Effect of increasing oxygen delivery postburn on oxygen consumption and oxidant-induced lipid peroxidation in the adult sheep

We studied the relationship between oxygen delivery (DO2) and oxygen consumption (VO2) in the early post-burn period. Unanesthetized sheep with a 15% total body surface (TBS) third-degree burn were resuscitated back to baseline VO2 and vascular pressures. DO2 was adjusted further by infusion and removal of whole blood. The response was compared to the same maneuver in nonburned sheep. We found that increasing DO2 after burns resulted in a 32% increase in VO2, while the same maneuver in controls produced no change in VO2. We then determined whether the increase in VO2, caused by volume loading, resulted in a further increase in postburn oxidant release and lipid peroxidation measured as conjugated dienes. Plasma conjugated dienes increased significantly and equally by 30% in burns maintained at baseline VO2 vs. the increased VO2. Therefore, the increased oxygen used is not simply resulting in further oxidant damage. VO2 was maintained equally in both burned animals and controls with a decrease in DO2 by increased oxygen extraction from Hgb. We conclude that standard burn resuscitation does not restore adequate DO2 for oxygen demands. The 30% increase in VO2 achieved by increasing DO2 does not lead to a further release of oxidants from burn tissue and is therefore potentially beneficial for cell function.     

Effect of dobutamine on oxygen consumption and fluid and protein losses after endotoxemia

OBJECTIVE: To determine the effect of a dobutamine infusion on the relationship between oxygen consumption (VO2) and oxygen delivery (DO2) after endotoxin administration, as well as the rate of fluid and protein loss from permeability-injured tissue. METHODS: Unanesthetized adult sheep with lung and soft-tissue lymph fistulas were given 5 micrograms/kg Escherichia coli endotoxin alone, or E. coli endotoxin plus a continuous infusion of dobutamine (10 to 15 micrograms/kg.min) beginning at 3 hrs. Lymph flow reflected the vascular permeability and surface area perfused. Data were compared with dobutamine alone and with controls. Filling pressures were maintained at baseline. RESULTS: Dobutamine alone produced a 75% increase in DO2, a transient 10 +/- 4% increase in VO2, but no increase in lung or soft-tissue lymph flow. Beginning at 3 hrs after endotoxin alone, a significant increase in protein-rich lung and soft-tissue lymph flow was noted, but only a transient 14 +/- 5% increase in VO2. Plasma proteins were slightly decreased. With the addition of dobutamine at 3 hrs postendotoxin, DO2 increased by greater than 50% for the 3-hr infusion period, while VO2 increased for a 30-min period by 25 +/- 8%, which was not different than endotoxin alone. Lung and soft-tissue lymph flow did not increase further, but plasma proteins did decrease significantly compared with controls and with endotoxin alone. CONCLUSION: Increasing DO2 with dobutamine postendotoxin does not increase the surface area perfused or the edema process, at least in lung and soft tissue. Therefore, no microvessels in these tissues are reopened with dobutamine when normal filling pressures are present. Dobutamine administration does not increase VO2 more than the increase seen with endotoxin alone.     

Effect of sequential early burn wound excision and closure on postburn oxygen consumption

OBJECTIVE: To determine the effect of early excision and closure of burns on postburn hypermetabolism, measured as oxygen consumption (VO2). METHODS: Twelve patients with deep burns of 30% to 50% of total body surface underwent sequential excisions and wound coverage, beginning 1 to 3 days after burn. The majority of the deep burn was removed by day 7, but with the addition of a donor site area of 20% to 25% of total body surface. RESULTS: No decrease in VO2 was noted in relation to the percent removal of burn tissue. In addition, a transient further increase in VO2 was noted early after excision, especially with surgical procedures performed after 5 days. This response could not be attributed to wound manipulation-induced bacteremias. CONCLUSION: We conclude that early surgical excision and closure of burns in excess of 30% to 50% of total body surface do not decrease postburn hypermetabolism in proportion to the area closed. It is possible that remaining open wounds in the form of donor sites and nonexcised burn are sufficient to perpetuate the hypermetabolic process, once established.     

