PtiO2 Values Research Articles

Pathophysiological central nervous system changes in a porcine model of acetaminophen-induced acute liver failure

BackgroundCritical care management of patients suffering from acute liver failure (ALF) continues to be challenging. Animal models studying the pathophysiological central nervous system alterations during the course of ALF provide an opportunity to improve diagnostic and therapeutic strategies. The aim of this study was to analyse the course of cerebral oxygenation in addition to conventional neuromonitoring during the course of acetaminophen-induced ALF. MethodsALF was induced by intrajejunal acetaminophen administration in 20 German landrace pigs. All animals underwent invasive hemodynamic and neuromonitoring and were maintained under standardized intensive care support. Neuromonitoring consisted of continuous intraparenchymatous recording of intracranial pressure and brain partial oxygen pressure. Hemodynamic and ventilation parameters were continuously recorded; laboratory parameters were analysed every eight hours. Mean values were compared using the Wilcoxon test. ResultsAcute liver failure occurred in all intoxicated animals after 23±2h, resulting in death due to ALF after further 15±2h. Continuous neuromonitoring was performed in all animals during the whole experiment without observing signs of intracranial haemorrhage. Two hours after manifestation of ALF an increase in brain tissue oxygen (PtiO2) was observed. Brain oxygenation stayed stable until nine hours before death. Intracranial pressure (ICP) remained basically at a plateau level until manifestation of ALF. In the following ten hours a linear and slow increase was observed until five hours before death, followed by a fast and continuous rise in ICP to a final level of 35±1mmHg. Cerebral perfusion pressure (CPP) began to decrease 25h prior to exitus, further decreasing to 18±2mmHg at the end of the experiment. A strong negative linear correlation was found between PtiO2 and ICP (R=0.97). Arterial partial pressure of oxygen (PaO2) below 100mmHg was associated with lower PtiO2 levels. Changes in arterial partial pressure of carbon dioxide (PaC02) did not influence PtiO2 values. Hemoglobin values below 7g/dl were associated with lower PtiO2 values. ConclusionsThe results of our experiments demonstrate that ICP and PtiO2 measurements indicate impending damage well before serious complications occur and their use should be considered in order to protect endangered brain function in the presence of acetaminophen-induced ALF.

Cerebral metabolism during experimental endotoxin shock and after preconditioning with monophosphoryl lipid A

PurposePreconditioning with low doses of monophosphoryl lipid A (MPL) has been shown to induce endotoxin tolerance and to reduce the metabolic and hemodynamic consequences of endotoxin shock. However, no data are available about the effects of endotoxin preconditioning on cerebral metabolism during endotoxemia. The study was designed to determine the effects of endotoxin preconditioning with MPL on cerebral metabolism via microdialysis compared to muscle tissue metabolism during experimental endotoxemia. MethodsIn a controlled animal study, continuous endotoxin infusion (1μg/kg b.w. per h) was administrated to 7 female mixed-breed pigs after pretreatment with MPL in incremental doses of endotoxin during days 5–2 before the experiments. In the control group, 7 animals received a saline pretreatment. In addition to hemodynamic monitoring and blood gas analyses, interstitial lactate, pyruvate, glucose and glycerol concentrations in muscle and cerebral tissue were measured using in vivo microdialysis. ResultsThere were no significant differences between the two groups with respect to hemodynamic parameters, while mixed venous oxygen saturation (SvO2), arterial blood pH and mean pulmonary arterial pressure (MPAP) were significantly higher in the preconditioned group. Cerebral perfusion pressure (CPP) and brain tissue oxygen pressure (ptiO2) values stayed stable throughout the experiment with no inter-group differences. While interstitial concentrations of lactate and glycerol as well as the lactate/pyruvate (LP) and the lactate/glucose (LG) ratio in muscle tissues were significantly increased in control animals compared to those who had been pretreated with MPL; the results of cerebral microdialysis showed no significant changes in interstitial lactate or glycerol levels in both groups. However, the lactate/glucose (LG) ratio in the control group showed a significantly higher increase than in the preconditioned group. ConclusionsPreconditioning with low doses of MPL ameliorates the negative metabolic effects of endotoxin shock in muscle tissue. With regard to cerebral metabolism, the present study suggests that MLP preconditioning provides moderate advantages, at least in an experimental model of endotoxin shock.

