Diagnostic utility of sublingual PCO2 for detecting hemorrhage in penetrating trauma patients

BACKGROUND: Hemorrhage results in early compromise of splanchnic circulation. Studies have shown that sublingual Pco2 (SLCO2) correlates with gut perfusion. We tested SLCO2's ability to detect hemorrhage. We compared SLCO2 with arterial base deficit (BD) and lactate (LAC). METHODS: This was a prospective study of patients with penetrating torso trauma. SLCO2 was measured at triage. Blood loss was defined as none (group 1), minimal to moderate (<1,500 mL) (group 2), or severe (>/=1,500 mL) (group 3). Data were reported as mean (95% confidence interval) and compared by analysis of variance. Receiver operating characteristic curves compared diagnostic performance between SLCO2, BD, and LAC. RESULTS: One hundred eight patients were enrolled. There was a significant difference (p < 0.001) in SLCO2 between all blood loss groups: group 1, 46.9 mm Hg (44.9-49.0 mm Hg); group 2, 53.5 mm Hg (50.8-56.2 mm Hg); and group 3, 66.0 mm Hg (53.1-78.9 mm Hg). There were no significant (p > 0.05) differences for receiver operating characteristic curves between SLCO2, BD, or LAC. CONCLUSION: SLCO2 differentiated blood loss groups. SLCO2 may be useful in triage of penetrating trauma patients.     

The relation between intracranial pressure,mean arterial pressure and cerebral blood flow in patients with severe head injury

In patients with severe head injuries ICP, MAP and CBF were measured continuously. In most patients there was a positive vasopressor response to increasing ICP, but the ICP/MAP ratio varied considerably in individual cases. CBF was diminished either by increasing ICP or by decreasing MAP. This effect was more marked with ICP above 40 mm Hg or MAP below 110 mm Hg. In terminal stages there was often a negative MAP/ICP ratio accompanied by massive cerebral hyperaemia. Key words: Severe head injury--intracranial pressure--mean arterial pressure--cerebral blood flow--cerebral perfusion pressure--critical limit of ICP and CBF. Abbreviations: ICP equals intracranial pressure (mm Hg); CBF, Flow equals cerebral blood flow (ml/min); MAP equals mean arterial pressure (mm Hg); CPP equals cerebral perfusion pressure (mm Hg) (difference between MAP and ICP); BP equals blood pressure.     

不同程度过度通气对蛛网膜下腔出血犬脑氧代谢的影响

目的 评价不同程度过度通气对蛛网膜下腔出血犬脑氧代谢的影响.方法 健康雄性犬,体重12～18 kg,采用枕大池二次注血法制备犬蛛网膜下腔出血模型,取模型制备成功犬24只,随机分为4组(n=6):正常通气组[N组,呼气末二氧化碳分压(PETCO2)35～40 mm Hg]、轻度过度通气组(L组,PETCO2 30～35 mm Hg)、中度过度通气组(M组,PETCO2 25～30 mm Hg)和重度过度通气组(H组,PETCO220～25 mm Hg).调整呼吸机参数使各组PETCO2分别达到所需数值,维持机械通气4 h.分别于二次注血完毕稳定后30 min(T0)、机械通气1、2、3、4 h(T1～4)时记录基本生命体征,测定颅内压、颈静脉血氧饱和度(SjvO2)、颈静脉血氧分压(PjvO2)、颈动脉-静脉血氧含量差(Da-jvO2)、脑氧摄取率(ERO2)和颈静脉-动脉血乳酸浓度差(Djv-aL).分别于T0～4机械通气结束后4、12、20、44、92和188 h(T5～10)时采集前肢内侧皮下头静脉血测定S-100B蛋白浓度.结果 与N组比较,其余各组T1～4时颅内压降低,M组和H组Da-jvO2、ERO2升高,H组Djv-aL升高,M组T2～4时Djv-aL升高,H组T2,3时SjvO2降低,H组T1～10时血清S-100B蛋白浓度升高(P<0.05);与T0时比较,N组、M组和H组T5～8时、L组T4～8时血清S-100B蛋白浓度升高(P<0.05).结论 对蛛网膜下腔出血犬,轻度及中度过度通气不会加重脑损伤;重度过度通气时脑氧供需失衡,脑损伤加重.     

Metabolic and hemodynamic effects of CO2 pneumoperitoneum in a controlled hemorrhage model.

