The Influence of Hyperoxic Ventilation during Sodium Nitroprusside-induced Hypotension on Skeletal Muscle Tissue Oxygen Tension

Background: Increasing inspired oxygen concentrations might provide a simple and effective intervention to increase oxygen tension in tissues during controlled hypotension. To test this hypothesis, the influence of hyperoxic ventilation (100% O2) on skeletal muscle oxygen partial pressure (Ptio2) in patients receiving sodium nitroprusside-induced controlled hypotension was studied.

Methods: Forty-two patients undergoing radical prostatectomy were prospectively studied and randomly divided into three groups as follows: (1) Controlled hypotension induced by sodium nitroprusside (mean arterial blood pressure, 50 mmHg) and hyperoxic ventilation (CH-100%; n = 14); (2) controlled hypotension and ventilation with 50% O2 in nitrous oxide (CH-50%; n = 14); and (3) standard normotensive anesthesia with 50% O2 in nitrous oxide (control; n = 14). Ptio2 values were measured continuously in all patients using implantable polarographic microprobes. Arterial blood gases and lactate concentrations were analyzed in 30-min intervals.

Results: Surgical blood loss and transfusion requirements were significantly reduced in both groups receiving hypotensive anesthesia. During surgery, arterial partial pressure of oxy-gen and arterial oxygen content were significantly higher in patients of the CH-100% group. Baseline values of Ptio2 were comparable between the groups (CH-50%: 25.0 +/- 0.7 mmHg; CH-100%: 25.2 +/- 0.2 mmHg; control: 24.5 +/- 0.2 mmHg). After a transient increase in Ptio2 in the CH-100% group during normotension, Ptio2 values returned to baseline and remained unchanged in the control group. Ptio2 decreased significantly during the hypotensive period in the CH-50% group. The lowest mean Ptio2 values were 15.0 +/- 4.1 mmHg in the CH-50% group, 24.2 +/- 4.9 mmHg in the CH-100% group, and 23.5 +/- 3.8 mmHg in the control group. There were no significant changes in lactate plasma concentrations in any group throughout the study period.     

尼卡地平、硝普钠用于控制性降压对鼻内镜手术脑氧代谢的影响

目的比较鼻内镜手术中应用尼卡地平、硝普钠行控制性降压对脑氧代谢的影响。方法选择鼻息肉行内镜手术者30例,随机分为两组,分别采用尼卡地平(A组,n=15)和硝普钠(B组,n=15)行控制性降压。于不同时段降压前(T0)、降压后10 min(T1)、降压后30 min(T2)及停止降压后10 min(T3)行动静脉血气分析。结果①T1、T2时,B组HR明显快于T0时,且在此两时点HR明显快于A组(P<0.05)。②A组D(a-jv)O2、CERO2在T1、T2时较T0时明显下降,且在此两时点上明显低于B组(P<0.05)。结论尼卡地平、硝普钠均可安全用于鼻内镜手术中的控制性降压,都能降低脑氧代谢,但在降低脑氧代谢、改善脑氧合方面,尼卡地平优于硝普钠,有较好的脑保护作用。     

Recovery of Evoked Potential Amplitude after Cerebral Arterial Air Embolism in the Rabbit: A Comparison of the Effect of Cardiopulmonary Bypass with Normal Circulation

Background: Cerebral arterial air embolism (CAAE) may cause neurologic injury during cardiac surgery. It is not known whether cardiopulmonary bypass (CPB) increases or decreases brain injury from CAAE compared with the normal circulation.

Methods: A model of CAAE was produced by injection of 50 micro liter/kg air into the internal carotid artery of methohexital-anesthetized New Zealand white rabbits. Somatosensory-evoked potential (SSEP) amplitude was measured serially as a marker of neurologic recovery. In experiment A, saline rather than air was injected to control for surgical manipulation and time in CPB (n = 4) and nonheparinized non-CPB (n = 4) animals. In experiment B, 50 micro liter/kg air was injected in CPB (n = 11) and nonheparinized non-CPB (n = 11) animals. In experiment C, non-CPB animals (n = 6) were given heparin according to the same protocol as for CPB.

Results: In experiment A, SSEP latencies and amplitudes did not differ between CPB and non-CPB conditions. In experiment B, there was no SSEP recovery 5 min after CAAE in either CPB or non-CPB animals. Thereafter, SSEP recovery was less in CPB animals than in non-CPB animals at 30 min (9 +/- 12% vs. 29 +/- 20%; P = 0.009) and 60 min (18 +/- 15% vs. 39 +/- 22%; P = 0.030) after CAAE. Ninety-minute SSEP recovery did not differ between CPB and non-CPB groups (at 24 +/- 19% vs. 39 +/- 24%, respectively; P = 0.146). In experiment C (heparinized non-CPB), SSEP recovery 5, 30, 60, and 90 min after CAAE was 67 +/- 48%, 72 +/- 47%, 80 +/- 35%, and 77 +/- 35%, respectively.     