口服补液对犬50%TBSA烧伤休克期循环氧动力学指标的影响

目的 研究口服补液对50%TBSA烧伤休克期循环氧动力学指标的影响,为提高烧伤休克口服补液的复苏效果提供依据.方法 成年雄性Beagle犬18只,先期无菌手术行颈动、静脉置管,24 h后用凝固汽油燃烧法造成50%体表面积Ⅲ度烧伤.随机分为不补液组(n=6)、口服补液组(n=6)和静脉补液组(n=6).伤后第一个24 h不补液组无治疗,口服补液组和静脉补液组根据Parkland公式分别从胃内或静脉输注葡萄糖-电解质溶液;伤后24 h起三组均实施延迟静脉补液.测定动物非麻醉状态下的平均动脉压(MAP)、红细胞压积(HCT)和血乳酸(LAC)含量,抽取动脉和混合静脉血测定动、静脉氧分压和血氧含量.计算氧供量(DO2)、氧耗量(VO2)和氧摄取(Oext),并统计3 d死亡率.结果 不补液组伤后8 h MAP比伤前降低77.1%,HCT和血乳酸分别升高48.5%和533.7%;DO2,VO2和Oext水平伤后进行性降低,24 h内动物全部死亡.两补液组上述指标逐渐恢复,伤后72 hMAP和HCT恢复至伤前(P＞0.05),但血乳酸水平仍显著高于伤前(P＜0.01).伤后24 h内同期比较,口服补液组MAP,DO2,VO2和Oext水平显著高于不补液组(P＜0.01),但低于静脉补液组;血乳酸低于不补液组,但高于静脉补液组(P＜0.01).伤后24 h起Do2与静脉补液组差异无统计学意义(P＞0.05),但VO2和Oext仍显著低于静脉补液组(P＜0.01).72 h死亡率:不补液组100%、口服补液组50%(3/6),而静脉补液组为零.结论 50%TBSA烧伤休克期采用口服补液能显著改善动物循环氧动力学指标,减轻高乳酸血症,降低动物的病死率.     

The relationship between oxygen delivery and oxygen consumption during fluid resuscitation of burn-related shock

Although burn-related shock resuscitation based on invasive hemodynamic monitoring has been reported at an increased rate, little is known about appropriate hemodynamic end points. Shock resuscitation based on oxygen transport criteria has been widely used for patients with trauma and patients who undergo surgery, and supranormal values of oxygen delivery (DO2) have been reported in association with an improved survival rate. This improved survival rate has been attributed to a shifting of the critical threshold of DO2 to higher values in these patients. In patients with thermal injuries, the effects of the manipulation of hemodynamics to optimize oxygen transport have not been proven. It is still unclear whether these patients exhibit delivery-dependent oxygen consumption (VO2) during the shock phase. The goal of this study was to evaluate the existence of oxygen supply dependency and to determine critical levels of DO2 in patients with burns. In a prospective study that included 16 patients with serious thermal injuries, we studied the effects of volume loading on DO2 and VO2. A transpulmonary double dilution technique was used for hemodynamic monitoring, and resuscitation end points included a normalization of preload and cardiac output parameters within 24 hours of the thermal injury. Fluid loading with crystalloids and colloids, according to our resuscitation protocol, was used to augment cardiac output and DO2. Of the 16 patients with a mean of 46% total body surface area burned (range, 22%-80%), 8 patients survived and 8 patients died. With the use of progressive fluid loading, cardiac index was restored within 24 hours of admission in all of the patients. Successful resuscitation was associated with increased levels of DO2 and VO2 and with declining serum lactate levels. VO2 appeared to be dependent on DO2 during the resuscitation period (r = 0.596), and the correlation was significantly stronger in the patients who survived (r = 0.744) than in the patients who died (r = 0.368; P < .05). A critical threshold of oxygen supply could not be identified. We concluded that increasing DO2 by fluid resuscitation increases VO2 during hypovolemic shock after a severe burn injury.     

