Moderately prolonged permissive hypotension results in reversible metabolic perturbation evaluated by intracerebral microdialysis - an experimental animal study

Jakobsen, Rasmus Peter; Nielsen, Troels Halfeld; Mölström, Simon; Nordström, Carl‐Henrik; Granfeldt, Asger; Toft, Palle

doi:10.1186/s40635-019-0282-x

Cited by 6 publications

(13 citation statements)

References 31 publications

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“…(B): Brain tissue oxygen tension (PbtO 2 ), and lactate/pyruvate (LP) ratio obtained in brain tissue (intracerebral) and superior sagittal sinus (sinus) during reversible hemorrhagic shock. Data from ( 94 , 95 ) are shown as Mean ± SEM.…”

Section: Microdialysis Of Cerebral Venous Blood—experimentalmentioning

confidence: 99%

Bedside interpretation of cerebral energy metabolism utilizing microdialysis in neurosurgical and general intensive care

et al. 2022

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The microdialysis technique was initially developed for monitoring neurotransmitters in animals. In 1995 the technique was adopted to clinical use and bedside enzymatic analysis of glucose, pyruvate, lactate, glutamate and glycerol. Under clinical conditions microdialysis has also been used for studying cytokines, protein biomarkers, multiplex proteomic and metabolomic analyses as well as for pharmacokinetic studies and evaluation of blood-brain barrier function. This review focuses on the variables directly related to cerebral energy metabolism and the possibilities and limitations of microdialysis during routine neurosurgical and general intensive care. Our knowledge of cerebral energy metabolism is to a large extent based on animal experiments performed more than 40 years ago. However, the different biochemical information obtained from various techniques should be recognized. The basic animal studies analyzed brain tissue homogenates while the microdialysis technique reflects the variables in a narrow zone of interstitial fluid surrounding the probe. Besides the difference of the volume investigated, the levels of the biochemical variables differ in different compartments. During bedside microdialysis cerebral energy metabolism is primarily reflected in measured levels of glucose, lactate and pyruvate and the lactate to pyruvate (LP) ratio. The LP ratio reflects cytoplasmatic redox-state which increases instantaneously during insufficient aerobic energy metabolism. Cerebral ischemia is characterized by a marked increase in intracerebral LP ratio at simultaneous decreases in intracerebral levels of pyruvate and glucose. Mitochondrial dysfunction is characterized by a moderate increase in LP ratio at a very marked increase in cerebral lactate and normal or elevated levels of pyruvate and glucose. The patterns are of importance in particular for interpretations in transient cerebral ischemia. A new technique for evaluating global cerebral energy metabolism by microdialysis of the draining cerebral venous blood is discussed. In experimental studies it has been shown that pronounced global cerebral ischemia is reflected in venous cerebral blood. Jugular bulb microdialysis has been investigated in patients suffering from subarachnoid hemorrhage, during cardiopulmonary bypass and resuscitation after out of hospital cardiac arrest. Preliminary results indicate that the new technique may give valuable information of cerebral energy metabolism in clinical conditions when insertion of an intracerebral catheter is contraindicated.

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Section: Microdialysis Of Cerebral Venous Blood—experimentalmentioning

confidence: 99%

Bedside interpretation of cerebral energy metabolism utilizing microdialysis in neurosurgical and general intensive care

et al. 2022

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“…The porcine model of haemorrhagic shock and the surgical preparations have been described previously [16][17][18]. Instrumentation and anaesthesia were the same in the control group and NE group.…”

Section: Anaesthesia Mechanical Ventilation and Surgical Preparationmentioning

confidence: 99%

“…Vital parameters were recorded every 10 min. Following a 60 min baseline period haemorrhagic shock was achieved by bleeding the animals to a pre-defined MAP of approximately 40 mm Hg at a rate of 2.15 mL/kg/min over 7 min, and then 1.15 mL/kg/min over the remaining period [15,16]. The depth and duration of haemorrhagic shock necessary for producing cerebral ischemia that caused compromised energy state was based on previous experiments [15].…”

Section: Experimental Protocolmentioning

confidence: 99%

“…The objective of this study was to investigate the effect of the vasopressor norepinephrine on MAP, cerebral energy metabolism evaluated from intracerebral microdialysis, cerebral tissue oxygen tension (PbtO 2 ) and intracranial pressure (ICP) in an experimental model of induced haemorrhagic shock. The experimental model has been used in previous studies of cerebral energy metabolism during haemorrhagic shock [15,16].…”

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Effects of norepinephrine infusion on cerebral energy metabolism during experimental haemorrhagic shock