Cerebral Oxygen Extraction and Autoregulation during Extracorporeal Whole Body Hyperthermia in Humans

Background: The effects of hyperthermia on the human brain are incompletely understood. This study assessed the effects of whole body hyperthermia on cerebral oxygen extraction and autoregulation in humans.

Methods: Nineteen patients with chronic hepatitis C virus infection, not responding to interferon treatment, were subjected to experimental therapy with extracorporeal whole body hyperthermia at 41.8[degrees]C for 120 min under propofol anesthesia (23 sessions total). During treatment series A (13 sessions), end-tidal carbon dioxide was allowed to increase during heating. During series B (10 sessions), end-tidal carbon dioxide was maintained approximately constant. Cerebral oxygen extraction (arterial to jugular venous difference of oxygen content) and middle cerebral artery blood flow velocity were continuously measured. Cerebral pressure-flow autoregulation was assessed by static tests using phenylephrine infusion and by assessing the transient hyperemic response to carotid compression and release.

Results: For treatment series A, cerebral oxygen extraction decreased 2.2-fold and cerebral blood flow velocity increased 2.0-fold during heating. For series B, oxygen extraction decreased 1.6-fold and flow velocity increased 1.5-fold. Jugular venous oxygen saturation and lactate measurements did not indicate cerebral ischemia at any temperature. Static autoregulation test results indicated loss of cerebrovascular reactivity during hyperthermia for both series A and series B. The transient hyperemic response ratio did not decrease until the temperature reached approximately 40[degrees]C. Per degree Celsius temperature increase, the transient hyperemic response ratio decreased 0.07 (95% confidence interval, 0.05-0.09; P = 0.000). This association remained after adjustment for variations in arterial partial pressure of carbon dioxide, mean arterial pressure, and propofol blood concentration.     

Effects of Hypothermia, Pentobarbital, and Isoflurane on Postdepolarization Amino Acid Release during Complete Global Cerebral Ischemia

Background: Hypothermia and anesthetics may protect the brain during ischemia by blocking the release of excitatory amino acids. The effects of hypothermia (28 degrees C), pentobarbital, and isoflurane on postischemic excitatory amino acid concentrations were compared.

Methods: Rats were anesthetized with 0.8% halothane/50% N2 O, vascular catheters were placed, and a glass microelectrode and microdialysis cannula were inserted into the cerebral cortex. Experimental groups were: (1) control, pericranial, t = 38 degrees C; (2) hypothermia, t = 28 degrees C; (3) pentobarbital, t = 38 degrees Celsius; and (4) isoflurane, t = 38 degrees C. Halothane/N2 O was continued in groups 1 and 2, whereas a deep burst-suppression or isoelectric electroencephalogram was achieved with the test drugs in groups 3 and 4. Cerebral metabolic rates were similar in groups 2, 3, and 4. After a baseline dialysis sample was collected, animals were killed with potassium chloride. The time to terminal depolarization was recorded, after which three consecutive 10-min dialysate samples were collected. Glutamate, aspartate, gamma-aminobutyric acid, and glycine concentrations were measured using high-performance liquid chromatography.

Results: Times to terminal depolarization were shorter in both pentobarbital and isoflurane groups than with hypothermia (103+/- 15 and 127+/-10 vs. 195+/-20 s, respectively, mean +/-SD). However, times to terminal depolarization in all three groups were longer than in control subjects (control = 70+/-9 s). Postdepolarization concentrations of all compounds were lower in hypothermic animals (vs. normothermic control animals), but no reductions in glutamate, aspartate, or glycine concentrations were noted in pentobarbital or isoflurane groups. gamma-aminobutyric acid concentrations were reduced by both anesthetics, but not to the same degree as with hypothermia.     

Influence of Changes in Arterial PCO2 on Cerebral Blood Flow and Cerebral Energy State during Hypothermia in the Rat