Arterial lactate above 2 mM is associated with increased brain lactate and decreased brain glucose in patients with severe traumatic brain injury.

Lactate fuels cerebral energy-consuming processes and it is neuroprotective. The impact of arterial lactate on brain metabolism determined by microdialysis was investigated retrospectively in patients with severe traumatic brain injury (TBI). Cerebral microdialysis (glucose, lactate), neuromonitoring (ICP, CPP, ptiO2, SjvO2) and blood gas data collected in 20 patients during pharmacologic coma were grouped within predefined arterial lactate clusters (<1, 1-2, >2 mM). Microdialysis samples were only taken from time points characterized by normoventilation (paCO2 34.5-42 mmHg), sufficient oxygenation (paO2 >75 mmHg) and hematocrit (≥24%) to exclude confounding influences. Elevated arterial lactate ≥2 mM was associated with significantly increased brain lactate which coincided with markedly decreased brain glucose despite significantly increased arterial glucose levels and sufficient cerebral perfusion indirectly determined by normal SjvO2 and ptiO2 values. At elevated arterial lactate levels signs of significantly increased cerebral lactate uptake coincided with markedly decreased cerebral glucose uptake. Infused lactate above 50 mM per 24 hours was associated with significantly decreased cerebral glucose. Increased arterial lactate levels were associated with increased cerebral lactate uptake and elevated brain lactate. At the same time brain glucose uptake and brain glucose were significantly reduced. It remains unclear whether arterial lactate is the driving force for the increased cerebral lactate levels or if the reduced glucose uptake also contributed to the increased cerebral lactate levels. Further studies are required to assess the impact of lactate infusion under clinical conditions.

Monitoring of brain tissue oxygenation in surgery of middle cerebral artery incidental aneurysms

Introduction:The management of incidental unruptured aneurysms remains a matter of controversy; middle-sized or large anterior circulation incidental aneurysms, in young or middle age patients, should be considered for treatment. Surgical clipping is an accepted treatment for middle cerebral artery unruptured aneurysms. Ischemic events can occur even in cases of incidental aneurysm surgery. Since regional cerebral blood flow can be compromised due to temporary arterial clipping or to incorrect placement of defi nitive clip, we performed intra-operative monitoring of brain tissue oxygen concentration (PtiO2), to detect changes in brain oxygenation due to reduced blood fl ow, eventually leading to ischemia, during surgery of middle cerebral artery incidental aneurysms.Methods:PtiO2 monitoring was performed during surgery of eight patients harboring incidental MCA aneurysms, using a polarographic microcatheter (Licox, GMS – Kiel, Germany), placed in the temporal lobe on the side of the lesion, from dural opening to dural closure.Results:Basal values varied between 2.3 and 27.3 mmHg; these values are lower than those previously described in the literature as “normal” for uninjured brain or in cases of subarachnoid hemorrhage. In all patients, a significant decrease in PtiO2 was found in every period of temporary clipping of MCA. Post-operative infarction in the territory of middle cerebral artery occurred in one patient and, in that case, there was a persistent minimum value of 0.6 mmHg, without recovery after the placement of the definitive clip. In another patient, an incorrect placement of the definitive clip could be predicted by a decrease in PtiO2 value.Conclusions:PtiO2 monitoring during aneurysm surgery shows brain tissue perfusion in real time and there is a correlation between any episode of reduced blood flow to the affected vascular territory during surgery and a decrease of PtiO2 values. Unexpected low basal values were obtained in “uninjured” brain, with no influence from subarachnoid hemorrhage. The values of risk for brain infarction during temporary arterial occlusion still need further studies, but an incomplete recovery or a persistent fall in PtiO2 values after definitive clipping should be considered as an indication for verification of the position of the clip.

Brain Tissue Oxygen Pressure and Prognosis in Spontaneous Intracerebral Hematomas

Spontaneous intracerebral hematomas are one of the major causes of morbidity and mortality in the modern world. The purpose of our study is to investigate the usefulness of tissue oxygen tension (PtiO2)-monitoring in the prognosis of sponta- neous intracerebral hematomas. Thirty-one patients (22 males and 9 females) were included in the study. The Glasgow Coma Scale on admission was r8 (n = 27) or r12 (n = 4), followed by an early deterioration. A 3 lumen bolt was used to introduce the catheters of cerebral monitoring into the brain parenchyma. The outcome was assessed with the Glasgow Outcome Scale at 3 and 6 months of follow-up. From the patients included, only 6 had a favorable outcome (Glasgow Outcome Scale = 4 to 5) and the remaining 25 had an unfavorable outcome. Twenty-one out of them died during the first 6 months after the ictus. Unfavorable outcome was correlated with the presence of an episode of PtiO2 values 30 min) and with the relative total duration of PtiO2 values below that level. PtiO2 monitoring in patients with spontaneous intracerebral hemato- mas may be a reliable tool for their prognosis.

