Increased cerebral blood flow velocities assessed by transcranial Doppler examination is associated with complement activation after cardiopulmonary bypass.

The role of complement activation on the cerebral vasculature after cardiopulmonary bypass (CPB) is unclear. The goal of the study was to assess whether heparin-coated CPB reduces complement activation, and influences cerebral blood flow velocities (CBFV). Twenty-four patients undergoing coronary surgery were randomly allocated to non-coated (NC-group) or heparin-coated (HC-group) CPB. Complement activation was assessed by measuring sC5b-9. Transcranial Doppler (TCD) was performed on middle cerebral arteries before and after CPB. Systolic (SV), diastolic (DV) and mean (MV) CBFV were measured. Significant increase of sC5b-9 (p=0.003) was observed in the NC-group and CBFV increased after CPB (SV by 27%, p=0.05; DV by 40%, p=0.06; MV by 33%, p=0.04) whereas no changes were detected in the HC-group. TCD values were higher in the NC-group than in the HC-group (SV, p=0.04; DV, p=0.03; MV, p=0.03) although cardiac index, systemic vascular resistance, haematocrit and pCO(2) were similar. Postoperative SV, DV and MV were significantly correlated with sC5b-9 (r=0.583, p=0.009; r=0.581, p=0.009; r=0.598, p=0.007, respectively). Increased CBFV after CPB are correlated to the level of complement activation and may be controlled by heparin-coated circuits.

[Cerebral metabolism and brain injury]. / Métabolisme énergétique et agression cérébrale.

Brain energy metabolism and signal transduction are intimely intricated. At the cellular level this is reflected by the interdependent metabolism of glutamate and glucose and the energetic compartmentalization between astrocytic glycolysis and neuronal metabolism. Astrocytes appear to have a particular importance in brain metabolism by regulating microcirculation and the repartition of energetic substrates in function of synaptic activity. The high level of O(2) consumption compared to the mass of tissue confers a particular vulnerability of brain to oxidative stress. The synthesis of glutathione, the main anti-oxidant of brain, appears to be dependent of the regulation of synaptic glutamate concentration by astrocytes. Deficiencies of astrocytes functions appear to play a key role in the physiopathology of brain injury.

[Conventional and diffusion magnetic resonance imaging in the acute phase of severe traumatic brain injury]. / Apports de l'IRM conventionnelle et de l'IRM de diffusion à la phase aiguë du traumatisme crânien grave.

Neuro-imaging is essential for the initial evaluation and subsequent control in the acute stage of severe head injury. In these indications tomodensitometry (TDM) has a pivotal role. Despite the well recognized contribution of magnetic resonance imaging (MRI) to the investigation of most of acute neurological pathologies, MRI is not still a routine procedure for the initial investigation of patients with acute head injury. The superiority of morphological and functional MRI on TDM in this indication is discussed.

Changes in cerebral blood flow during PaCO2 variations in patients with severe closed head injury: comparison between the Fick and transcranial Doppler methods.

OBJECT: The aim of this study was to reassess whether middle cerebral artery blood flow velocity (MCAv) variations measured by transcranial Doppler ultrasonography during acute PaCO2 manipulation adequately reflect cerebral blood flow (CBF) changes in patients with severe closed head injury. METHODS: The study was performed by comparing MCAv variations to changes in CBF as assessed by measurements of the difference in the arteriovenous content in oxygen (AVDO2). The authors initiated 35 CO2 challenges in 12 patients with severe closed head injury during the acute stage. By simultaneous recording of systemic and cerebral hemodynamic parameters, 105 AVDO2 measurements were obtained. Patients were stratified into two groups, "high" and "low," with respect to whether their resting values of MCAv were greater than 100 cm/second during moderate hyperventilation. Four patients displayed an elevated MCAv, which was related to vasospasm in three cases and to hyperemia in one case. The PaCO2 and intracranial pressure levels were not different between the two groups. The slope of the regression line between 1 divided by the change in (delta)AVDO2 and deltaMCAv was not different from identity in the low group (1/deltaAVDO2 = 1.08 x deltaMCAv - 0.07, r = 0.93, p < 0.001) and significantly differed (p < 0.05) from the slope of the high group (1/deltaAVDO2 = 1.46 x deltaMCAv - 0.4, r = 0.83, p < 0.001). CONCLUSIONS: In patients with severe closed head injury, MCAv variations adequately reflect CBF changes as assessed by AVDO2 measurements in the absence of a baseline increase in MCAv. These observations indicate that both moderate variations in PaCO2 and variations in cerebral perfusion pressure do not act noticeably on the diameter of the MCA. The divergence from the expected relationship in the high group seems to be due to the heterogeneity of CO2-induced changes in cerebrovascular resistance between differing arterial territories.

