanism also was studied at a cellular level. RESULTS: Propofol relaxed coronary rings that were contracted by KCl, norepinephrine (NE), serotonin (5-HT), or carbachol (CCh). The minimal concentrations of propofol that produced significant vasorelaxation ranged from 3.16 x 10(-7) M to 3.16 x 10(-6) M. Vasodilation was more pronounced in rings contracted by NE, 5-HT, and CCh than by KCl. Propofol (10(-5) M) attenuated coronary vasoconstriction in response to cumulative concentrations of KCl, NE, 5-HT, and acetylcholine. Maximal contractions produced by NE and 5-HT were inhibited to a greater degree than contractions produced by KCl. Propofol at concentrations of 10(-5) M and higher attenuated a contraction in response to CaCl2 in vascular rings depolarized by KCl, but concentrations of 10-M did not attenuate contractions. Vasoconstriction in response to calcium entry in the presence of NE (and nifedipine 10(-6) M) was attenuated by propofol at concentrations of 10(-6) M and higher. Caffeine-induced contraction, caused by intracellular calcium release, was attenuated only at 10(-4) M of propofol. CONCLUSIONS: Propofol possesses vasodilator effect and attenuates the effects of vasoconstrictor agents in porcine coronary artery. Further, an antagonism of calcium channels may be responsible for these effects of propofol.

Enzyme inhibition by analgesic and hypnotic agents on anaerobic dehalogenation of halothane.

Enzyme inhibition on anaerobic dehalogenation of halothane by various analgesic or hypnotic agents was investigated in vitro using rat liver microsomal fraction. The production rate of chloro-difluoro-ethylene (CDE) and chloro-trifluoro-ethane (CTE), anaerobic metabolites of halothane, was measured when various concentrations of analgesic or hypnotic agents (fentanyl, morphine, pentazocine, buprenorphine, ketamine, diazepam, chlorpromazine and hydroxyzine) were supplemented. Inhibitor constant (Ki) of each agent was calculated and compared with each other. The activity of NADPH-cytochrome c reductase (fp(2)) and NADH-ferricyanide reductase (fp(1)) was measured when each agent was added. The values of inhibitor constants (Ki) for CDE and CTE formation were in the following order from large to small values; morphine (656 microM and 2570 microM), chlorpromazine (49.7 microM and 68.1 microM), ketamine (24.9 microM and 64.4 microM), fentanyl (23.9 microM and 34.6 microM), hydroxyzine (19.2 microM and 50.8 microM), diazepam (17.0 microM and 13.9 microM), buprenorphine (11.2 microM and 22.4 microM), and pentazocine (1.96 microM and 6.67 microM) respectively. Pentazocine inhibited the formation of CDE 300 fold greater than morphine. The activity of fp(2) and fp(1) did not change by the addition of these analgesic or hypnotic agents. These results indicate that various analgesic or hypnotic agents, which are commonly used with halothane in clinical anesthesia, suppress the anaerobic dehalogenation of halothane in vitro. They also imply that the suppression of production of halothane metabolites is the result of direct enzyme inhibition on cytochrome P-450, since these agents did not affect the activity of fp(2) and fp(1) which are flavoproteins existing in the microsomal electron transport system.

Effects of bienzyme complex formation of cysteine synthetase from escherichia coli on some properties and kinetics.

Some properties and kinetics of the free and bound serine acetyltransferases (SATs) and O-acetylserine sulfhydrylase-As (OASS-As) from Escherichia coli were investigated. In some cases, SATdeltaC20, deleting 20 amino acid residues from the C-terminus of the wild-type SAT (Biosci. Biotechnol. Biochem., 63, 168-179 (1999)) was tested for comparison. The optimum pH and stability against some reagents for the free and bound wild-type SATs were similar except for the resistance to cold inactivation. The kinetics for the wild-type SAT and SATdeltaC20 followed a Ping-Pong Bi Bi mechanism with a mixed-type inhibition by L-cysteine. The kinetics and kinetic constants for the wild-type SAT were not changed by the complex formation with OASS-A. The optimum pH for OASS-A was shifted towards an alkaline pH by the complex formation. Thermal stability and stability against some reagents for the free and bound OASS-As were almost the same. On the other hand, the maximum velocity for OASS-A was lowered and dissociation constants for the substrates and products were increased by forming the complex with the wild-type SAT, although the kinetics for the free and bound enzymes followed the same Ping-Pong Bi Bi mechanism. From comparisons of computed courses of L-cysteine formation from L-serine using SAT (wild-type SAT and SATdeltaC20) and OASS-A with the experimental results and changes in the stability of the wild-type SAT by the complex formation, we discuss the role and significance of a complex formation for the cysteine synthetase.

Usefulness of transesophageal echocardiography for guiding pulmonary artery catheter placement in the operating room.

