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Biomedical subjects

Hiroshi Morisaki

Publications and source records attributed to Hiroshi Morisaki.

At least 19 recordsLinked to original sources

Contribution of high-mobility group box-1 to the development of ventilator-induced lung injury.

RATIONALE: Proinflammatory cytokines play an important role in ventilator-induced lung injury (VILI). High-mobility group box-1 (HMGB1) is a macrophage-derived proinflammatory cytokine that can cause lung injury. OBJECTIVES: This study tested the hypothesis that HMGB1 is released in intact lungs ventilated with large Vt. A second objective was to identify the source of HMGB1. A third objective was to examine the effects of blocking HMGB1 on the subsequent development of VILI. METHODS: Bronchoalveolar lavage fluid (BALF) and lung tissues were obtained from rabbits mechanically ventilated for 4 h with a small (8 ml/kg) versus a large (30 ml/kg) Vt. BALF was also obtained from rabbits with intratracheal instillation of anti-HMGB1 antibody before the initiation of large Vt ventilation. MEASUREMENTS AND MAIN RESULTS: The concentrations of HMGB1 in BALF were fivefold higher in the large than in the small Vt group. Immunohistochemistry and immunofluorescence studies revealed expression of HMGB1 in the cytoplasm of macrophages and neutrophils in lungs ventilated with large Vt. Blocking HMGB1 improved oxygenation, limited microvascular permeability and neutrophil influx into the alveolar lumen, and decreased concentrations of tumor necrosis factor-alpha in BALF. CONCLUSIONS: These observations suggest that HMGB1 could be one of the deteriorating factors in the development of VILI.

Bronchoalveolar Lavage Fluid↗

Platelet dysfunction during cardiopulmonary bypass assessed by a novel whole-blood aggregometer.

OBJECTIVE: The purpose of this study was to assess perioperative platelet function with 2 types of monitors (a whole-blood aggregometer [WBA analyzer; Mebanix, Tokyo, Japan]) and the Sonoclot monitor [Sienco, Wheat Ridge, CO]) in patients undergoing hypothermic cardiopulmonary bypass (CPB). DESIGN: Prospective, observational study. SETTING: Single-center study at a university hospital. PARTICIPANTS: Twenty-six patients who underwent coronary artery bypass grafting or valve replacement under hypothermic CPB without platelet transfusion or fresh frozen plasma administration. INTERVENTIONS: Blood sampling was performed at the following time periods: after anesthetic induction, after CPB, and on the first postoperative day. These samples were assessed with the WBA analyzer and the Sonoclot. MEASUREMENTS AND MAIN RESULTS: Significant attenuation of adenosine diphosphate-induced platelet aggregation was detected shortly after CPB by 2 WBA analyzer-derived parameters: a decrease in the filtration pressure rate and an increase in the platelet aggregatory threshold index. Platelet aggregation returned to the preoperative level on the next day. There was no correlation between the amount of postoperative mediastinal drainage and defects in platelet aggregation. On the other hand, time to peak obtained by the Sonoclot did not show any significant changes. CONCLUSIONS: Whole-blood aggregation measured with the WBA analyzer detected transient platelet dysfunction shortly after CPB, whereas the Sonoclot was less sensitive to this change.

Adenosine Diphosphate↗

Activation of a neutrophil-derived inflammatory response in the airways during cardiopulmonary bypass.

Cardiopulmonary bypass (CPB) is believed to cause postoperative lung dysfunction. To more closely examine the inflammatory processes occurring in the airways during CPB, we serially measured inflammatory mediators, with the assistance of a new bronchoscopic microsample probe, in 11 patients undergoing repair of aortic arch aneurysms. Epithelial lining fluid (ELF) and arterial blood were sampled simultaneously after induction of anesthesia, at the time of pulmonary reperfusion, and at the end of surgery. A decrease in the PaO2/FiO2 ratio was observed at the end of surgery (P = 0.029). Although the ELF concentrations of interleukin (IL)-8, IL-6, and neutrophil elastase had increased significantly at the end of surgery (median = 23,200, 1818, and 12,900 microg/mL, respectively), they did not correlate with the degree of hypoxemia. Neutrophil elastase increased significantly at the time of pulmonary reperfusion, before IL-8 and IL-6, and independently of blood transfusions. At the end of surgery, IL-6 in ELF correlated with total blood transfusion volume (rho = 0.731, P = 0.011). These results indicate that a neutrophil-derived inflammatory response is activated in the airway in the early phase of CPB.

