The Effects of Hypercapnia and Hypocapnia upon the Cerebrospinal Fluid Lactate and Pyruvate Concentrations and upon the Lactate, Pyruvate, ATP, ADP, Phosphocreatine and Creatine Concentrations of Cat Brain Tissue

Granholm, Lars; Siesjö, Bo K.

doi:10.1111/j.1748-1716.1969.tb04379.x

Cited by 116 publications

(27 citation statements)

References 33 publications

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“…Cerebral venous oxygen tension was elevated in our experiments (Table III) and is usually related closely to cerebral blood flow as measured by xenon-133 clearance (13). Although Plum and Posner (15) and others (16)(17)(18) have found that passive hyperventilation may lead to decreased cerebral blood flow and increased CSF lactate, this association was not observed (17) at Pco2 values as high as those we observed in the presence of increased CSF lactate (Table I). Another possible source of increased lactic acid production is the phagocytosing inflammatory cells in the meninges (19).…”

Section: Respiration and Circulation In Meningitiscontrasting

confidence: 50%

Effect of Experimental Pneumococcal Meningitis on Respiration and Circulation in the Rabbit

Sears¹,

O’Donoghue²,

Fisher³

et al. 1974

J. Clin. Invest.

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Section: Respiration and Circulation In Meningitiscontrasting

confidence: 50%

Effect of Experimental Pneumococcal Meningitis on Respiration and Circulation in the Rabbit

Sears¹,

O’Donoghue²,

Fisher³

et al. 1974

J. Clin. Invest.

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“…The elevation of the L=P in the brain is considered a reliable indicator of cerebral ischemia (Granholm and Siesjo, 1969;Persson and Hillered, 1992;Enblad et al, 1996). The L=P is elevated, at least in the early course of sTBI, as an indicator of brain injury and a compromised microcirculation.…”

Section: Discussionmentioning

confidence: 99%

“…The specific aim of the study was to establish whether the treatment with low-dose epoprostenol would reduce a L=P as measured by cerebral microdialysis after 24 h of treatment. The L=P is considered the most reliable marker for the redox state of the brain (Granholm and Siesjo, 1969;Persson and Hillered, 1992;Enblad et al, 1996). Secondly, the changes in microdialysis parameters over time in the epoprostenol and placebo groups were studied.…”

Section: à=àmentioning

confidence: 99%

Prostacyclin Treatment in Severe Traumatic Brain Injury: A Microdialysis and Outcome Study

Olivecrona

Rodling-Wahlström

Naredi

et al. 2009

Journal of Neurotrauma

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Prostacyclin (PGI 2 ) is a potent vasodilator, inhibitor of leukocyte adhesion, and platelet aggregation. In trauma the balance between PGI 2 and thromboxane A 2 (TXA 2 ) is shifted towards TXA 2 . Externally provided PGI 2 would, from a theoretical and experimental point of view, improve the microcirculation in injured brain tissue. This study is a prospective consecutive double-blinded randomized study on the effect of PGI 2 versus placebo in severe traumatic brain injury (sTBI). All patients with sTBI were eligible. Inclusion criteria: verified sTBI, Glasgow Coma Score (GCS) at intubation and sedation of 8, age 15-70 years, a first-recorded cerebral perfusion pressure (CPP) of !10 mm Hg, and arrival within 24 h of trauma. All subjects received an intracranial pressure (ICP) measuring device, bilateral intracerebral microdialysis catheters, and a microdialysis catheter in the abdominal subcutaneous adipose tissue. Subjects were treated according to an ICP-targeted therapy based on the Lund concept. 48 patients (mean age of 35.5 years and a median GCS of 6 [3-8]) were included. We found no significant effect of prostacyclin (epoprostenol, Flolan) on either the lactate-pyruvate ratio (L=P) at 24 h or the brain glucose levels. There was no significant difference in clinical outcome between the two groups. The median Glasgow Outcome Score (GOS) at 3 months was 4, and mortality was 12.5%. The favorable outcome (GOS 4-5) was 52%. The initial L=P did not prognosticate for outcome. Thus our results indicate that there is no effect of PGI 2 at a dose of 0.5 ng=kg=min on brain L=P, brain glucose levels, or outcome at 3 months.