Brain Tissue Oxygen Pressure Monitoring in Awake Patients during Functional Neurosurgery: The Assessment of Normal Values

Local brain tissue oxygen (ptiO2) monitoring is frequently applied in patients at risk for cerebral ischemia. To identify ischemic thresholds, the normal range of local brain tissue oxygen pressure (ptiO2) values needs to be established. Ideally, such normal values are determined in healthy and awake subjects, so as to eliminate the possible influences of anesthetics on cerebral physiology or ptiO2. Thus far, however, such measurements have not been conducted, and to fill this void, we determined the ptiO2 values in normal white matter of awake patients undergoing functional stereotactic brain surgery. In 25 otherwise healthy patients, who underwent functional neurosurgery for treatment of a refractory movement disorder under local anesthesia, the ptiO2 of white matter was recorded continuously using a polarographic Clark type electrode monitoring system. Preoperative screening ruled out cognitive dysfunction or structural cerebral lesions. Reliable intraoperative ptiO2 values were obtained in 22 patients. After an adaptation period of 118+/-35 min (range, 47-171 min), we found an average normal ptiO2 of 22.6+/-7.2 mm Hg in the frontal white matter. In 11 patients, ptiO2 measurements were continued postoperatively for 24 h. During this period, a similar normal ptiO2 value of 23.1+/-6.6 mm Hg was found. No iatrogenic complications occurred. In conclusion, the normal ptiO2 of cerebral white matter is most likely lower than previously assumed. Further, the long adaptation time renders this widely applied monitoring instrument unreliable in detecting ischemia early after insertion and limits its usefulness for intraoperative monitoring.

Impact of age of transfused blood on cerebral oxygenation in male patients with severe traumatic brain injury*

Prolonged erythrocyte storage time might reduce the efficacy of transfusion. In this study, the effects of transfusion of erythrocytes with four different storage periods (<10 days, n = 18; 10-14 days, n = 15; 15-19 days, n = 17; and >19 days, n = 16 patients) on brain tissue oxygen tension (PtiO2) in stable male patients with severe traumatic brain injury were investigated during a 24-hr follow-up period. Prospective, observational study. Neurotrauma critical care unit of a university hospital. Sixty-six male, nonbleeding, hemodynamically stable anemic patients (hemoglobin <95 g/L) with Glasgow Coma Scale score <9. None. PtiO2, cerebral perfusion pressure, mean arterial pressure, intracranial pressure, peripheral oxygen saturation, CO2 pressure at the end of expiration, and intracerebral temperature were recorded in all patients at baseline, immediately after the completion of transfusion, and 1, 2, 3, 4, 5, 6, 12, and 24 hrs posttransfusion. All four groups were homogeneous with respect to multiple baseline variables, except for storage time of transfused erythrocytes (p < .0001). There was a significant short-lasting (3-4 hrs) increase in PtiO2 values after transfusion of erythrocytes stored for <10 days, 10-14 days, or 15-19 days, compared with those at baseline. In contrast, no significant changes in PtiO2 were observed after transfusion of erythrocytes stored >19 days. Transfusion of erythrocytes increased cerebral oxygenation in patients with severe traumatic brain injury, except in those transfused with erythrocytes stored >19 days.

A Comparison of Epinephrine Only, Arginine Vasopressin Only, and Epinephrine Followed by Arginine Vasopressin on the Survival Rate in a Rat Model of Anaphylactic Shock