Jakobsen

Hansen

Nielsen

et al. 2022

ICMx

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Background The use of norepinephrine in the case of life-threatening haemorrhagic shock is well established but widely discussed. The present study was designed to compare the effects of early norepinephrine treatment vs. no treatment on cerebral energy metabolism during haemorrhagic shock. Methods Twelve pigs were subjected to haemorrhagic shock, 4 in the control group and 8 in the norepinephrine (NE) group. Following a 60 min baseline period haemorrhagic shock was achieved by bleeding all animals to a pre-defined mean arterial blood pressure (MAP) of approximately 40 mm Hg. When mean arterial pressure had decreased to 40 mmHg NE infusion started in the treatment group. After 90 min, NE infusion stopped, and all pigs were resuscitated with autologous blood and observed for 2.5 h. During the experiment cerebral tissue oxygenation (PbtO2) was monitored continuously and variables reflecting cerebral energy metabolism (glucose, lactate, pyruvate, glutamate, glycerol) were measured by utilizing intracerebral microdialysis. Results All 12 pigs completed the protocol. NE infusion resulted in significantly higher MAP (p < 0.001). During the shock period lactate/pyruvate (LP) ratio group increased from 20 (15–29) to 66 (38–82) (median (IQR)) in the control group but remained within normal limits in the NE group. The significant increase in LP ratio in the control group remained after resuscitation. After induction of shock PbtO2 decreased markedly in the control group and was significantly lower than in the NE group during the resuscitation phase. Conclusion NE infusion during haemorrhagic shock improved cerebral energy metabolism compared with no treatment.

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“…Moreover, H 2 S and the oxytocin (OT)/ oxytocin receptor (OTR) systems interact in trauma in the heart and the brain (11)(12)(13)(14)(15) and are both reported to have anti-oxidative, and vasculo-protective effects (15). Hence, activation of either system could be beneficial in HS, since severe hypovolemia can induce at least transitory cerebral tissue hypoxia events (16- 19), redox imbalance (20), barrier dysfunction (18,21) and, upon resuscitation, ischemia/reperfusion (I/R) injury (22).…”

Section: Introductionmentioning

confidence: 99%

Brain Histology and Immunohistochemistry After Resuscitation From Hemorrhagic Shock in Swine With Pre-Existing Atherosclerosis and Sodium Thiosulfate (Na2S2O3) Treatment

et al. 2022

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BackgroundThe hydrogen sulfide (H2S) and the oxytocin/oxytocin receptor (OT/OTR) systems interact in the central nervous and cardiovascular system. As a consequence of osmotic balance stress, H2S stimulates OT release from the paraventricular nuclei (PVN) in the hypothalamic regulation of blood volume and pressure. Hemorrhagic shock (HS) represents one of the most pronounced acute changes in blood volume, which, moreover, may cause at least transient brain tissue hypoxia. Atherosclerosis is associated with reduced vascular expression of the main endogenous H2S producing enzyme cystathionine-γ-lyase (CSE), and, hence, exogenous H2S administration could be beneficial in these patients, in particular after HS. However, so far cerebral effects of systemic H2S administration are poorly understood. Having previously shown lung-protective effects of therapeutic Na2S2O3 administration in a clinically relevant, long-term, porcine model of HS and resuscitation we evaluated if these protective effects were extended to the brain.MethodsIn this study, available unanalyzed paraffin embedded brain sections (Na2S2O3N = 8 or vehicle N = 5) of our recently published HS study were analyzed via neuro-histopathology and immunohistochemistry for the endogenous H2S producing enzymes, OT, OTR, and markers for brain injury and oxidative stress (glial fibrillary acidic protein (GFAP) and nitrotyrosine).ResultsNeuro-histopathological analysis revealed uninjured brain tissue with minor white matter edema. Protein quantification in the hypothalamic PVN showed no significant inter-group differences between vehicle or Na2S2O3 treatment.ConclusionsThe endogenous H2S enzymes, OT/OTR co-localized in magnocellular neurons in the hypothalamus, which may reflect their interaction in response to HS-induced hypovolemia. The preserved blood brain barrier (BBB) may have resulted in impermeability for Na2S2O3 and no inter-group differences in the PVN. Nonetheless, our results do not preclude that Na2S2O3 could have a therapeutic benefit in the brain in an injury that disrupts the BBB, e.g., traumatic brain injury (TBI) or acute subdural hematoma (ASDH).

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Moderately prolonged permissive hypotension results in reversible metabolic perturbation evaluated by intracerebral microdialysis - an experimental animal study

Cited by 6 publications

References 31 publications

Bedside interpretation of cerebral energy metabolism utilizing microdialysis in neurosurgical and general intensive care

Bedside interpretation of cerebral energy metabolism utilizing microdialysis in neurosurgical and general intensive care

Effects of norepinephrine infusion on cerebral energy metabolism during experimental haemorrhagic shock

Brain Histology and Immunohistochemistry After Resuscitation From Hemorrhagic Shock in Swine With Pre-Existing Atherosclerosis and Sodium Thiosulfate (Na2S2O3) Treatment

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