The usefulness of transesophageal echocardiography (TEE) for guiding the placement of a pulmonary artery (PA) catheter was evaluated in 31 patients (TEE group); 31 patients who were treated before TEE guidance was used (control group). In the control group, use of the PA catheter was abandoned in two patients; because of an unstable condition and marked arrhythmias, respectively. The key findings for TEE guidance were: (1) pulsatile to-and-fro movement of the balloon, i.e., "shuttle movement" and (2) loss of shuttle movement at wedging of the balloon, i.e., "anchoring sign." When the PA catheter did not enter the right vertricle (RV), the balloon was found to be in the inferior vena cava or the right atrium (RA) without shuttle movement. Coiling of the catheter was suggested in the latter situation. Coiling also occurred in the RV, often associated with frequent arrhythmias. These findings indicate that the catheter should be withdrawn once. TEE allowed for readjustment of the catheter tip position by enabling the balloon to be wedged twice. An excessively deep placement of the catheter tip was seen in 5 of the controls, but in none of the TEE group. Biplane TEE was found to be advantageous for guiding PA catheter placement and for visualizing the RV inflow and outflow tract in a single view, with the shuttle movement of the balloon in its long axis. TEE acts as an "eye" in the operating room, as does fluoroscopy, enabling smooth placement of the PA catheter.

Fentanyl attenuates porcine coronary arterial contraction through M3-muscarinic antagonism.

The "antimuscarinic effect" of fentanyl and its dependence on subtypes of receptors were characterized in isolated porcine coronary arteries. Left anterior descending coronary arteries were dissected from the hearts of 60 adult pigs obtained at a slaughterhouse and prepared for isometric tension studies. The effects of fentanyl on the cumulative concentration-response curve for acetylcholine were obtained in the presence and absence of muscarinic blockade by atropine. Fentanyl shifted the concentration-response curve to the right in a concentration-dependent fashion. Atropine shifted the concentration-response curve to the right, and no further shift was caused by fentanyl. To investigate the dependence on muscarinic receptor subtypes, the effect of fentanyl on acetylcholine-induced contraction was examined in the presence of specific M1-, M2-, and M3-muscarinic antagonists. The pA2 values for fentanyl decreased significantly in the presence of atropine (a nonspecific antagonist) and also in the presence of p-F-HHSiD (an M3-antagonist). In contrast, no significant change of pA2 value for fentanyl was observed in the presence of both pirenzepine (an M1-antagonist) and methoctramine (an M2-antagonist). We conclude that fentanyl has an antimuscarinic effect, and that this antagonism occurs in a competitive manner. Furthermore, the significant decrease of the pA2 value for fentanyl in the presence of M3-, but not in the presence of M1 + M2-antagonists, suggests that the attenuation of cholinergic contraction of porcine coronary arteries by fentanyl is mediated through the M3-muscarinic receptor subtype.

Effects of opioids on vasoresponsiveness of porcine coronary artery.

Myocardial ischemia during surgery can be caused by coronary vasospasm. Neurohumoral mechanisms are involved in this phenomenon, and various substances have been suggested as possible causes, including acetylcholine, histamine, and norepinephrine. The responses of isolated porcine coronary arteries (from 117 pig hearts) with (E+) and without (E-) endothelium to these agents were investigated in the presence of fentanyl, sufentanil, and morphine. Fentanyl significantly shifted to the right, in a concentration-dependent fashion, the concentration-response curve to acetylcholine. This effect was not different between E+ and E- rings. Neither sufentanil nor morphine altered acetylcholine-induced contraction of porcine coronary arteries. Naloxone did not antagonize the suppressive effect of fentanyl on acetylcholine-induced contraction. The response of porcine coronary arteries to norepinephrine was decreased only at very high concentrations of fentanyl. Neither sufentanil nor morphine altered norepinephrine-induced contraction of porcine coronary arteries. Fentanyl, sufentanil, and morphine had no effect on histamine-induced contraction. We conclude that fentanyl antagonized acetylcholine-induced contraction of porcine coronary arteries. This effect of fentanyl seems to be caused by a direct effect on smooth muscle cells and is not opioid-receptor mediated.

Purification and characterization of serine acetyltransferase from Escherichia coli partially truncated at the C-terminal region.

Incubation of serine acetyltransferase (SAT) from Escherichia coli at 25 degrees C in the absence of protease inhibitors yielded a truncated SAT. The truncated SAT was much less sensitive to feedback inhibition than the wild-type SAT. Analyses of the N- and C-terminal amino acid sequences found that the truncated SAT designated as SAT delta C20 was a resultant form of the wild-type SAT cleaved between Ser 253 and Met 254, deleting 20 amino acid residues from the C-terminus. Based on these findings, we constructed a plasmid containing an altered cysE gene encoding the truncated SAT. SAT delta C20 was produced using the cells of E. coli JM70 transformed with the plasmid and purified to be homogeneous on an SDS-polyacrylamide gel. Properties of the purified SAT delta C20 were investigated in comparison with those of the wild-type SAT and Met-256-Ile mutant SAT, which was isolated by Denk and Böck but not purified (J. Gen. Microbiol., 133, 515-525 (1987)). SAT delta C20 was composed of four identical subunits like the wild-type SAT and Met-256-Ile mutant SAT. Specific activity, optimum pH for reaction, thermal stability, and stability to reagents for SAT delta C20 were similar those for the wild-type SAT and Met-256-Ile mutant SAT. However, SAT delta C20 did not form a complex with O-acetylserine sulfhydrylase-A (OASS-A), a counterpart of the cysteine synthetase and did not reduce OASS activity in contrast to the wild-type SAT and Met-256-Ile mutant SAT.