Epinephrine and more recently arginine vasopressin (AVP) alone or in combination have been proposed in patients with anaphylactic shock, but few experimental data exist. The authors investigated the effects of epinephrine only, AVP only, or epinephrine followed by AVP in a model of anaphylactic shock. Ovalbumin-sensitized Brown Norway rats were anesthetized, intubated, and shock induced with ovalbumin. Rats (n = 6/group) were randomly allocated to receive 5 min after shock onset: (1) saline (no-treatment group); (2) two boluses of epinephrine followed by continuous infusion (epinephrine group); (3) AVP bolus followed by continuous infusion (AVP group); (4) epinephrine bolus followed by AVP continuous infusion (epinephrine + AVP group). Mean arterial pressure (MAP) and skeletal muscle oxygen pressure (PtiO2) were measured. Continuous infusion rates were titrated to reach MAP values of 60 mmHg. Survival was analyzed. Without treatment, MAP and PtiO2 decreased rapidly with 0% survival. In the epinephrine group, MAP and PtiO2 recovered after an initial decrease, with 84% survival. In the AVP group, MAP was partially restored and subsequently decreased; PtiO2 values decreased to values similar to those in the no-treatment group; survival was 0%. In the epinephrine + AVP group, MAP and PtiO2 values increased more slowly as compared with the epinephrine group; survival was 100%. In this model of anaphylactic shock, early treatment with epinephrine followed by continuous epinephrine or vasopressin infusion resulted in an excellent survival rate, whereas vasopressin only resulted in a 100% death rate. These experimental results suggest that epinephrine must still be considered as the first-line drug to treat anaphylactic shock.

Resuscitation of severe but brief haemorrhagic shock with PFC in rabbits restores skeletal muscle oxygen delivery and does not alter skeletal muscle metabolism

Studies have demonstrated that perfluorocarbon (PFC) emulsions associated with hyperoxia improved whole body oxygen delivery during resuscitation of acute haemorrhagic shock (HS). Nevertheless the microcirculatory effects of PFC and the potential deleterious effects of hyperoxic reperfusion are still of concern. We investigated (i) the ability of a newly formulated, small sized and highly stable PFC emulsion to increase skeletal muscle oxygen delivery and (ii) the effect of hyperoxic reperfusion on skeletal muscle metabolism after a brief period of ischaemia using an original, microdialysis-based method that allowed simultaneous measurement tissue oxygen pressure (PtiO2) and interstitial lactate and pyruvate. These measurements were carried out in anaesthetised and ventilated (FiO2 = 1) rabbits subjected to acute HS (50% of blood volume withdrawal) and either resuscitated with a PFC emulsion diluted with a 5% albumin solution (16.2 g PFC per kg body weight) (n = 10) or with a modified fluid gelatin solution (Gelofusine) (n = 10). We found no difference between the two groups for the haemodynamic and haematological variables (except for the venous oxygen partial pressure). However, a significant difference was observed in the slope of the regression linear relationship exhibited between the mean arterial pressure (MAP) and the PtiO2, PFC group showing a much steeper slope than Gelofusine group. In addition, PtiO2 values increased linearly with decreasing haematocrit (Hct) values in PFC-resuscitated animals and decreased linearly with decreasing Hct values in Gelofusine-resuscitated animals. There were no differences between the two groups concerning the blood and interstitial lactate/pyruvate ratios suggesting no deleterious effect of hyperoxic resuscitation in skeletal muscle. In conclusion these results suggest that resuscitation of severe, but brief, HS with PFC increased skeletal muscle oxygen delivery without measurable deleterious effects.

Continuous assessment of cerebrovascular autoregulation after traumatic brain injury using brain tissue oxygen pressure reactivity*

To evaluate whether two newly developed indexes of brain tissue oxygen pressure reactivity (ORx and bPtio2) provide information on the status of cerebrovascular autoregulation after traumatic brain injury. This was accomplished by analyzing the relationship between these indexes and an index of cerebrovascular pressure reactivity (PRx). PRx is an established parameter for estimation of cerebrovascular autoregulation. Retrospective analysis of prospectively collected data. Neurosurgical intensive care unit of a university hospital. Twenty-seven patients suffering from severe traumatic brain injury. Continuous monitoring of mean arterial blood pressure, intracranial pressure, cerebral perfusion pressure, and partial pressure of brain tissue oxygen (Ptio2) was performed for an average of 6.5 days. ORx was calculated as a moving correlation coefficient between values of cerebral perfusion pressure and Ptio2. The bPtio2 was calculated as a moving value of the slope of the linear regression function between cerebral perfusion pressure and Ptio2. PRx was calculated as a moving correlation coefficient between values for intracranial pressure and mean arterial blood pressure. Outcome was assessed at 6 months after traumatic brain injury (Glasgow Outcome Scale). Both ORx and bPtio2 correlated significantly with PRx (r=.55 for ORx, r=.52 for bPtio2, p<.01). PRx and ORx showed a significantly negative correlation to the monitored Ptio2 values (r=-.42 for PRx, r=-.41 for ORx, p<.05) and outcome (r=-.52 for PRx, r=-.62 for ORx, p<.01), whereas bPtio2 did not. ORx and, to a lesser extent, bPtio2 correlated with the autoregulatory marker PRx and provide additional information about the status of cerebrovascular autoregulation after traumatic brain injury. The data also suggested that patients with impaired autoregulation are at increased risk for secondary cerebral hypoxia.