Lack of immediate effects of wound excision on the hyperdynamic circulation of burned patients

The high cardiac output (CO) observed during the chronic phase in burned patients has been ascribed, among other factors, to the elevated blood flow in the burn wound. The hemodynamic effects of wound excision to fascia have been studied in eight patients with second- and third-degree burns ranging from 42% to 70% total body surface area (TBSA) undergoing debridement and skin-grafting procedures. The study was performed on the 4th to the 51st postburn day when all patients were in a hyperdynamic state. Serial hemodynamic measurements, including arterial and mixed-venous blood O2 saturation and content, were made before induction of anesthesia, during surgery both before and after wound excision, and in the recovery room a few hours after surgery. During anesthesia, the elevated CO decreased probably as a consequence of decreased metabolic requirements, but no further hemodynamic change was observed following wound excision. The size of burn wound excised to fascia averaged 24% TBSA and ranged from one-third to more than one-half of the initial burn. With discontinuation of anesthesia, CO rose rapidly above preoperative values, apparently to meet a similar increase in oxygen consumption. The excision of large areas of burned tissue did not attenuate the hyperdynamic circulation in burned patients, at least during and immediately after surgery. The data suggest that the elevated blood flow in the burn wound does not play a significant role in the pathogenesis of the hyperdynamic state.     

Whole body oxygen consumption and critical oxygen delivery in response to prolonged and severe carbon monoxide poisoning

BACKGROUND: Carbon monoxide (CO) poisoning remains the leading cause of death by poisoning in the world. One of the major proposed mechanisms for CO toxicity is the binding of CO to cytochrome oxidase and interference with cellular oxygen utilization but evidence for this is inconclusive. AIM OF STUDY: This study examined the effects of prolonged CO exposure on the dynamics of whole body oxygen consumption (VO(2)) and oxygen delivery (DO(2)) in an attempt to observe if CO exposure results in a defect of oxygen utilization defect as determined by a reduction in VO(2) during the course of poisoning prior to reaching the point where VO(2) is directly dependent on DO(2). This critical level of DO(2) (DO(2)crit) produced by CO poisoning was compared to historical values produced by other insults, which decrease global body DO(2). METHODS: Five small dogs were ventilated for 2 h with 0.25% CO and room air followed by 0.5% CO until death. Cardiac index (Q), DO(2), VO(2), oxygen extraction ratio (OER), and systemic lactate were measured every 15 min until death. RESULTS: Carboxyhemoglobin (COHb) levels increased linearly over 2.5 h to values above 80% until death. VO(2) remained constant and not significantly different from baseline below a COHb of 80%. At COHb levels above 80%, VO(2) precipitously dropped. Similarly lactate levels were not significantly elevated from baseline until VO(2) dropped. DO(2) decreased by 78% (from 23+/-6 ml/kg/min to 5+/-4 ml/kg/min) over time despite an increase in Q by 58% until levels of COHb were above 80%. OER increased from 19+/-5% to 50+/-11% until death. The calculated DO(2)crit was 10.7+/-4 ml/min/kg, which is not significantly different from values ranging from 7 to 13 ml/min/kg reported in the literature due to other insults, which reduce DO(2). CONCLUSION: In this canine model of prolonged CO exposure, no gradual reduction in VO(2) or increase in systemic lactate prior to reaching DO(2)crit was noted. In addition, CO exposure does not appear to change the DO(2)crit. The combination of these findings does not support the theory that CO produces a whole body intracellular defect in oxygen utilization.     

Effect of blood transfusion on oxygen consumption in pediatric septic shock

Treatment plans for pediatric septic shock advocate increasing oxygen consumption (VO2). Recent studies in septic shock indicate that improving oxygen delivery (DO2) by increasing blood flow will increase VO2. We prospectively examined the effect on VO2 of improving DO2 by increasing oxygen content (CO2) with blood transfusion in eight hemodynamically stable septic shock patients. Transfusion consisted of 8 to 10 ml/kg of packed RBC over 1 to 2 h. Hemodynamic and oxygen transport measurements were obtained before and after blood transfusion. Transfusion significantly (p less than .05) increased Hgb and Hct from 10.2 +/- 0.8 g/dl and 30 +/- 2% to 13.2 +/- 1.4 g/dl and 39 +/- 4%, respectively (mean +/- SD). DO2 significantly (p less than .05) increased after transfusion (599 +/- 65 to 818 +/- 189 ml/min.m2), but VO2 did not change (166 +/- 68 to 176 +/- 74 ml/min.m2; NS). In pediatric septic shock patients, increasing CO2 by blood transfusion may not increase VO2.     