BACKGROUND: Intracavity infusion of fibrin sealant-based agents, as a novel modality to control internal bleeding, is associated with an increase of pneumoperitoneum (PP) pressure. The safe limit of such increase has not been well defined in hypovolemic subjects. The purpose of this study was to evaluate the hemodynamic and metabolic effects of increasing PP pressure and to define the limits of carbon dioxide (CO2) insufflation in a controlled hemorrhage rat model. METHODS: Ninety male rats (474 +/- 6 g, 37 degrees +/- 1 degrees C) were anesthetized, and mechanically ventilated. Animals were randomly distributed among 14 groups (n = 6-8) with an increasing amount of blood loss (0, 10, 15, and 17.5 mL/kg) and 15 minutes of CO2 insufflation at 0, 5, 10, and 15 mm Hg starting 15 minutes after hemorrhage, followed by desufflation. Mean arterial pressure (MAP), heart rate, and survival were recorded and arterial and venous blood samples were collected at baseline, at 15 minutes after hemorrhage, after insufflation, and after desufflation procedures to determine arterial blood gases and lactic acid levels. RESULTS: In nonhemorrhaged animals, increasing PP pressure up to 15 mm Hg produced only transient changes in MAP and no increase in lactate level. A moderate hemorrhage (10 mL/kg) limited the safe abdominal pressure to 10 mm Hg with metabolic changes that were restored 15 minutes after desufflation. Higher PP pressure (15 mm Hg) at this hemorrhage level produced a significant decline in MAP (42%, p < 0.001) and progressive metabolic acidosis with a 2.1-fold increase (p < 0.01) in lactate level. The more severe hemorrhage (15 mL/kg) further reduced the limits of PP pressure such that 10 and 15 mm Hg resulted in a progressive decline of blood pressures (52% and 54%, respectively; p < 0.001) and severe metabolic acidosis as manifested by 3.3- and 3.1-fold rises in lactate levels, respectively. In the most severe hemorrhaged animals (17.5 mL/kg), the 50% mortality was primarily determined by the severity of the blood loss and the additional PP at 5 mm Hg had no significant impact. CONCLUSION: The safe limit of PP pressurization with CO2 is dependent on the amount of blood loss. In this mechanically ventilated rat model, increasing the amount of blood loss from 0 to 15 mL/kg reduces the tolerable level of abdominal insufflation pressure from 15 mm Hg to 5 mm Hg. A 5-mm Hg PP pressure appears safe even in the most severely hemorrhaged animals.     

Regional cerebral blood flow and response to carbon dioxide during controlled hypotension with isoflurane anesthesia in the rat

Regional (frontal, parietal, occipital, cortical, and basal ganglia) cerebral blood flow (rCBF) was examined at 1.5 and 3.5 MAC inspired isoflurane/O2 anesthesia in the rat using the radioactive microsphere technique to determine the effects of controlled hypotension with deep isoflurane anesthesia on rCBF and the response of rCBF to changes in PaCO2 when mean blood pressure (BP) was decreased to levels below the lower limit of the autoregulatory threshold. Four groups of six rats were studied with rCBF 1 determined at 1.5 MAC (mean BP 80-90 mm Hg) followed by two rCBF determinations at 3.5 MAC (mean BP 46-48 mm Hg). For CBF 1 the regional CO2 response was a 3.1-3.9% increase in rCBF/mm Hg increase in CO2. Regional cerebral blood flow (ml/g/min) ranged from 0.64 +/- 0.05-0.83 +/- 0.15 at PaCO2 of 19 mm Hg to 1.34 +/- 0.11-1.80 +/- 0.33 at PaCO2 of 41 mm Hg to 2.61 +/- 0.26-3.72 +/- 0.37 at PaCO2 of 59 mm Hg (mean +/- SEM). With controlled hypotension (CBF 2) rCBF was unchanged during normocarbia, increased 100% during hypocarbia, P less than 0.01 vs CBF 1 and decreased 30% during hypercarbia, P less than 0.01 vs CBF 1. For rCBF 3 measurements, the BP and inspired concentration of isoflurane were kept constant, while PaCO2 was increased in two and decreased in two of the four groups. Within-group comparisons between rCBF 2 and rCBF 3 results demonstrated loss of CO2 responsiveness of the rat cerebrovasculature in every region during controlled hypotension to below the autoregulatory threshold at 3.5 MAC isoflurane/O2 anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)     