Anaphylactic Shock

The pathophysiology of anaphylactic shock during anesthesia is incompletely characterized. It is described as distributive by analogy with septic shock (anaerobic metabolism, high tissue oxygen pressure [Ptio2] values). The Ptio2 profile and its metabolic consequences during anaphylaxis are not known. Ovalbumin-sensitized anaphylactic shock rats (n = 11) were compared to nicardipine-induced hypotension rats (n = 12) for systemic hemodynamics, Ptio2, sympathetic nervous system activation, skeletal muscle blood flow, and interstitial lactate and pyruvate concentrations using combined microdialysis and polarographic Clark-type oxygen probes. In both groups, the time course and the magnitude of arterial hypotension were similar. The ovalbumin group but not the nicardipine group displayed decreased skeletal muscle blood flow (from 45 +/- 6.2 ml x 100 g(-1) x min(-1) to 24.3 +/- 5 ml x 100 g(-1) x min(-1); P < 0.0001) and Ptio2 values (from 42 +/- 5 to 5 +/- 2; P < 0.0001). The ovalbumin group had more intense sympathetic nervous system activation with higher plasma epinephrine and interstitial norepinephrine concentrations. For the ovalbumin group, there was skeletal muscle anaerobic metabolism (lactate concentration increased from 0.446 +/- 0.105 to 1.741 +/- 0.459 mm; P < 0.05) and substrate depletion (pyruvate concentration decreased from 0.034 +/- 0.01 mm to 0.006 +/- 0.002 mm; P < 0.05) leading to increased interstitial lactate/pyruvate ratios (from 17 +/- 6 to 311 +/- 115; P < 0.05). This profile suggests decreased skeletal muscle blood flow and oxygen delivery. Persistent energy consumption results in decreased Ptio2 and substrate depletion through anaerobic glycolysis leading to complete failure of cellular energy production. This could explain rapid organ dysfunction and resuscitation difficulties.

Relevance of ICP and ptiO2 for indication and timing of decompressive craniectomy in patients with malignant brain edema

The exact effects of decompressive craniectomy on intracranial pressure (ICP) and cerebral tissue oxygenation (ptiO2) are still unclear. Therefore, we have monitored ICP and ptiO2 intra-operatively and correlated these values to different operative steps during craniectomy. ICP and ptiO2 values have been monitored both, simultaneously and continuously, in 15 patients with cerebral edema due to posttraumatic or postischemic brain swelling. Indications for craniectomy were an increase in ICP above 25 mmHg or a decrease in ptiO2 below 10 mmHg resistant to conservative treatment (e.g. mannitol, hyperventilation, adequate arterial blood oxygenation, etc.). In all cases, we performed a fronto-temporo-parietal craniectomy (15 x 12 cm) and dura enlargement with galea-periosteum. During craniectomy, monitoring of ICP and ptiO2 in the affected hemisphere was continued. Values were recorded and correlated with the different operative steps. We performed craniectomy according to our treatment protocol in 5 patients. Prior to surgery, mean ICP values were 25.6 mmHg (range: 23-29 mmHg), mean ptiO2 values were 5.9 mmHg (range: 2.4-9.5 mmHg), and mean CPP values were 66 mmHg (range: 60-70 mmHg). After removing the bone flap, ICP values dropped to physiological values (mean: 7.4 mmHg), whereas ptiO2 values increased only slightly (mean: 11 mmHg). Opening of the dura resulted in a further decrease of ICP (mean 4.8 mmHg) and an increase of ptiO2 to normal limits (mean: 18.8 mmHg). After skin closure, mean ICP was 6.8 mmHg and mean ptiO2 was 21.7 mmHg, respectively. We found a significant decrease of ICP after craniectomy (p<0.042) and after dura enlargement (p<0.039) as well as a statistically significant increase in ptiO2 after craniectomy (p<0.043) and after dura enlargement (p<0.041). As a large bone flap in decompressive craniectomy is essential for adequate ICP reduction, the results of the presented cases suggest that dura enlargement is the crucial step to restore adequate brain tissue oxygenation and that ptiO2 monitoring could be an important tool for timing craniectomy in the future.