Aged↗

Effects of morphine and its metabolites on immune function in advanced cancer patients.

STUDY OBJECTIVE: To determine whether morphine and its active metabolites such as morphine-3-glucuronide (M-3-G) and morphine-6-glucuronide (M-6-G) modulate immune function in patients with advanced cancer who required morphine for pain relief. DESIGN: Prospective observational clinical study. SETTING: Pain clinic of a university hospital. PATIENTS: Fifteen patients who visited our clinic for control of advanced cancer pain. INTERVENTIONS: During the initiation or changes of morphine therapy, venous blood samples were obtained at the enrollment of this study, 1 and 3 weeks after the change of morphine dose or route. MEASUREMENTS: Lymphocyte subpopulation CD4+ and CD8+, activity of natural killer cell, phytohemagglutinin (PHA)-induced T-cell proliferation, and plasma immunoglobulin M and G concentrations were measured, as well as plasma concentrations of morphine, M-3-G, and M-6-G. MAIN RESULTS: At the entry of the study, 6 patients did not receive any type of morphine medication (group 1), whereas 9 patients were treated with morphine for 1 month (group 2). Cancer pain, rated as 4 at the entry period, was reduced to 2 of 10 (visual analogue scale) during the study periods. Although the plasma concentrations of M-3-G and M-6-G in Group 1 were significantly less than those in Group 2, plasma concentrations of immunologic markers were similar between the groups. In Group 1, Spearman linear regression analysis showed negative correlation between morphine-derived metabolites and immunoglobulins or PHA-induced T-cell proliferation, whereas poor correlation was found with all immunologic parameters in Group 2. Stepwise linear regression analyses showed that the metabolites, rather than morphine per se, modulated immune function, reflected by PHA-induced T-cell proliferation and immunoglobulin G concentration in Group 1. CONCLUSIONS: The present study suggests that some of humoral and cellular immunity are modulated by morphine-derived metabolites at the early phase of morphine therapy in patients with advanced cancer.

Adult↗

Infusion of the beta-adrenergic blocker esmolol attenuates myocardial dysfunction in septic rats.

OBJECTIVE: Since beta-blocker therapy is known to be effective in patients with an injured heart, such as infarction, we designed the present study to examine the protective effects of infusion of the beta1-selective blocker esmolol on myocardial function in peritonitis-induced septic rats using an isolated working heart preparation. DESIGN: Randomized animal study. SETTING: University research laboratory. SUBJECTS: Thirty-one rats treated with cecal ligation and perforation to evoke peritonitis. INTERVENTIONS: After cecal ligation and perforation, rats were randomly allocated to the control group (normal saline 2 mL/hr, n = 11), low-dose esmolol group (10 mg/kg/hr, n = 10), or high-dose esmolol group (20 mg/kg/hr, n = 10). After obtaining blood samples for measurement of arterial lactate and tumor necrosis factor-alpha at 24 hrs, we assessed cardiac output, myocardial oxygen consumption, and cardiac efficiency (cardiac output x peak systolic pressure/myocardial oxygen consumption) at various preloads in an isolated perfused heart preparation. MEASUREMENTS AND MAIN RESULTS: Esmolol infusion did not cause an elevation of arterial lactate levels but reduced tumor necrosis factor-alpha concentrations vs. the control group (p < .05). Both cardiac output and cardiac efficiency in the esmolol-treated rats were significantly higher throughout the study periods vs. the control group (p < .05). CONCLUSIONS: Esmolol infusion in sepsis improved oxygen utilization of myocardium and preserved myocardial function.

Adrenergic beta-1 Receptor Antagonists↗

Sivelestat, a neutrophil elastase inhibitor, attenuates neutrophil priming after hepatoenteric ischemia in rabbits.

Neutrophils play an important role in ischemia-reperfusion injury. The neutrophil elastase not only causes tissue damage, but also mediates neutrophil priming. In the present study, we use a rabbit model of hepatoenteric ischemia-reperfusion to test the hypothesis that neutrophil elastase inhibition ameliorates an ischemia-reperfusion injury by attenuating neutrophil priming and suppressing enzymatic activity. Twenty-four Japanese white rabbits underwent 30 min of supraceliac aortic cross-clamping and 180 min of reperfusion under isoflurane anesthesia. The rabbits randomly received the neutrophil elastase inhibitor, sivelestat (n = 10), or saline (n = 14). Neutrophil priming was then assayed with luminol-dependent neutrophil chemiluminescence. Hepatic, intestinal, renal, and pulmonary damages were assessed with serum transaminase, lactate dehydrogenase concentrations, urinary N-acetyl glucosaminidase activity, and protein concentration in post mortem bronchoalveolar lavage fluid. We discovered that neutrophil elastase inhibition suppressed plasma neutrophil elastase, and that lipid peroxide concentrations increased after reperfusion. It improved ischemia-reperfusion injuries in the liver, intestine, kidney, and lung. Furthermore, inhibition of neutrophil elastase with sivelestat significantly attenuated post-reperfusion neutrophil priming. The results of this study demonstrate that neutrophil elastase inhibition could effectively attenuate an ischemia-reperfusion injury caused by supraceliac aortic cross-clamping, most likely from the attenuation of neutrophil priming.