CO2气腹对动脉粥样硬化兔颈动脉血流量的影响

目的探讨CO2气腹对动脉粥样硬化兔颈动脉血流量的影响及其机理.方法将50只日本大耳白兔按随机数字表法分为正常对照组(n=13)和动脉粥样硬化组(n=37), 后者根据气腹压的不同[0、10及15 mm Hg(1 mm Hg=0.133 kPa)]分为3个亚组,n分别为12、12及13.通过高脂饮食制作兔动脉粥样硬化模型.采用电磁流量计检测实验兔颈动脉血流量变化,生化分析仪行血气分析.结果建立气腹后(10及15 mm Hg)各时点兔颈动脉血流量均明显高于0 mm Hg组及正常对照组(P＜0.05),且随气腹持续时间延长而增加,均明显高于气腹前(P＜0.05),解除气腹后30 min虽有下降,但仍高于气腹前(P＜0.05); 其中15 mm Hg组颈动脉血流量明显高于10 mm Hg组(P＜0.05); 0 mm Hg组与正常对照组颈动脉血流量差异无统计学意义(P>0.05).建立气腹后(10及15 mm Hg)各时点,动脉血PaCO2逐渐升高,pH值逐渐下降,均明显高于或低于气腹前、0 mm Hg组及正常对照组(P＜0.05); 各时点0 mm Hg组及正常对照组 pH值及PaCO2差异无统计学意义(P>0.05); 各组间及各时点间血HCO3-含量差异无统计学意义(P>0.05).结论动脉粥样硬化状态下,CO2气腹可引起颈动脉血流量增加,其机理可能与腹内压增高、CO2通过腹膜吸收导致PaCO2升高、pH降低、造成高碳酸血症等原因有关.     

The effect of photodynamic therapy on tumor oxygenation

Oxygen microelectrodes were used to measure tumor partial pressure of oxygen (PO2) before and after photodynamic therapy (PDT) in a rat transplantable subcutaneous chondrosarcoma. Before PDT there was a gradient of PO2 from the superficial layers of the tumor (PO2 = 46 +/- 6 mm Hg) toward the center of the tumor (PO2 = 10 +/- 1 mm Hg). Mean tumor PO2 (21 +/- 2 mm Hg) was significantly reduced to 3 +/- 1 mm Hg 1 hour after PDT, and this reduction in PO2 persisted 4 hours (8 +/- 2 mm Hg) and 24 hours (6 +/- 1 mm Hg) after PDT. The largest percentage decrease in PO2 occurred at a depth of only 50 microns into the tumor. Inasmuch as PDT has been shown to decrease blood flow, our data suggest that PDT actions on blood vessels in the peripheral areas of the tumor are of major importance for eliciting the tumor hypoxia that contributes to tumor necrosis after PDT.     

Blood flow and tissue oxygen pressures of liver and pancreas in rats: effects of volatile anesthetics and of hemorrhage.