Interleukin-1beta alters the oxygen delivery-oxygen consumption relationship in rabbits by increasing the slope of the supply-independent line

When systemic oxygen delivery (DO2) is reduced, oxygen consumption (VO2) is maintained until a critical level is reached (DO2crit). Sepsis is thought to shift DO2crit to the right and lengthen the supply-dependent portion. We tested the effect of interleukin (IL)-1beta, which is one of the key cytokines related to sepsis, on the DO2-VO2 relationship. Fifteen rabbits were subjected to stepwise cardiac tamponade to reduce DO2 to 10% by inflating a handmade balloon placed into the pericardial sac. Seven rabbits were given 10 microg/kg of IL-1beta intravenously (IL-1beta group) prior to the graded cardiac tamponade. The remainder received saline alone (control group). The DO2-VO2 relationship was analyzed by the dual-line method. IL-1beta significantly decreased mean arterial pressure (65 +/- 11 mmHg from baseline 85 +/- 7 mmHg) without altering cardiac output. The IL-1beta group showed significantly steeper supply-independent line slopes than did the control group (0.19 +/- 0.02 vs. 0.11 +/- 0.02, respectively), which resulted in a DO2crit shift to the left (IL-1beta group, 8.7 +/- 1.7 ml/kg x min vs. control, 11.7 +/- 0.7 ml/kg x min). The IL-1beta group also showed greater PO2 and plasma lactate levels in the portal vein than did the control group. These results indicate that IL-1beta impairs systemic oxygen uptake even before VO2 becomes supply-dependent, presumably due to maldistribution of the blood flow including the splanchnic circulation.     

Dopamine does not correct oxygen consumption/oxygen delivery relation abnormality during vasomotor shock induced by interleukin-1beta

We previously showed that interleukin 1beta (IL-1beta) induces vasomotor shock and impairs the oxygen consumption (VO2)/oxygen delivery (DO2) relation by increasing the slope of the supply-independent line in rabbits. In the present study, we investigated the inotropic effect of dopamine on the VO2/DO2 abnormality induced by IL-1beta. Twelve rabbits were divided into two groups (n = 6, each) and were given 10 microg/kg of IL-1beta or saline (control) intravenously. After baseline measurements were obtained, dopamine was infused continuously at a rate of 20 microg/kg/min throughout the study in both groups. All rabbits were subjected to stepwise cardiac tamponade to reduce the DO2 to <5 mL/min/kg by inflation of a handmade balloon placed into the pericardial sac. The VO2/DO2 relation was then analyzed by the dual-line method. Dopamine failed to correct the IL-1beta-induced decrease in mean arterial pressure to the baseline level. Dopamine significantly increased cardiac index in both groups, resulting in significant increases in DO2 (IL-1beta, 28.5 +/- 6.0 mL/min/kg from baseline 24.1 +/- 3.5 mL/min/kg; control, 27.7 +/- 2.9 mL/min/kg from baseline 22.9 +/- 2.9 mL/min/kg), but did not affect VO2 (IL-1beta, 10.0 +/- 0.5 mL/min/kg from baseline 9.9 +/- 0.7 mL/min/kg; control, 10.2 +/- 0.4 mL/min/kg from baseline 10.2 +/- 0.2 mL/min/kg). The IL-1beta group showed a significantly greater supply-independent line slope than that of controls (IL-1beta, y = 0.14x + 6.3; control, y = 0.06x + 8.6) during stepwise decreases in DO2. These results indicate that continuous infusion of dopamine at 20 microg/kg/min increases DO2 but does not correct the vasomotor disturbance or VO2/DO2 abnormality caused by IL-1beta.     

