Showing papers by "Benoit Vallet published in 2000"

Venoarterial CO2 difference during regional ischemic or hypoxic hypoxia

Abstract: To test the role of blood flow in tissue hypoxia-related increased veno-arterial Pco 2difference (ΔPco 2), we decreased O2 delivery (D˙o 2) by either decreasing flow [ischemic hypoxia (IH)] or arte...

A single endotoxin injection in the rabbit causes prolonged blood vessel dysfunction and a procoagulant state.

Abstract: OBJECTIVES To determine the duration of vascular blood vessel dysfunction and coagulation abnormalities after administration of endotoxin in a nonlethal septic rabbit model. DESIGN Randomized, controlled, interventional trial. SETTING University animal laboratory. SUBJECTS A total of 30 male New Zealand White rabbits, randomly assigned to one of two groups. INTERVENTIONS Male New Zealand White rabbits were randomly divided into control or lipopolysaccharide (LPS) (0.5 mg/kg iv bolus Escherichia coli endotoxin)-treated groups. Metabolic acidosis and coagulation activation confirmed the presence of septic shock. The abdominal aorta was removed at 24 hrs (day 1), day 5, or day 21 after LPS injection. Immunohistochemical staining for an endothelial cell marker (PECAM-1/CD31) was performed to assess endothelial injury. Endothelium-dependent vascular relaxation was analyzed by in vitro vascular reactivity studies. Responses to acetylcholine, to calcium ionophore (A-23187), and to sodium nitroprusside were studied. In addition, arterial blood samples were collected on day 1, day 5, and day 21 for measurement of clotting factors and tissue factor activity. MEASUREMENTS AND MAIN RESULTS LPS injection resulted in endothelial injury, with loss of approximately 25% of the endothelial area on day 5, which disappeared on day 21. LPS injection also caused a significantly reduced relaxation response to acetylcholine (44.9% +/-9.9% vs. 76.5%+/-5.4% for the control group; p < .005), which was restored on day 21. In contrast, vascular relaxation in response to A-23187 and sodium nitroprusside was not altered. A significant decrease in the platelet count was observed on day 1, associated with a decrease in factors II and V. On day 5, platelet count and factors II and V were corrected in conjunction with an elevated monocyte tissue factor activity in LPS-injected rabbits. On day 21, coagulation abnormalities were corrected. CONCLUSIONS A single endotoxin injection in the rabbit was responsible for prolonged aortic endothelial cell dysfunction, as well as a prolonged procoagulant state. The latter is a potential trigger for disseminated intravascular coagulation. Importantly, these features are associated with normalization of conventional biological evidence of septic shock.

Assessment of tissue oxygenation in the critically-ill.

Abstract: It is hypothesized that tissue dysoxia and O2 debt are major factors in the development and the propagation of multiple organ failure in critically ill patients. Dysoxia is the result of an abnormal relationship between O2 supply (DO2) and O2 demand and translates into increased anaerobic metabolism and tissue and blood lactate concentration. First-line therapeutic strategies used to avoid the development of an O2 debt involve correction of cardiac output, haemoglobin, and O2 saturation in order to increase DO2 above its critical value. They are not sufficient, however, to ensure appropriate end-organ perfusion and oxygenation. The adequacy of cardiac output towards tissue metabolic requirements may be appreciated by venous-to-arterial and gut mucosal-to-arterial PCO2 differences. This review details these strategies and discusses their usefulness in current practice.

Effect of L-arginine on endothelial injury and hemostasis in rabbit endotoxin shock.

Abstract: To investigate whether impaired endothelial function was related to alteration of nitric oxide (NO) formation during endotoxic shock, we studied the effects of supplementation of l-arginine (l-Arg)

Escherichia coli endotoxin reduces cytochrome aa3 redox status in pig skeletal muscle.

Abstract: ObjectiveTo assess the effect of endotoxin on cytochrome aa3 (C aa3) redox status in a controlled blood flow preparation of pig isolated hindlimb, at a constant oxygen delivery (˙Do2limb) (constant flow period) and during progressive ischemia (decreasing flow period).DesignRandomized, controlled exp

Epidural hematoma after catheter removal.

Abstract: results of three other studies (3–5) supports our conclusion that the incidence of PDPH is not increased with the CSE technique. Brownridge (6), who is credited with the first report of CSE, reviewed his experience with his first 1000 CSE anesthetics and did not detect any PDPH’s (3). Albright and Forster (4) reviewed the safety and efficacy of 6002 CSE anesthetics in a community hospital and found a 0.28% incidence of therapeutic blood patches, which was comparable to historic controls for epidural analgesia. Collis et al. (5) did not find any difference in the incidence of PDPH between women who received CSE and those who received epidural analgesia, nor did they find any PDPH’s in the CSE group. Although “common sense” may dictate that the incidence of PDPH should be more frequent with the CSE technique because of the intentional dural puncture, there are other reasons why the incidence of PDPH may not be greater with CSE. Norris et al. (2) suggested that the anesthesiologist may be more meticulous during CSE placement, which may lead to a lower incidence of accidental dural puncture. Brownridge (3) hypothesized that the introduction of subarachnoid opioid may “provide prophylaxis” against the development of PDPH. It is also possible that the epidural local anesthetic increases subarachnoid pressure, which may decrease the incidence of headache following the CSE technique. CSE analgesia has added a very powerful technique to our armamentarium for the woman in labor and current literature suggests that the incidence of complications, including PDPH, is not more frequent than that associated with standard epidural analgesia.