The object of this investigation was to compare the effects of volatile anesthetics and of hemorrhage at comparable arterial blood pressures on splanchnic blood flow (radioactive microspheres) and tissue oxygenation of the liver and pancreas (surface PO2 [PSO2] electrodes). In contrast to earlier studies, we did not use identical minimum alveolar anesthetic concentration multiples as a reference to compare volatile anesthetics; rather, we used the splanchnic perfusion pressure. Under general anesthesia (intravenous chloralose) and controlled ventilation, 12 Sprague-Dawley rats underwent laparotomy to allow access to abdominal organs. Mean arterial pressure was decreased from 84 +/- 3 mm Hg (mean +/- SEM) at control to 50 mm Hg by 1.0 +/- 0.1 vol% halothane, 2.2 +/- 0.2 vol% enflurane, and 2.3 +/- 0.1 vol% isoflurane in a randomized sequence. For hemorrhagic hypotension, blood was withdrawn gradually until a mean arterial pressure of 50 mm Hg was attained. Volatile anesthetics and hemorrhage reduced cardiac output, and hepatic arterial, portal venous, and total hepatic blood flows by comparable degrees. Mean hepatic PSO2 decreased significantly from 30.7 +/- 2.6 mm Hg at control to 17.4 +/- 2 and 17.5 +/- 2 mm Hg during enflurane and isoflurane (each P less than 0.05) anesthesia, respectively. The decrease to 11.5 +/- 2.5 mm Hg was more pronounced during halothane anesthesia. Hemorrhagic hypotension was associated with the lowest hepatic PSO2 (3.4 +/- 1.3 mm Hg) and the highest number of hypoxic (0-5 mm Hg 86%) and anoxic PSO2 values (0 mm Hg 46%). Pancreatic blood flow and oxygenation remained unchanged from control during halothane and enflurane administration, whereas isoflurane increased both variables. Hemorrhagic hypotension slightly reduced pancreatic flow (-8%) but significantly decreased PSO2 from 58 +/- 5 mm Hg at control to 36 +/- 3 mm Hg, with 7% of all measured values in the hypoxic range. Thus, volatile anesthetics preserved pancreatic but not hepatic blood flow and tissue oxygenation in this rat model. Despite comparable effects on perfusion, the PSO2 of the liver and pancreas was the least during hemorrhagic hypotension compared to that with the anesthetics. Because the volative anesthetic-induced hypotension has such a different effect on splanchnic tissue oxygenation compared with hemorrhagic-induced hypotension, the authors conclude that the method of inducing hypotension may have different effects on oxygenation of various tissues.     

重症急性胰腺炎早期目标治疗研究

目的 研究两种不同液体复苏目标在重症急性胰腺炎治疗中的差别.方法 选取2000年1月至2010年1月间80例重症急性胰腺炎患者,按时间顺序分为2组.A组治疗目标为24 h内:①血压控制在90/60 mm Hg(1 mm Hg=0.133 kPa)以上;②中心静脉压控制在8～12 mmHg;③尿量控制在0.5 ml·kg-1·h-1以上.B组治疗目标按照2004:年SSC早期目标治疗标准执行,6 h内:①平均动脉压大于65 mm Hg;②中心静脉压8～12 mm Hg;③尿量大于0.5 ml·kg-1·h-1以上;④中心静脉血氧饱和度大于70%.观察患者液体治疗3 d后的Marshall评分、APACHEⅡ评分及患者胰周感染率和病死率.结果 治疗3 d后,Marshall评分A组为6.82±4.69,B组为4.48±3.78,两者之间差异有统计学意义(P=0.02);APACHEⅡ评分A组为11.35±5.96,B组为8.22±4.53,两者之间差异有统计学意义(P=0.01).A组胰周感染率和病死率分别为44%和24%,B组胰周感染率和病死率分别为37%和17%,两者之间差异无统计学意义(P值分别为0.65和0.57).结论 按照SSC指南早期目标治疗标准对重症胰腺炎患者行液体复苏可以改善治疗3 d患者脏器功能,但不能显著改善患者的胰周感染率和病死率.

Abstract：

Objective To study the difference in outcomes between two treatment regimens of goal-directed fluid therapy in patients with severe acute pancreatitis. Methods From January 2000 to January 2010, 80 patients with severe acute pancreatitis were assigned into 2 groups. In group A,patients received fluid therapy aiming at the following goals in 24 hours: (1) Blood pressure >90/60 mm Hg;(2) CVP between 8-12 mm Hg;(3) Urine output >0. 5 ml · kg-1 · h-1. In group B, patients received fluid therapy aiming at the following goals in 6 hours (according to SSC guideline,2004): (1) mean arterial blood pressure >65 mm Hg;(2) CVP between 8-12 mm Hg;(3) Urine output >0. 5 ml · kg-1 · h-1 ;(4) central venous oxygen saturation >70%. After therapy for 3 days we measured the Marshall score, APACHE Ⅱ score, and the peri-pancreatic infection and mortality rates. Results The Marshall score was 6. 82±4. 69 and 4. 48±3. 78 in group A and B, respectively (P=0. 02). The APACHE Ⅱ score was 11. 35±5. 96 and 8. 22±4. 53 in group A and B, respectively (P=0. 01). The peri-pancreatic infection rate was 44% and 37% in group A and B, respectively, and there was no significant difference between the 2 groups (P = 0. 65). The mortality rate was 24% and 17% in group A and B. There was no significant difference between the 2 groups(P=0. 57). Conclusion Goal-directed fluid therapy in patients with severe acute pancreatitis according to the SSC guideline improved organ function but it did not reduce peri-pancreatic infection and mortality rates.     