Acetylglucosaminidase↗

Epidural analgesia prevents endotoxin-induced gut mucosal injury in rabbits.

In the present study, we evaluated the effect of epidural analgesia on the alterations of gut barrier function elicited by endotoxin in rabbits. After the placement of an epidural catheter, 28 male rabbits were randomized into either 0.5% lidocaine (group E) or saline (group C) group. The solutions (0.4 mL/kg) were epidurally injected, followed by continuous infusion (0.1 mL . kg(-1) . h(-1)) throughout the study period. Under a continuous infusion of lipopolysaccharide (15 microg . kg(-1) . h(-1)), mean arterial blood pressure, intramucosal pH, and plasma thrombomodulin concentrations were measured. At 4 h, mean arterial blood pressure was lower (P < 0.05), intramucosal pH was higher (P < 0.01), and the progression of hemodilution more profound (P < 0.05) in group E versus group C, whereas plasma thrombomodulin levels were increased to a similar extent between the groups. With less wet-to-dry weight ratio of ileum, histopathological injury scores of gut mucosa were significantly less in group E versus group C (P < 0.01). In a separate series of experiments (n = 10 each group), mucosal permeability in group E was significantly less compared with group C (P < 0.05). Collectively, these studies showed that despite a significant decrease of perfusion pressure and arterial oxygen content, epidural analgesia minimized endotoxin-induced functional and structural injury of gut mucosa possibly through endothelium-independent mechanisms.

Algorithms↗

Tissue oxygen delivery and the microcirculation.

In health, acute anemia is accompanied by changes in the distribution of blood flows at all of the central, regional, and microcirculatory levels. This redistribution in blood flows provides the capacity to maintain tissue oxygenation with hematocrit as low as 21%. What is not known with certainty is whether the capacity to maintain tissue oxygenation in the presence of acute anemia can be influenced significantly by concurrent disease such as sepsis and cardiac disease. The single clinical trial found an apparent survival benefit by not exposing patients with sepsis to blood transfusions until the hemoglobin concentration was less than 70 g/L. The question remains as to whether this observation was the consequence of a protective effect anemia or an injurious effect of transfusing old stored blood.

Anemia↗

The effectiveness of continuous epidural infusion of low-dose fentanyl and mepivacaine in perioperative analgesia and hemodynamic control in mastectomy patients.

STUDY OBJECTIVES: To investigate, in mastectomy patients, the effectiveness of continuous cervical epidural block using a low-dose fentanyl infusion in combination with local anesthetics. DESIGN: Prospective, observational study. SETTING: 450-bed, university-affiliated hospital. PATIENTS: 21 ASA physical status I and II female patients undergoing modified radical mastectomy. INTERVENTIONS: An epidural catheter was inserted at the C(7)-Th(1) interspace before the induction of anesthesia. Anesthesia was maintained using a low concentration of sevoflurane with nitrous oxide-oxygen (N(2)O-O(2)). A mixture of 100 microg fentanyl and 49 mL of 1% mepivacaine was prepared, and 7 mL of this solution was epidurally injected before the initial incision. This same solution was continuously infused at a rate of 7 mL/hr (fentanyl 17.5 microg/hr) throughout the anesthesia, and at 2 mL/hr (fentanyl 5 microg/hr) postoperatively. MEASUREMENTS AND MAIN RESULTS: Intraoperative mean arterial pressure (MAP) and heart rate (HR), postoperative pain and analgesic use, and the frequency of postoperative side effects of anesthesia, including nausea, dizziness, and respiratory depression, were recorded. The protocol described provided stable intraoperative hemodynamic control with no or low-dose nicardipine infusion. Sufficient postoperative analgesia was achieved in 18 of 21 patients. One patient reported postoperative nausea, and no other side effects were reported. CONCLUSIONS: Continuous epidural infusion of the low-dose fentanyl mixture described above provides adequate intraoperative hemodynamic control and postoperative pain relief, with a low rate of side effects in mastectomy patients.