Persistent carotid-vertebrobasilar anastomoses: how and why differentiating them?

The persistent carotid-vertebrobasilar anastomoses (PCVBA) can be explained by an interruption of the vertebrobasilar system (VBS) embryogenesis. We present two very rare cases of persistent anastomoses: a hypoglossal artery and a type I proatlantal artery, insisting on the angiographic criteria allowing differentiation. After a brief review of the embryogenesis of the VBS, we describe the different types of persistent anastomoses (hypoglossal, type I and II proatlantal, trigeminal and otic arteries). We will insist on the potential risks, not well-known, but typical of each anastomosis. PCVBA usually are incidental findings but imaging follow-up may be required since aneurysms may develop.

[Treatment of cerebral oedema]. / Traitement de l'oedème cérébral.

Progress in brain imaging, monitoring and physiopathology allows the identification of brain oedema from brain swelling, determination of its interstitial or intracellular nature, as well as blood-brain barrier permeability and the evaluation of the impact on cerebral haemodynamic. Common treatment of all types of cerebral oedema is based on prevention of self-sustained disorders due to increased intracranial pressure resulting in ischemic cerebral oedema. The specific treatment of each type of cerebral oedema is reviewed. Optimization of conventional anti-oedematous strategies is based on the precise determination of the nature of the cerebral oedema and of the blood-brain barrier status.

[Monitoring of severely head-injured patients during the first 24 hours]. / Monitorage du traumatisé crânien grave durant les 24 premières heures.

Monitoring of severely head-injured patients is essential to optimize cerebral haemodynamics and thus to limit intracranial hypertension and to prevent the occurrence of secondary systemic cerebral injuries. It includes continuous measurement of intracranial pressure, mean arterial pressure and venous jugular oxygen saturation. Assessment of circulatory velocity in the arteries of the polygon of Willis allows identification of intracranial hypertension, and later, a vasospasm in case of subarachnoid haemorrhage. Near infrared spectroscopy is an indirect indicator of cerebral oxygenation. This technique has not yet been validated. Direct tissue measurement of cerebral oxygen content is the most recently developed monitoring tool. Its clinical range of application has still to be specified. These basic monitoring techniques are a standard. They are essential for an undelayed and efficient treatment of complications occurring in head trauma patients.

[Cardiovascular effects of a calcium channel blocker in hypoxia caused by altitude]. / Effets cardiovasculaires d'un bloqueur calcique en hypoxie d'altitude.

OBJECTIVE: High altitude pulmonary oedema can be successfully treated and prevented by calcium channel blockers. Moreover, calcium entering in the cells could explain the congestive phenomena of acute mountain sickness (AMS). These findings led us to study the action of a calcium channel blocker, isradipine, in the prevention of non-complicated AMS. METHODS: In a double blind randomized study, 20 healthy volunteers received 5 mg of isradipine (n = 6) or placebo (n = 6) for 8 days. After 5 days of treatment in normoxia, the subjects were rapidly transported to an altitude of 4350 m. The efficiency of the treatment was then estimated by the AMS symptom score, haemodynamic parameters and renal function. RESULTS: The administration of isradipine did not significantly modify AMS symptom score nor most of other parameters measured in high altitude hypoxia. Heart rate was an average of 15 b/min lower in the isradipine group, probably because of a direct action of isradipine on the sinus node. Otherwise, the effects of hypoxia were similar in both groups and were in accordance with the literature. There was no clear explanation for the increase in cardiac output and stroke volume when the subjects moved from supine to standing position. Renal blood flow, measured by Doppler or para-aminohippuric acid clearance was not modified by hypoxia. Cerebral blood flow was elevated, due to the direct vasodilator effect of hypoxia. However this increase did not seem to be the main mechanism responsible for the congestive phenomena. On the other hand, the increase in capillary permeability (demonstrated by the increased transcapillary escape rate of albumin, and albuminuria) appeared to play a major role in the pathogenesis of AMS and high altitude cerebral oedema. Isradipine had no protective effect on these phenomena and its use should be restricted to the treatment of high altitude pulmonary oedema.