重症急性胰腺炎血流动力学和氧代谢变化的实验研究

目的 观察重症急性胰腺炎(SAP)猪的血流动力学和氧代谢变化特点,为临床治疗提供理论依据。方法 通过向主胰管逆行注入含质量分数为4％牛磺胆酸钠和质量分数为1％胰蛋白酶的生理盐水溶液(1 ml／kg)诱导猪SAP模型(n=8);通过Swan-Ganz导管和心电监护仪,连续监测心率(HR)、中心静脉压(CVP)、平均动脉压(MAP)、肺动脉楔压(PAWP)、平均肺动脉压(MPAP)和心排血量,计算心脏指数(CI);通过对制模前(0 h)和制模后6、12、24及36 h的动脉及混和静脉血的血气分析,计算出相应的全身氧输送(DO2)、氧耗(VO2)和氧摄取率(O2ext),分析上述各指标的变化。结果 制模12 h MAP和CI与0 h比较显著下降(P均<0.05)。动脉氧分压(PaO2)和DO2都有下降的趋势。与0 h比较,PaO2在制模后6 h以后下降显著,DO2在制模后24 h下降最显著(P均<0.05)。VO2和O2ext的走势一致,都在制模后6 h上升至最高水平(P均<0.05),然后一直下降,制模后24 h较6 h差异具有显著性(P均<0.05)。结论SAP时不仅有血流动力学紊乱,而且有氧代谢障碍。SAP导致多器官功能障碍综合征(MODS)的因素可能与VO2和O2ext下降有关。     

重型乙型肝炎患者原位肝移植围手术期全身氧代谢的变化

目的 探讨重型乙型肝炎（乙肝）与其他肝病患者原位肝移植围术期全身氧代谢变化的特点。方法 12例重型乙肝患者为试验组。10例其他肝病患者为对照组。以咪唑安定、异丙酚、芬太尼、维库溴铵诱导全麻，术中吸入异氟醚维持麻醉。维库溴铵维持肌松，行改良背驼式原位肝移植术。左桡动脉穿刺测有创动脉压，右颈内静脉穿刺置入漂浮导管。分别于术前、无肝前10min、无肝期25min、新肝期30min和术毕监测动脉和混合静脉血氧分压（PaO2和Pv^-O2）、动脉和混合静脉血氧含量（CaO2和Pv^-O2）及动-静脉血氧含量差（CA-vO2）、氧供（DO2）、氧供指数（DO2I）、氧消耗（VO2）、氧耗指数（VO2I）、氧摄取指数（O2EI）和氧摄取率（O2ER）。结果 ①试验组：与术前相比，无肝前期Pv^-O2上升，Ca-vO2、O2EI、O2ER下降，DO2和VO2无明显变化；无肝期DO2、DO2I、VO2和VO2I均明显下降，DO2、VO2分别下降43％和21％，O2EI和O2ER均明显上升；新肝期PvO2上升，DO2和DO2I明显上升。VO2和VO2I回升至术前水平；术毕时DO2和DO2I依然高于术前水平。②对照组：无肝前期PvO2上升。DO2和VO2无明显变化，O2EI和O2ER下降；无肝期DO2、DO2I、VO2和VO2I均明显下降，DO2下降25％，VO2则下降12％；新肝期PvO2上升，Ca-vO2下降，DO2、DO2I明显上升，VO2和VO2I回升至术前水平；术毕时DO2和DO2I依然高于术前水平。结论肝移植围术期中，全身DO2变化大于VO2变化；重型乙肝患者的全身DO2和VO2变化较其他肝病患者剧烈。     

Comparison of systemic oxygen delivery and uptake with NIR spectroscopy of brain during normovolemic hemodilution in the rabbit.

Incremental hyperoxic normovolemic hemodilution was utilized to progressively decrease oxygen delivery (DO2) in anesthetized rabbits. At decreasing DO2, we compared systemic responses related to the adequacy of DO2, i.e. mixed venous oxygen saturation (SvO2), oxygen consumption (VO2), and arterial lactate concentrations, to near infrared spectroscopy (NIRS) of the brain, a regional measure of intracellular oxygen availability. We sought concomitantly to define critical SvO2 and DO2, beyond which whole body VO2 begins to decline and arterial lactate concentrations increase. NIR Spectroscopy provided the means to test the hypothesis that systemic indicators of inadequate DO2 would not accurately reflect the oxygenation of a critical organ such as the brain. In thirteen rabbits anesthetized with fentanyl, paralyzed and artificially ventilated at an FIO2 of 0.60, hemodilution produced an early decrease in mixed venous oxygen saturation. When mixed venous oxygen saturation decreased below approximately 50%, arterial lactate concentrations began to increase significantly. Further decreases in oxygen delivery precipitated a decline in systemic VO2. Finally, NIRS revealed an increase in the reduction level of brain cytochrome a,a3 after systemic parameters of oxygen delivery had been altered. Analysis of the data indicated that falling SvO2 predicted inadequate DO2 to tissue during early hemodilution under narcotic/relaxant anesthesia and that the brain showed evidence of intracellular hypoxia only after systemic parameters such as SvO2 were affected markedly.     