Analgesia, Epidural↗

Neutrophil depletion attenuates interleukin-8 production in mild-overstretch ventilated normal rabbit lung.

OBJECTIVE: Acute lung injury induced by lung overstretch is associated with neutrophil influx, but the pathogenic role of neutrophils in overstretch-induced lung injury remains unclear. DESIGN: To assess the contribution of neutrophils, we compared the effects of noninjurious large tidal volume (Vt) ventilation on lungs in normal and neutrophil-depleted animals. SETTING: Research animal laboratory. SUBJECTS: Twenty-six male Japanese white rabbits. INTERVENTIONS: Animals were mechanically ventilated for 4 hrs with one of the three following protocols: large Vt (20 mL/kg), small Vt (8 mL/kg), and large Vt (20 mL/kg) with neutrophil depletion achieved by a single dose of vinblastine injection (0.75 mg/kg) intravenously 4 days before the experiment. MEASUREMENTS AND MAIN RESULTS: Large Vt ventilation produced alveolar neutrophil influx compared with low Vt (p =.002) without evidence of edema or increased epithelial permeability. The neutrophil influx was accompanied by increases in interleukin-8 in bronchoalveolar lavage fluid (p =.04). Immunohistochemistry of large Vt lungs showed increased interleukin-8 staining in bronchial epithelial cells, alveolar epithelium, alveolar macrophages, and smooth muscles of pulmonary vessels. Neutrophil depletion attenuated the interleukin-8 increase in the lung. Large Vt did not increase plasma interleukin-8 or tumor necrosis factor-alpha in plasma and bronchoalveolar lavage fluid. No expression of p-selectin or intercellular adhesion molecule-1 was observed. CONCLUSIONS: Cyclic overstretching of normal rabbit lungs with noninjurious large Vt produced neutrophil influx and interleukin-8 increase in bronchoalveolar lavage fluid. Production of pulmonary interleukin-8 by lung overstretch might require the interaction between resident lung cells and migrated neutrophils. This study suggests that large Vt ventilation potentiates the predisposed, subclinical lung injury, such as nosocomial pneumonia or aspiration of gastric contents.

Animals↗

A mycobacterial virulence gene cluster extending RD1 is required for cytolysis, bacterial spreading and ESAT-6 secretion.

Initiation and maintenance of infection by mycobacteria in susceptible hosts are not well understood. A screen of Mycobacterium marinum transposon mutant library led to isolation of eight mutants that failed to cause haemolysis, all of which had transposon insertions in genes homologous to a region between Rv3866 and Rv3881c in Mycobacterium tuberculosis, which encompasses RD1 (Rv3871-Rv3879c), a known virulence gene cluster. The M. marinum mutants showed decreased virulence in vivo and failed to secrete ESAT-6, like M. tuberculosis RD1 mutants. M. marinum mutants in genes homologous to Rv3866-Rv3868 also failed to accumulate intracellular ESAT-6, suggesting a possible role for those genes in synthesis or stability of the protein. These transposon mutants and an ESAT-6/CFP-10 deletion mutant all showed reduced cytolysis and cytotoxicity to macrophages and significantly decreased intracellular growth at late stages of the infection only when the cells were infected at low multiplicity of infection, suggesting a defect in spreading. Direct evidence for cell-to-cell spread by wild-type M. marinum was obtained by microscopic detection in macrophage and epithelial monolayers, but the mutants all were defective in this assay. Expression of M. tuberculosis homologues complemented the corresponding M. marinum mutants, emphasizing the functional similarities between M. tuberculosis and M. marinum genes in this region that we designate extRD1 (extended RD1). We suggest that diminished membranolytic activity and defective spreading is a mechanism for the attenuation of the extRD1 mutants. These results extend recent findings on the genomic boundaries and functions of M. tuberculosis RD1 and establish a molecular cellular basis for the role that extRD1 plays in mycobacterial virulence. Disruption of the M. marinum homologue of Rv3881c, not previously implicated in virulence, led to a much more attenuated phenotype in macrophages and in vivo, suggesting that this gene plays additional roles in M. marinum survival in the host.

Animals↗

Massive hepatic infarction in preeclampsia: successful treatment with continuous hemodiafiltration and corticosteroid therapy.