Mild hypothermia protects liver against ischemia and reperfusion injury

To determine whether mild hypothermia could protect liver against ischemia and reperfusion injury in pigs. Twenty-four healthy pigs were randomly divided into normothermia, mild hypothermia and normal control groups. The experimental procedure consisted of temporary interruption of blood flow to total hepatic lobe for different lengths of time and subsequent reperfusion. Hepatic tissue oxygen pressure (PtiO2) and aspartate aminotransferase (AST) values were evaluated, and ultrastructural analysis was carried out for all samples. Serum AST was significantly lower, and hepatic PtiO2 values were significantly higher in the mild hypothermia group than in the normothermia group during liver ischemia-reperfusion periods (P=0.032, P=0.028). Meanwhile, the histopathologic injury of liver induced by ischemia-reperfusion was significantly improved in the mild hypothermia group, compared with that in the normothermia group. Mild hypothermia can protect the liver from ischemia-reperfusion injury in pigs.

Brain tissue oxygen guided treatment supplementing ICP/CPP therapy after traumatic brain injury

Objective: To evaluate the effects of a brain tissue oxygen (Ptio2) guided treatment in patients with traumatic brain injury. Methods: Ptio2 was monitored in 93 patients with severe traumatic brain...

Effects of cerebral perfusion pressure and increased fraction of inspired oxygen on brain tissue oxygen, lactate and glucose in patients with severe head injury.

The purpose of the study was to measure the effects of increased inspired oxygen on patients suffering severe head injury and consequent influences on the correlations between CPP and brain tissue oxygen (PtiO2) and the effects on brain microdialysate glucose and lactate. In a prospective, observational study 20 patients suffering severe head injury (GCS< or =8) were studied between January 2000 and December 2001. Each patient received an intraparenchymal ICP device and an oxygen sensor and, in 17 patients brain microdialysis was performed at the cortical-subcortical junction. A 6 h 100% oxygen challenge (F IO2 1.0) ( Period A) was performed as early as possible in the first 24 hours after injury and compared with a similar 6 hour period following the challenge ( Period B). Statistics were performed using the linear correlation analysis, one sample t-test, as well as the Lorentzian peak correlation analysis. F IO2 was positively correlated with PtiO2 (p < 0.0001) over the whole study period. PtiO2 was significantly higher (p < 0.001) during Period A compared to Period B. CPP was positively correlated with PtiO2 (p < 0.001) during the whole study. PtiO2 peaked at a CPP value of 78 mmHg performing a Lorentzian peak correlation analysis of all patients over the whole study. During Period A the brain microdialysate lactate was significantly lower (p = 0.015) compared with Period B. However the brain microdialysate glucose remained unchanged. PtiO2 is significantly positively correlated with F IO2, meaning that PtiO2 can be improved by the simple manipulation of increasing F IO2 and ABGAO2. PtiO2 is positively correlated with CPP, peaking at a CPP value of 78 mmHg. Brain microdialysate lactate can be lowered by increasing PtiO2 values, as observed during the oxygen challenge, whereas microdialysate glucose is unchanged during this procedure. Extension of the oxygen challenge time and measurement of the intermediate energy metabolite pyruvate may clarify the metabolic effects of the intervention. Prospective comparative studies, including analysis of outcome on a larger multicenter basis, are necessary to assess the long term clinical benefits of this procedure.

Volume expansion with modified hemoglobin solution, colloids, or crystalloid after hemorrhagic shock in rabbits: effects in skeletal muscle oxygen pressure and use versus arterial blood velocity and resistance.