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“…3 -*• 23,24 According to MacMillan and Siesjo's observations, 23 cerebral lac tate in rats was increased to 3.42 mM/kg at paC0 2 21.1 mmHg and 5.25 mM/kg at paC0 2 …”

Section: Cerebral Blood Flowmentioning

confidence: 99%

Effects of hyperventilation on cerebral blood flow and brain tissue metabolism in normotensive and spontaneously hypertensive rats.

Ishitsuka¹,

Fujishima²,

Nakatomi³

et al. 1982

Stroke

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SUMMARY Cerebral vascular carbon dioxide (CO2) reactivities were compared in normotensive (NTR) and hypertensive (SHR) rats. Cerebral bloodflow (CBF) in cortex and thalamus were evaluated before and during one hour of hyperventilation. After one hour of hyperventilation brain lactate, pyruvate, and ATP concentrations were also determined. Significant and similar reductions of CBF due to hyperventilation induced hypocapnia were found in both NTR and SHR groups. In contrast the percent increase in cerebrovascular resistance (CVR) per unit decrease in paC0 2 was significant, indicating that hypocapnia induced vasoconstriction is greater in NTR than in SHR groups. During hyperventilation the average value for lactate in the NTR group was 3.98 mM/kg. In contrast it was 3.15 mM/kg in the SHR group, a significant difference (p < 0.05). When paCC>2 fell below 15 mm Hg the cerebral lactate increased strikingly in the NTR group and cortical CVR was reduced suggesting that an accumulation of the ischemic metabolites caused dilatation of the constricted cerebral vessels. In contrast the SHR group disclosed no such changes. The increase CVR characteristic of SHR appeared to diminish the cerebral vasoconstrictive response to hypo capnia. As a result ischemic metabolites in the brain do not increase in this group to the degree that they do in NTR.Stroke Vol 13, No 5, 1982 IT HAS BEEN KNOWN that hyperventilation leads to cally ventilated with a gas mixture of 70% N 2 0 and vasoconstriction of cerebral arteries with reduced cere 30% of 0 2 . One femoral artery was cannulated to bral blood flow (CBF) and cerebral oxygen tension, 1 ' 2 measure blood pressure and for anaerobic sampling of and consequently alters the brain metabolism. '• 3 4 The arterial blood for pC0 2 , p0 2 and pH determinations electroencephalographic changes during hyperventila with a Model 113 IL meter. The body temperature, tion are indistinguishable from those observed during measured in the rectum, was kept close to 37°C cerebral hypoxia. 5,6 throughout the experiment. Our previous studies 7-10 have demonstrated that The animals were divided into two experimental spontaneously hypertensive rats (SHR) are more sus groups: one for measurements of local CBF and the ceptible to cerebral ischemia than normotensive rats other for determinations of brain tissue metabolites. (NTR) following bilateral carotid occlusion, suggest ing that the cerebral vasoreactivities to changes of the Cerebral Blood Flowperfusion pressure might be different between SHR Twenty-two NTR and 22 SHR were used for this and NTR. In fact, the lower limit of cerebral autoregupurpose. The animal's head was fixed in a head holder, lation is significantly higher in SHR than NTR, and the and two small burr holes were made on the skull 2 mm increased cerebral vascular resistance due to the persis lateral to the bregma on each side for stereotaxic inser tent high blood pressure is responsible for such upward tion of teflon-coated platinum electrodes, one in the shift of the autoregulation in SHR...

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The Effects of Hypercapnia and Hypocapnia upon the Cerebrospinal Fluid Lactate and Pyruvate Concentrations and upon the Lactate, Pyruvate, ATP, ADP, Phosphocreatine and Creatine Concentrations of Cat Brain Tissue

Cited by 116 publications

References 33 publications

Effect of Experimental Pneumococcal Meningitis on Respiration and Circulation in the Rabbit

Effect of Experimental Pneumococcal Meningitis on Respiration and Circulation in the Rabbit

Prostacyclin Treatment in Severe Traumatic Brain Injury: A Microdialysis and Outcome Study

Effects of hyperventilation on cerebral blood flow and brain tissue metabolism in normotensive and spontaneously hypertensive rats.

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