Blood transfusion and oxygen consumption in surgical sepsis

OBJECTIVE: To evaluate the use of serum lactic acid values to predict flow-dependent increases in oxygen consumption (VO2) in response to increasing oxygen delivery (DO2) after blood transfusion in surgical sepsis. DESIGN: Prospective study. SETTING: Tertiary care, trauma center. PATIENTS: Twenty-one patients, postsurgical or posttrauma, judged septic by defined criteria. INTERVENTIONS: Serum lactic acid concentrations, DO2, and VO2 were measured before and after transfusion therapy. MEASUREMENTS AND MAIN RESULTS: Overall, the DO2 increased from 532 +/- 146 to 634 +/- 225 (SD) mL/min.m2 (p less than .001), and the VO2 increased from 145 +/- 39 to 160 +/- 56 mL/min.m2 (p = .02). These changes occurred with an Hgb increase from 9.3 +/- 1.1 to 10.7 +/- 1.5 g/dL (p less than .001). The patients were grouped by their pretransfusion serum lactic acid values. In those patients with normal (less than 1.6 mmol/dL) serum lactic acid (n = 10), DO2 increased from 560 +/- 113 to 676 +/- 178 mL/min.m2 (p less than .02), and VO2 increased from 150 +/- 25 to 183 +/- 46 mL/min.m2 (p less than .02). However, in the increased serum lactic acid group (n = 17), VO2 was not significantly changed after transfusion (143 +/- 46 to 146 +/- 58 mL/min.m2) despite increased DO2 (515 +/- 163 to 609 +/- 251 mL/min.m2, p less than .01). CONCLUSIONS: Blood transfusion can be used to augment DO2 and VO2 in septic surgical patients. Increased serum lactic acid values do not predict patients who will respond. The absence of lactic acidosis should not be used in this patient population to justify withholding blood transfusions to improve flow-dependent VO2. Patients who have increased lactate concentrations may have a peripheral oxygen utilization defect that prevents improvement in VO2 with increasing DO2.     

Time course of alterations in lung lymph and bronchial blood flows after inhalation injury

The effects of inhalation injury on the pulmonary microvascular fluid flux and bronchial blood flow were examined in a long-term study of sheep (N = 13). They were insufflated with either 48 breaths of cotton smoke (n = 8) or air (n = 5) while they were deeply anesthetized with halothane. After injury, anesthesia was discontinued and the animals were mechanically ventilated throughout the experimental period (24 hours). Bronchial blood flow increased significantly at all time points recorded and reached its peak 20 minutes after the inhalation trauma (11 +/- 1 ml/hr to 106 +/- 18 ml/hr; p less than 0.05). Thereafter, bronchial blood flow decreased to a value that was six to eight times above the baseline measurement for the remainder of the study period. With these changes in blood flow, there was a concomitant increase in lung lymph flow. This variable gradually increased and was 633% of the baseline value (6 +/- 1 ml/hr to 44 +/- 8 ml/hr) 24 hours after the challenge with smoke. The control animals showed little or no change in cardiopulmonary function during the experimental period. There is no correlation between the increase in bronchial blood flow and lung lymph flow patterns after cotton smoke inhalation injury.     