The effect of insufflation pressure on CO(2) pneumoperitoneum and embolism in piglets

We conducted this study to investigate the effect of insufflation pressure on the pathophysiology of CO(2) pneumoperitoneum and embolism in an infant model. Twenty anesthetized piglets had stepwise intraperitoneal insufflation with CO(2) for 15 min at pressures ranging from 5 to 20 mm Hg. The piglets were ventilated to baseline normocarbia (ETCO(2) = 30 mm Hg, PaCO(2) = 38 mm Hg) before beginning each insufflation. CO(2) was then insufflated IV in 15 of these piglets at the same pressures. There was no reduction of blood pressure or cardiac output with intraperitoneal insufflation, but the stroke volume declined significantly (*P < 0.05) from (mean +/- SE) 10.6 +/- 1.3 mL to 8.5 +/- 1.3* mL and from 10.0 +/- 1.4 mL to 7.2 +/- 1.2* mL at 15 and 20 mm Hg insufflation pressure, respectively. Abdominal insufflation at 5, 10, 15, and 20 mm Hg caused an increase in ETCO(2) to 31.7 +/- 0.8 mm Hg, 35.6 +/- 1.2* mm Hg, 37.5 +/- 1.5* mm Hg, and 40.1 +/- 1.8* mm Hg and in PaCO(2) to 41.1 +/- 1.3* mm Hg, 44.2 +/- 1.4* mm Hg, 49.9 +/- 1.8* mm Hg, and 53.0 +/- 2.1* mm Hg, respectively. In contrast, the ETCO(2)decreased to 19.4 +/- 1.5* mm Hg, 20.4 +/- 1.4 mm Hg, 15.2 +/- 2.1* mm Hg, and 10.6 +/- 2.0* mm Hg with IV insufflation using the same pressures. IV insufflation caused marked hypotension and mortality. As the insufflation pressure increased, the mortality increased (0 in 15, 1 in 15, 1 in 14, and 6 in 13* at 5, 10, 15, and 20 mm Hg; *P < 0.05 vs 0 in 15, 1 in 15, and 1 in 14). This study suggests that although intraperitoneal insufflation up to 20 mm Hg may be tolerated hemodynamically, the lowest possible pressure should be used to reduce hypercarbia. A low insufflation pressure may also prevent mortality from CO(2) embolism. IMPLICATIONS: The lowest pressure possible should be used when inflating the abdomen with CO(2) to perform a laparoscopy in babies. A low pressure allows better ventilation and may prevent mortality if CO(2) is accidentally injected into a vein.     

CO2气腹对正常大鼠脑组织S-100、NSE mRNA和蛋白水平的影响

目的研究在不同CO2气腹压及不同时段下大鼠血和脑脊液S-100蛋白(S-100)、神经元特异性烯醇化酶(NSE)水平的变化对中枢神经系统的影响。方法Wistar大鼠建立气腹模型,光镜和电镜观察大鼠脑组织胶质细胞和神经元细胞组织学变化;抗体夹心法检测血液和脑脊液中S-100、NSE水平变化,RT-PCR技术和免疫组织化学的方法观察脑组织中S-100、NSEmRNA和蛋白水平表达的变化。结果CO2气腹后,A5-1组与对照组比较,海马区胶质细胞和神经元细胞均无明显变化,A10-2组胶质细胞和神经元细胞在光镜下呈轻度水样变,电镜下线粒体轻度肿胀;血液和脑脊液中S-100、NSE在CO2气腹压力后逐渐增加,但差异无统计学意义(P>0.05),S-100和NSE在血液和脑脊液中水平变化分别呈正相关(P<0.05);S-100、NSEmRNA在CO2气腹后逐渐增加,但与对照组比较差异无统计学意(P>0.05);脑组织S-100、NSE表达阳性面积随气腹时间及压力增加而逐渐增加,在A5-1组和A10-2组与对照组比较差异无统计学意义(P>0.05)。结论在10mmHg2h范围,CO2气腹对正常大鼠中枢神经系统无损害,CO2气腹在这一范围内应用对中枢神经系统是安全的。     

Continuous arterial P(O2) and P(CO2) measurements in swine during nitrous oxide and xenon elimination: prevention of diffusion hypoxia