Massive hepatic infarction associated with pregnancy is extremely rare, but is potentially fatal. A 35-year-old primigravida with mild preeclampsia developed acute right upper quadrant pain and marked elevation of liver enzymes at 26 weeks' gestation. After emergent cesarean section, her condition was complicated by oliguric renal failure and pulmonary edema with further deterioration of hepatic function (aspartate transaminase 4339 IU/L; alanine transaminase 3489 IU/L; lactate dehydrogenase 10780 IU/L). The contrast-enhanced computed tomography revealed non-enhancing low attenuation throughout the right lobe of liver, compatible with infarction. Continuous hemodiafiltration was initiated as renal support on postpartum day one. However, excessive fluid accumulation persisted, and she developed severe edema formation in both lung and systemic body surface. To ameliorate microvascular endothelial injury, corticosteroid therapy was begun on postpartum day five. Following treatment initiation, her renal and hepatic function showed steady improvement, accompanied by drastic resolution of edema formation. She was discharged five weeks postpartum with no additional treatment, and is without sequelae six months later. Massive hepatic infarction should be considered in preeclamptic patients who present acute abdominal pain and severe hepatic dysfunction, and continuous hemodiafiltration with corticosteroid therapy may improve the maternal outcome.

Abdominal Pain↗

Enhancement of the endotoxin recognition pathway by ventilation with a large tidal volume in rabbits.

Ventilation with a small tidal volume (V(t)) is associated with better clinical outcomes than with a large V(t), particularly in critical settings, including acute lung injury. To determine whether V(t) influences the lipopolysaccaharide (LPS) recognition pathway, we studied CD14 expression in rabbit lungs and the release of TNF-alpha by cultured alveolar macrophages after 240 min of ventilation with a large (20 ml/kg) vs. a small (5 ml/kg) V(t). We also applied small or large V(t) to lungs instilled with 50 microg/kg of LPS. The alveolar macrophages collected after large V(t) ventilation revealed a 20-fold increase in LPS-induced TNF-alpha release compared with those collected after small V(t) ventilation, whereas TNF-alpha was undetectable without LPS stimulation. In animals ventilated with a large V(t), the expression of CD14 mRNA in whole lung homogenates and the expression of CD14 protein on alveolar macrophages, assessed by immunohistochemistry, were both significantly increased in the absence of LPS stimulation. A large V(t) applied to LPS-instilled lungs increased the pulmonary albumin permeability and TNF-alpha release into the plasma. These results suggest that mechanical stress caused by a large V(t) sensitizes the lungs to endotoxin, a phenomenon that may occur partially via the upregulation of CD14.

Albumins↗

Elevation of KL-6, a lung epithelial cell marker, in plasma and epithelial lining fluid in acute respiratory distress syndrome.

KL-6 is a pulmonary epithelial mucin more prominently expressed on the surface membrane of alveolar type II cells when these cells are proliferating, stimulated, and/or injured. We hypothesized that high levels of KL-6 in epithelial lining fluid and plasma would reflect the severity of lung injury in patients with acute lung injury (ALI). Epithelial lining fluid was obtained at onset (day 0) and day 1 of acute respiratory distress syndrome (ARDS)/ALI by bronchoscopic microsampling procedure in 35 patients. On day 0, KL-6 and albumin concentrations in epithelial lining fluid were significantly higher than in normal controls (P < 0.001), and the concentrations of KL-6 in epithelial lining fluid (P < 0.002) and in plasma (P < 0.0001) were higher in nonsurvivors than in survivors of ALI/ARDS. These observations were corroborated by the immunohistochemical localization of KL-6 protein expression in the lungs of nonsurvivors with ALI and KL-6 secretion from cultured human alveolar type II cells stimulated by proinflammatory cytokines. Because injury to distal lung epithelial cells, including alveolar type II cells, is important in the pathogenesis of ALI, the elevation of KL-6 concentrations in plasma and epithelial lining fluid could be valuable indicators for poor prognosis in clinical ALI.

Adult↗

Olprinone, a phosphodiesterase III inhibitor, reduces gut mucosal injury and portal endotoxin level during acute hypoxia in rabbits.