Hemodynamic and metabolic effects of dobutamine in 18 patients after open heart surgery

Low cardiac output syndrome frequently follows cardiopulmonary bypass (CPB) surgery. In the present study, we used dobutamine to increase cardiac index (CI) and oxygen delivery (DO2) in 18 patients after open heart surgery. Using increasing doses of dobutamine up to 10 micrograms/kg.min-1, we observed statistically significant (p less than .01) increases in mean CI (2.50 +/- 0.10 to 3.56 +/- 0.18 L/min.m2) and in mean heart rate (HR) (83 +/- 3 to 105 +/- 3 beat/min). Mean systemic vascular resistance index decreased significantly (p less than .01) in all patients (2271 +/- 101 to 1648 +/- 83 dyne.sec/cm5.m2). Pulmonary vascular resistance index did not change in the ten coronary artery bypass graft patients, but decreased significantly (p less than .01) in the eight valve replacement patients (561 +/- 98 to 421 +/- 79 dyne.sec/cm5.m2). Mean DO2 increased in all patients, although there was no concomitant increase in oxygen consumption (VO2) in four patients. We observed a significant (p less than .01) increase in mean VO2 in the remaining 14 patients (110 +/- 6 to 148 +/- 12 ml/min.m2), in spite of significant decreases in PaO2 and increases in right-to-left intrapulmonary shunting. Although increases in HR and ventricular arrhythmias may limit its use, dobutamine increases CI and DO2 in patients after CPB. In the present study, dobutamine's varying metabolic effect exemplifies the need for close monitoring of hemodynamic and metabolic variables when using vasoactive drugs in the postoperative period.     

Hepatic and splanchnic oxygen consumption during acute hypoxemic hypoxia in anesthetized pigs

OBJECTIVE: To compare the hepatosplanchnic oxygen consumption (VO2) with the hepatic and splanchnic VO2 and to calculate the critical oxygen delivery (DO2crit) below which VO2 decreases in the hepatic, splanchnic, and hepatosplanchnic regions in a model of hypoxemic hypoxia. DESIGN: Prospective animal study. SETTING: University research laboratory. SUBJECTS: Anesthetized and ventilated pigs (n = 7). INTERVENTIONS: The right carotid artery was cannulated to measure mean arterial pressure. A pulmonary artery catheter was inserted to measure mean pulmonary arterial pressure and cardiac output. After a midline abdominal incision, two flow probes were positioned around the portal vein and the hepatic artery to measure portal vein blood flow and hepatic artery blood flow. Oxygen and lactate contents in the carotid artery, the portal vein, and the hepatic vein were measured in blood samples obtained from the appropriate catheters. MEASUREMENTS AND MAIN RESULTS: After a 2-hr stabilization period, hemodynamic and biological variables were recorded during acute hypoxemic hypoxia (FIO2 = 0.5, 0.4, 0.3, 0.21, 0.15, 0.10, and 0.07). VO2, DO2, and DO2crit were determined in the hepatic, splanchnic, and hepatosplanchnic regions. The hepatosplanchnic VO2 was 48 +/- 5 mL/min at high FIO2 (40% for the liver and 60% for the splanchnic organs) and decreased below FIO2 of 0.15. Lactate uptake in the whole hepatosplanchnic region remained steady at FIO2 values of 0.5 to 0.15 and then switched to a lactate release at low FIO2. However, the splanchnic region released lactate, whereas lactate was taken up by the liver. DO2crit in the hepatic, splanchnic, and hepatosplanchnic regions was 24 +/- 3, 38 +/- 2, and 49 +/- 4 mL/min, but the systemic DO2crit, below which regional VO2 became oxygen supply dependent, did not differ in the liver, splanchnic, and hepatosplanchnic regions. CONCLUSIONS: The variables of oxygenation and lactate flux measured in the hepatosplanchnic region summarize the metabolic changes of various organs that may vary in different ways during hypoxemic hypoxia.     

Decreased supply-dependent oxygen consumption in the skeletal muscle of the spontaneously hypertensive rat during acute hypoxia