BACKGROUND: During nitrous oxide (N2O) elimination, arterial oxygen tension (PaO2) decreases because of the phenomenon commonly called diffusive hypoxia. The authors questioned whether similar effects occur during xenon elimination. METHODS: Nineteen anesthetized and paralyzed pigs were mechanically ventilated randomly for 30 min using inspiratory gas mixtures of 30% oxygen and either 70% N2O or xenon. The inspiratory gas was replaced by a mixture of 70% nitrogen and 30% oxygen. PaO2 and carbon dioxide tensions were recorded continuously using an indwelling arterial sensor. RESULTS: The PaO2 decreased from 119+/-10 mm Hg to 102+/-12 mm Hg (mean+/-SD) during N2O washout (P<0.01) and from 116+/-9 mm Hg to 110+/-8 mm Hg during xenon elimination (P<0.01), with a significant difference (P<0.01) between baseline and minimum PaO2 values (deltaPaO2, 17+/-6 mm Hg during N2O washout and 6+/-3 mm Hg during xenon washout). The PaCO2 value also decreased (from 39.3+/-6.3 mm Hg to 37.6+/-5.8 mm Hg) during N2O washout (P<0.01) and during xenon elimination (from 35.4+/-1.6 mm Hg to 34.9+/-1.6 mm Hg; P< 0.01). The deltaPaCO2 was 1.7+/-0.9 mm Hg in the N2O group and 0.5+/-0.3 mm Hg in the xenon group (P<0.01). CONCLUSION: Diffusive hypoxia is unlikely to occur during recovery from xenon anesthesia, probably because of the low blood solubility of this gas.     

Systemic and mesenteric hemodynamics, metabolism, and intestinal tonometry in a rat model of supraceliac aortic cross-clamping and declamping

OBJECTIVE: To describe systemic and mesenteric hemodynamics, metabolism, and intestinal tonometry in a rat model of supraceliac aortic cross-clamping and declamping. DESIGN: Prospective, randomized, experimental study. SETTING: University cardiovascular research laboratory. PARTICIPANTS: Twelve male anesthetized and ventilated Sprague-Dawley rats. INTERVENTION: Supraceliac aortic cross-clamping was performed for 30 minutes, followed by declamping and reperfusion for 180 minutes or sham clamping and sham declamping. MEASUREMENTS AND MAIN RESULTS: Mean arterial blood pressure; abdominal aortic, superior mesenteric, and carotid artery blood flow; intestinal mucosal tonometry; hemoglobin; lactate; and blood gases were measured before and after 30 minutes of aortic cross-clamping and 15, 30, 60, 120, and 180 minutes after declamping during reperfusion. Aortic cross-clamping induced an increase in mean arterial pressure (117+/-20 mm Hg to 147+/-12 mm Hg), an increase in right atrial hemoglobin saturation(66%+/-11% to 81%+/-6%), an increase in lactate levels (1.7+/-0.7 mmol/L to 4.3+/-1.3 mmol/L), and an increase in tonometric PCO2 (49.6+/-5.0 mm Hg to 75.6+/-8.6 mm Hg). Three hours of reperfusion after declamping resulted in significantly decreased mean arterial pressure (38+/-10 mm Hg); decreased aortic (101+/-12 mL/min/kg to 57+/-32 mL/min/kg), mesenteric (19+/-4 to 13+/-6 mL/min/kg), and carotid (12+/-4 mL/min/kg to 5+/-3 mL/min/ kg) blood flows; and elevated lactate levels (4.2+/-2.0 mmol/L). Tonometric PCO2 had normalized to baseline levels (51.9+/-3.8 mm Hg), but PCO2 gap was significantly higher than in sham clamped rats (17.9+/-7.8 mm Hg v. 7.0+/-2.6 mm Hg). CONCLUSIONS: Hemodynamic and metabolic effects of aortic cross-clamping and declamping known from large animal models are reproducible using a rat model. Intestinal tonometry indicated mesenteric ischemia during aortic cross-clamping, which was reversible to preclamp values within 30 minutes of reperfusion after declamping.     

Carotid blood flow in anesthetized rats: effects of carotid ligation and anastomosis.