Therapeutic goals for hemorrhagic shock resuscitation are the increase of cardiac output and oxygen delivery. The possibility exists that because of microcirculatory effects, different volume expanders result in different tissue oxygen delivery and oxygen use. In a rabbit model of resuscitation from hemorrhagic shock (50% blood loss), we compared the effects of an hemoglobin-based O2-carrying solution (HbOC) with those elicited by albumin, hydroxyethyl starch (HES), or saline on systemic hemodynamics, skeletal muscle O2 pressure (PtiO2), and interstitial concentration of lactate (LACi) through the combined implantation of a microdialysis probe and a sensitive O2 electrode into the hind limb. Hemorrhagic shock induced a 50% decrease in mean arterial pressure (MAP), femoral artery blood flow (BF), and PtiO2. After resuscitation, there were statistically significant differences among the volume expanders. The increase in MAP was faster with HbOC and colloids, and slower with saline, mainly obtained by vasoconstriction for HbOC and by increased BF with albumin and HES. The maximum MAP values were significantly higher for HbOC compared with the other volume expanders. HbOC and colloids induced a faster increase in PtiO2 as compared with saline, but maximum PtiO2 values were not different among the volume expanders. Tissue oxygen use as estimated by LACi increased transiently at the beginning of volume expansion with similar maximum values. Animals resuscitated with saline had significantly higher LACi concentrations after the onset of volume expansion as compared with HbOC but not with colloids. Our results demonstrate that there are measurable differences in MAP and BF upon resuscitation with the four different solutions and there is a slower increase in tissue PtiO2 with saline than with colloids associated with significantly increased LACi consistent with delayed reoxygenation upon resuscitation with saline.

Therapeutic aspects of brain tissue pO2 monitoring after subarachnoid hemorrhage.

Prolonged phases of brain tissue hypoxia (ptiO2 < 10 mmHg) lead to cerebral infarction. Therefore, the present study investigates the role of ptiO2--monitoring to guide hypervolemic hypertensive therapy in patients suffering from severe subarachnoid hemorrhage (SAH). Besides transcranial doppler, neuromonitoring of ICP/CPP was supplemented by ptiO2 monitoring. The ptiO2 catheter was inserted into viable tissue in the vascular territory with the highest risk for vasospasm. Patients were divided in an infarction (n = 21) and a non-infarction group (n = 11). Critical CPP (< 70 mmHg) as well as hypoxic ptiO2 (< 10 mmHg) was significantly more frequent in the infarction group (CPP: 25 vs 13%, p < 0.001; ptiO2: 16 vs 7%, p < 0.001). In both groups, over 25% of the critical ptiO2 values occurred at a CPP > 90 mmHg. In the infarction group, 13 patients showed transient phases of hypoxia which normalized under induced hypervolemic hypertension and 5 patients developed persistent hypoxia. In the non-infarction group 6 patients showed transient hypoxia and in 5 patients no hypoxic values could be found. In conclusion, monitoring of ptiO2 provides an additional independent parameter to detect hypoxic events and to guide therapy.

PtiO2 and CMRO2 changes in cortex and hippocampus of aging gerbil brain.

Tissue O2 partial pressure (PtiO2) and O2 disappearance rates (dPO2/dt) after bilateral carotid artery occlusion were measured with recessed cathode O2 microelectrodes (tips < 3 microns) in gerbil brains (n = 38) from three age groups: young (Y, 3-6 mo), mature (M, 10-12 mo), and older (O, 18-21 mo). Mean PtiO2 values were 18.4 +/- 1.2 (SE), 14.0 +/- 0.8 (P < 0.005), and 21.2 +/- 1.0 (NS) Torr for Y, M, and O groups, respectively, in the cortex and 14.1 +/- 0.8, 15.6 +/- 0.8 (NS), and 16.1 +/- 0.8 (NS) Torr in the hippocampus (Mann-Whitney comparisons with Y). In the cortex, mean dPO2/dt declined significantly with age: -19.2 +/- 1.1, -14.2 +/- 0.9 (P < 0.001), and -12.4 +/- 0.5 (P < 0.001) Torr/s for Y, M, and O, respectively (ANOVA comparisons with Y). In the hippocampus, the respective mean dPO2/dt values were -16.4 +/- 0.8, -15.6 +/- 1.9, and -13.9 +/- 2.2 Torr/s. Although the time trend for dPO2/dt was significant (P < 0.05), mean hippocampal differences compared by ANOVA were not. In Y, mean PtiO2 and dPO2/dt were lower in the hippocampus than in the cortex (P < 0.05). Apparent Michaelis-Menten constants for O2 were estimated from the O2 disappearance curves. These constants were significantly higher for the O group in the hippocampus (5.1 +/- 0.8 Torr) than in the cortex (2.7 +/- 0.6 Torr, P < 0.05).