The purpose of this study was to correlate microvascular oxygen delivery (DO2) and consumption (VO2) in the skeletal muscle of spontaneously hypertensive rats (SHRs) and Wistar Kyoto rats (WKY) with hemodynamics during acute hypoxia. We expected greater abnormalities in central and microvascular hemodynamics during hypoxic induced shock in the SHR compared with the WKY due to microvascular rarefaction. The inspired oxygen fraction (FiO2) was lowered from 0.21 to 0.15, 0.1, 0.08, and 0.05 in anesthetized, mechanically ventilated rats. Lactate and base deficit values were similar for both groups at 0.21 and 0.15 FiO2, but higher in SHR at lower FiO2. Baseline aortic blood flow (SHR, 56.2+/-4.0 mL min; WKY, 61.8+/-5.3 mL min) and systemic DO2 (SHR, 9.02+/-0.82 mL min; WKY, 9.32+/-0.54 mL min) increased similarly when FiO2 was lowered to 0.15. Further reductions in FiO2 caused lower aortic flow and systemic DO2 in the SHR than WKY at 0.08 and 0.05 FiO2. Spinotrapezius blood flow increased from baseline (SHR, 24.8+/-1.8 nL s; WKY, 22.7+/-2.1 nL s) in both groups when FiO2 was reduced to 0.15; further reductions in FiO2 decreased blood flow in both groups, with lower values in the SHR group at 0.1 and 0.08 FiO2. The SHR group demonstrated higher venous oxygen saturation at low values of FiO2 compared with WKY. This reduced oxygen extraction in SHR resulted in a lower supply-dependent VO2 at low values of spinotrapezius DO2, perhaps attributed to arteriolar thickening and rarefaction seen in chronic hypertension.     

Aerosolized alpha-tocopherol ameliorates acute lung injury following combined burn and smoke inhalation injury in sheep

Victims of fire accidents who sustain both thermal injury to the skin and smoke inhalation have gross evidence of oxidant injury. Therefore, we hypothesized that delivery of vitamin E, an oxygen superoxide scavenger, directly into the airway would attenuate acute lung injury postburn and smoke inhalation. Sheep (N = 17 female, 35 +/- 5 kg) were divided into 3 groups: (1) injured, then nebulized with vitamin E (B&S, Vitamin E, n = 6); (2) injured, nebulized with saline (B&S, Saline, n = 6); and (3) not injured, not treated (Sham, n = 5). While under deep anesthesia with isoflurane, the sheep were subjected to a flame burn (40% total body surface area, 3rd degree) and inhalation injury (48 breaths of cotton smoke, <40 degrees C). All groups were resuscitated with Ringer lactate solution (4 mL/kg/%burn/24 h) and placed on a ventilator [positive end-expiratory pressure (PEEP) = 5 cm H2O, tidal volume = 15 mL/kg] for 48 h. B&S injury halved the lung alpha-tocopherol concentrations (0.9 +/- 0.1 nmol/g) compared with sham-injured animals (1.5 +/- 0.3), whereas vitamin E treatment elevated the lung alpha-tocopherol concentrations (7.40 +/- 2.61) in the injured animals. B&S injury decreased pulmonary gas exchange (PaO2/FiO2 ratios) from 517 +/- 15 at baseline to 329 +/- 49 at 24 h and to 149 +/- 32 at 48 h compared with sham ratios of 477 +/- 14, 536 +/- 48, and 609 +/- 49, respectively. Vitamin E treatment resulted in a significant improvement of pulmonary gas exchange; ratios were 415 +/- 34 and 283 +/- 42 at 24 and 48 h, respectively. Vitamin E nebulization therapy improved the clinical responses to burn and smoke inhalation-induced acute lung injury.     

Usefulness of warm fluid in acute burn resuscitation: an experimental study in dogs

Hypothermia is a common complication in patients with extensive burns, receiving massive volumes of fluid for resuscitation at ambient temperature. It is therefore important to maintain the body temperature of patients with extensive burns. The present study was performed to evaluate the usefulness of warm fluid for burn injury resuscitation. Ten dogs were used in this study. Full-thickness burns, involving 40% of the body surface, were generated in the backs of the animals. In the control group (n = 5), the fluid temperature was maintained at about 23 degrees C, while in other group (n = 5), the temperature of the fluid was maintained at 39 degrees C with a warming device. Cardiac output and urinary output were measured in both groups for up to 24 hours. The cardiac output decreased in all animals during the first two hours following injury. The cardiac dynamics remained depressed in the control group. By contrast, in animals treated with warm fluid, the cardiac output returned to the baseline level within 4 hours of resuscitative measures and then decreased slightly for the subsequent 20 hours. The urinary output was better in animals treated with warm fluid, indicating the improved hemodynamic state in these animals. These results suggested that the hemodynamic state in acute burn shock was ameliorated by the use of warm fluid. Therefore, warmed fluid resuscitation might be useful to perform immediate excision and grafting for the patients with extensive burns in acute burn shock.