In order to study the relationship between arterial P_CO2 and cerebral blood flow (CBF) in hypothermia, the body temperature of artificially ventilated rats was decreased to 22C, and changes in CBF were evaluated from arteriovenous differences in oxygen content (AVD_O2) at Pa_CO2 values of 15, 30, 40 and 60 mm Hg. The results were compared to those obtained at normal body temperature (37C) over the Pa_CO2 range 15–60 mm Hg. Separate experiments were performed to evaluate CBF and CMR_O2 at 22C and a Pa_CO2 of 15 mm Hg, using an inert gas technique for CBF. The tissue contents of phosphocreatine, ATP, ADP, AMP and lactate were measured in hypothermic animals at Pa_co2values of 15, 30 and 60 mm Hg.
The results showed that changes in CBF were of the same relative magnitude in hypothermia and normothermia when Pa co2 was increased from about 35 to about 60 mm Hg. However, with a decrease in Pa_CO2 the reduction in CBF was much more pronounced in hypothermia, and at Pa_CO2 15 mm Hg CBF was less than 20 % of the value measured in normothermic and normocapnic animals. The results of the metabolite measurements gave no evidence of tissue hypoxia in spite of the pronounced reduction in CBF. Although the results demonstrate that the brain of a hypothermic animal is protected against the harmful effects of a lowered CBF, it may not warrant recommending hyperventilation in clinical cases of hypothermia, especially not in patients with arteriosclerosis or cerebrovascular diseases.     

Accuracy of Cerebral Monitoring in Detecting Cerebral Ischemia during Carotid Endarterectomy: A Comparison of Transcranial Doppler Sonography, Near-infrared Spectroscopy, Stump Pressure, and Somatosensory Evoked Potentials

Background: This study compares the accuracy of cerebral monitoring systems in detecting cerebral ischemia during carotid endarterectomy.

Methods: The authors compared transcranial Doppler sonography (TCD), near-infrared spectroscopy (NIRS), stump pressure (SP) measurement, and somatosensory evoked potentials (SEP) in 48 patients undergoing carotid surgery during regional anesthesia. Cerebral ischemia was assumed when neurologic deterioration occurred. During clamping, the minimum mean middle cerebral artery velocity (TCDmin), its percentage change (TCD%), the minimum regional saturation of oxygen (NIRSmin), its percentage change (NIRS%), the mean SP, and the changes of SEP amplitude were recorded. To analyze the corresponding sensitivity and specificity of each parameter, the authors performed receiver operating characteristic analysis.

Results: Neurologic deterioration occurred in 12 patients. SP and NIRS were successfully performed in all patients. TCD monitoring was not possible in 10 (21%); SEP was not possible in 2 patients (4%). All parameters provided the ability to distinguish between ischemic and nonischemic patients. TCD% and NIRS% showed significantly better discrimination than TCDmin and NIRSmin (P < 0.05). The highest area under the curve (AUC) was found for TCD% (AUC = 0.973), but there was no significant difference compared with NIRS% (AUC = 0.905) and SP (AUC = 0.925). The lowest AUC was found for SEP (AUC = 0.749), which was significantly lower than that for TCD%, NIRS%, and SP.     

Effects of Temperature on Cerebral Tissue Oxygen Tension, Carbon Dioxide Tension, and pH during Transient Global Ischemia in Rabbits

Background: A decrease in brain temperature (Tbrain) causes a decrease in the cerebral metabolic rate for oxygen (CMRO2) and provides potent neuroprotection against ischemic damage. In the present study, the effects of mild to moderate hypothermia on cerebral tissue oxygen tension (PO2 brain), carbon dioxide tension (PCO2 brain), and pH (pHbrain) were monitored during short episodes of global cerebral ischemia.

Methods: After approval by the Animal Care and Use Committee, 10 New Zealand white rabbits were anesthetized (1% halothane in air) and mechanical ventilation was adjusted to maintain the arterial carbon dioxide tension at 35 mmHg (alpha-stat). A sensor to measure PO2 brain, PCO2 brain, pHbrain, and Tbrain was inserted into the brain through a burr hole in the skull. Tbrain was adjusted to 38 [degree sign] Celsius, 34.4 [degree sign] Celsius, and 29.4 [degree sign] Celsius in a random sequence in each animal. PO2 brain, PCO sub 2 brain, and pHbrain (all variables are reported at the actual Tbrain) were recorded every 10 s during a 5-min baseline, 3 min of cerebral ischemia induced by inflation of a neck tourniquet, and 10 min of reperfusion at each level of Tbrain. Analysis of variance and Dunnett's test were used for statistical analysis. Data are presented as means +/- SD.

Results: During ischemia, PO2 brain decreased from 56 +/- 3 to 33 +/- 2 mmHg at 38 [degree sign] Celsius, from 58 +/- 3 to 32 +/- 3 mmHg at 34.4 [degree sign] Celsius, and from 51 +/- 2 to 32 +/- 2 mmHg at 29.4 [degree sign] C (p = NS). PCO2 brain increased by 6.7 +/- 2 mmHg at 38 [degree sign] Celsius, by 5.1 +/- 1.4 mmHg at 34.4 [degree sign] Celsius, and by 2.3 +/- 0.8 mmHg at 29.4 [degree sign] Celsius. pH sub brain inversely followed the trend of PCO2 brain.