BACKGROUND: Preservation of gut integrity has become a therapeutic goal to obviate bacterial translocation in the critically ill. The authors examined whether olprinone, a phosphodiesterase III inhibitor, protected functional and structural integrity of gut mucosa against acute progressive hypoxia. METHODS: Thirty-two animals were randomly allocated to a control group (n = 12), a low-dose group (0.2 microg x kg-1 x min-1 olprinone; n = 10), or a high-dose group (0.6 microg x kg-1 x min-1 olprinone; n = 10) after preparatory surgery. Ascending aortic and portal blood flow, intramural pH of the ileum, and portal endotoxin levels were measured at normoxia and through three stages of progressive hypoxia (fraction of inspired oxygen = 0.17, 0.13, and 0.10). RESULTS: At normoxia, ascending aortic flow in the high-dose group was approximately 20% higher than in the control and low-dose groups. During progressive hypoxia, both ascending aortic and portal flow in the control group were depressed, whereas olprinone infusion attenuated such alterations and redistributed blood to the splanchnic area in a dose-dependent manner. On the contrary, the reduction of intramural pH of the ileum and the elevation of portal endotoxin levels observed in the control group were significantly minimized in both the low- and high-dose groups to a similar extent during acute hypoxia. Histopathologic alterations of gut mucosa observed in the control group were minimized by olprinone infusion dose-independently, accompanied by reduction of mortality rate of the animals. CONCLUSIONS: Olprinone slows progression of intestinal mucosal acidosis and gut barrier dysfunction, concurrently with preservation of microscopic structures, through both flow-dependent and -independent mechanisms under acute hypoxia. Such properties of olprinone may serve to protect the host under insult.

3',5'-Cyclic-AMP Phosphodiesterases↗

Performance of noninvasive partial CO2 rebreathing cardiac output and continuous thermodilution cardiac output in patients undergoing aortic reconstruction surgery.

BACKGROUND: In the partial CO(2) rebreathing method, monitored changes in CO(2) elimination and end-tidal CO(2) in response to a brief rebreathing period are used to estimate cardiac output. However, dynamic changes in CO(2) production during ischemia and reperfusion may affect the accuracy of these estimates. This study was designed to compare measurements of cardiac output as produced by the partial CO(2) rebreathing (NICO), bolus (BCO), and continuous thermodilution (CCO) methods of monitoring cardiac output. METHODS: Cardiac output was continuously monitored using both NICO and CCO in 28 patients undergoing aortic reconstruction. BCO measurements were taken at the following intervals when hemodynamic stability was achieved: (1) after anesthetic induction; (2) during aortic cross-clamp; (3) at reperfusion of the iliac artery; and, (4) during peritoneal closure. RESULTS: The bias and precision (1 SD) derived from all the measurements between NICO and BCO was -0.58 +/- 0.9 l/min, whereas for CCO and BCO it was 0.38 +/- 1.17 l/min. The bias between NICO and BCO was small after anesthetic induction and during cross-clamp, but increased following reperfusion. The bias between CCO and BCO was relatively small until reperfusion but increased significantly at peritoneal closure. CONCLUSIONS: Results indicate that in aortic reconstruction surgery the performance of NICO monitoring is comparable with that of CCO; however, the direction of bias in these continuous measurement devices is the opposite.

Aged↗

Comparative effect of 6% hydroxyethyl starch (containing 1% dextrose) and lactated Ringer's solution for cesarean section under spinal anesthesia.

PURPOSE: This study aimed to compare low-molecular weight hydroxyethyl starch containing 1% dextrose (HES) infusion and lactated Ringer's solution (LR) in the prevention of hypotension associated with spinal anesthesia for cesarean section. METHODS: Sixty-seven patients scheduled for cesarean section under spinal anesthesia were randomly allocated to receive either LR ( n= 35) or HES ( n= 32) infusion before cesarean delivery. Infusion of the fluid was started immediately after arrival at the operating room, through two fully open i.v. routes of 18 or 16 gauge. The two groups were compared in terms of the incidence of hypotension; ephedrine dose; cord and maternal blood gas, hemoglobin, and glucose; and Apgar scores. RESULTS: Intravenous fluid volume until delivery in the LR group was significantly greater than that in the HES group (1298 +/- 503 and 973 +/- 339 ml, respectively) in spite of the similar periods of intravenous infusion (18.1 +/- 3.9 and 18.2 +/- 4.1 min). The incidence of hypotension, and the ephedrine dose, blood gas analyses, and Apgar scores were not significantly different between the groups. The ephedrine dose correlated with the anesthesia level by spinal anesthesia (P < 0.05). CONCLUSION: This study did not show an advantage of HES compared with LR in the prevention of hypotension or in the reduction of ephedrine dose during cesarean section under spinal anesthesia. The anesthesia level, rather than the choice of intravenous fluid solution, might be related to the ephedrine dose.

Clinical Trial↗