An experimental model was developed for continuous measurement of the common carotid blood flow, in the anesthetized rat, with an electromagnetic flowmeter. The mean carotid blood flow for 41 rats averaged 3.2 +/- 0.2 ml/min at an average mean arterial pressure of 101 +/- 2.5 mm Hg and arterial pO2 of 106 +/- 3.4 mm Hg, pCO2 of 38 +/- 1.2 mm Hg, and pH of 7.36 +/- 0.02. This model allowed short- and long-term carotid hemodynamic changes to be recorded after contralateral carotid ligation or end-to-side carotid anastomosis. After ligation of the contralateral carotid, blood flow through the intact carotid increased 25% (at about 1 week) and 45% (at about 5-6 months), whereas, after anastomosis, carotid blood flow increased 76% and 89% at periods comparable to those after ligation. Arterial pressure and gases did not change throughout the experimental periods. Probable mechanisms involved in these carotid hemodynamic changes are discussed.     

Effects of ethanol on spinal cord blood flow in the rat

This study examines the effects of low and high concentrations of ethanol on spinal cord blood flow (SCBF) in the rat. SCBF was measured in the following blood pressure ranges: (a) <60 mm Hg, (b) 60-90 mm Hg, (c) 90-120 mm Hg, (d) 120-150 mm Hg, and (e) >150 mm Hg. Rats were anesthetized with 1.4% isoflurane in air and randomly assigned to the following treatment groups: group 1 (n = 12), intraperitoneal (i.p.) saline injection; group 2 (n = 10), 1 g/kg of ethanol i.p.; and group 3 (n = 14), 4 g/kg of ethanol i.p. Blood pressure was increased by intravenous phenylephrine infusion or lowered by a combination of intravenous trimethaphan and blood withdrawal. The SCBF was measured in cervical, thoracic, and lumbar segments using radioactive microspheres. The plasma ethanol concentration was 0 mg/ml for group 1, 0.64 +/- 0.06 mg/ml (mean +/- SEM) in group 2, and 4.18 +/- 0.11 mg/ml in group 3. In control rats, the cervical SCBF was higher than the thoracic or lumbar SCBF, evaluated over the entire blood pressure range (analysis of variance, p <0.05). This difference in regional SCBF was abolished by ethanol. Ethanol produced a significant decrease in cervical and lumbar SCBF (p <0.05) but not thoracic SCBF (p = 0.07). This decrease in SCBF was most pronounced at high blood pressures. These results suggest that ethanol produces vasoconstriction in the spinal cord that is countered by autoregulatory vasodilation at low blood pressures.     

Cerebral and spinal cord blood flow in awake and fentanyl-N2O anesthetized rats: evidence for preservation of blood flow autoregulation during anesthesia

Blood flow responses to alterations in mean arterial blood pressure (MABP) were measured in the cerebral cortex, subcortex, midbrain, and spinal cord of awake rats. Data were compared with those of rats anesthetized with an i.v. fentanyl infusion and inspired nitrous oxide (N2O). Regional cerebral blood flow was measured using radioactive microspheres in the following blood pressure ranges: (a) <40 mm Hg; (b) 40-60; (c) 60-80; (d) 80-100; (e) 100-120; (f) 120-140; (g) 140-160; and (h) >160. Blood pressure was increased with phenylephrine or decreased with trimethaphan combined with blood withdrawal. Cerebral blood flow was not measured when MABP was less than 60 mm Hg in awake rats. Autoregulation was seen in all brain areas between 60 and 140 mm Hg in both treatment groups. Although regional cerebral blood flow was not different between the two treatment groups, PaCO2 was 2-4 mm Hg lower in awake rats. This suggests that PaCO2-corrected cerebral blood flow may be 10-20% lower with fentanyl-N2O anesthesia.     

Methylmethacrylate blood levels in patients with femoral neck fracture

The blood levels of monomeric methylmethacrylate were measured in 20 patients with fracture of the femoral neck, treated with a Thompson prosthesis under spinal anesthesia. Monomeric methylmethacrylate was detected in the blood stream in all patients; the maximum levels (mean 6.44 micrograms/ml, range 0.05-31.89 micrograms/ml) were measured 30 s after insertion of the Thompson prosthesis. A moderate drop in systolic blood pressure and a marked reduction of arterial oxygen tension was noted after cementation and insertion of the prosthesis; the mean maximum drops were 10.1 mm Hg (range 0-32 mm Hg) and 6.1 mm Hg (range 0-13.5 mm Hg) No dose-dependent correlation could be established between the levels of monomeric methylmethacrylate and the drop in arterial blood pressure or arterial oxygen tension.     

Continuous measurement of intraarterial pHa, PaCO2, and PaO2 in the operating room

Miniaturized sensors based upon the principles of optical fluorescence can measure the pH, PCO2, and PO2 of liquid or gas media. A prototype of a three-component fiberoptic sensor has been developed for intraarterial application by CDI, 3M Health Care, Irvine, California. We report the first study of this continuous intraarterial monitor in patients undergoing surgical procedures under general anesthesia. Fourteen patients participated in the study. The fiberoptic sensor was calibrated before insertion and then passed through an existing 18-gauge radial artery cannula. Blood samples were drawn at frequent intervals through the same cannula for in vitro blood gas analysis. For each of the 87 arterial blood gas samples obtained, the in vitro values of pHa, PaCO2, and PaO2 were compared with simultaneous readings from the fiberoptic sensor. For pHa, the mean error (error = fiberoptic value minus in vitro value) or "bias" of the fiberoptic data was -0.032 and the standard deviation of error or "precision" was 0.042. For PaCO2, the bias was -3.8 mm Hg and the precision was 4.7 mm Hg. For PaO2, the bias was -9.0 mm Hg and the precision was 23.3 mm Hg. For PaO2 values less than 175 mm Hg, the bias was -8.5 mm Hg and the precision was 8.3 mm Hg. Expressed in terms of percentage errors, the bias +/- precision values were -11.5% +/- 13.3% for PaCO2, and -6.2% +/- 10.0% for PaO2. The duration of the surgical procedures ranged from 1.6 to 8 h with an average of 4.2 h.(ABSTRACT TRUNCATED AT 250 WORDS)     

Tissue pressure measurements as a determinant for the need of fasciotomy.

An experimental and clinical tehcnique of measuring tissue pressures within closed compartments demonstrates a normal tissue pressure is approximately zero mmHg, and increased markedly in compartmental syndromes. There is inadequate perfusion and relative ischemia when the tissue pressure within a closed compartment rises to within 10-30 mm Hg of the patient's diastolic blood pressure. Fasciotomy is usually indicated, therefore, when the tissue pressure rises to 40-45 mm Hg in a patient with a diastolic blood pressure of 70 mm Hg and any of the signs or symptoms of a compartmental syndrome. There is no effective tissue perfusion within a closed compartment when the tissue pressure equals or exceeds the patient's diastolic blood pressure. A fasciotomy is definitely indicated in this circumstance, although distal pulses may be present. The measurement of tissue pressure aids in the early diagnosis and appropriate treatment of compartmental syndromes.     

Do ancillary properties of antihypertensive drugs explain the outcome results of recent trials?

BACKGROUND: In a quantitative overview of published trials, we investigated whether some pharmacological properties of antihypertensive drugs, besides reduction in blood pressure, explain cardiovascular outcomes in hypertensive or high-risk patients. METHODS: Across trials, using meta-regression, we correlated odds ratios with differences in systolic blood pressure between study groups. We then compared odds ratios of benefit observed in recent trials with those predicted by metaregression on the basis of the differences in systolic pressure between randomised groups. RESULTS: Significant differences in systolic pressure between randomised groups (experimental minus reference) were observed in the ALLHAT (-2/+1), CAPPP(-3/-1) and NORDIL (-3.1/+0.2) trials. Furthermore, the differences in achieved systolic and/or diastolic pressure between study groups were also significant in the hypertension trials which involved untreated control patients, as well as in MIDAS (-3.5/ approximately 0 mm Hg), HOPE (-3.3/-1.0 mm Hg), PART2 (-5/-4 mm Hg), and SCAT (4/-2 mm Hg) (1). The differences between the observed odds ratios and those predicted by the meta-regression between outcome and difference in systolic pressure did not reach statistical significance except for the NORDIL trial, in which the risk of stroke was lower on diltiazem than on the older drugs despite a 3.1 mm Hg higher systolic pressure on the calcium-channel blocker. CONCLUSIONS: The finding that in the reviewed trials blood pressure reduction largely accounted for outcome emphasizes the desirability of blood pressure control. The hypothesis that converting-enzyme inhibitors or alpha-blockers might influence cardiovascular prognosis over and beyond their antihypertensive effect remains unproved.