Assessing Vascular Permeability during Experimental Cerebral Malaria by a Radiolabeled Monoclonal Antibody Technique

Heyde, Henri C. van der; Bauer, Philippe R.; Sun, Guan; Chang, Wun-Ling; Yin, Lijia; Fuseler, John W.; Granger, D. Neil

doi:10.1128/iai.69.5.3460-3465.2001

Cited by 42 publications

(30 citation statements)

References 32 publications

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“…Vascular permeability related to lung injury was measured using the Evans Blue dye extravasation assay, as previously described [20]. The animals were anesthetized with a combination of ketamine (24 mg/kg) and xylazine (36 mg/kg), and received 30 mg/kg Evans Blue dye dissolved in 0.9% saline at a final concentration of 20 mg/ml by jugular vein injection, 10 min before sacrifice.…”

Section: Methodsmentioning

confidence: 99%

Deficiency in type 1 insulin-like growth factor receptor in mice protects against oxygen-induced lung injury

et al. 2005

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Background: Cellular responses to aging and oxidative stress are regulated by type 1 insulin-like growth factor receptor (IGF-1R). Oxidant injury, which is implicated in the pathophysiology of a number of respiratory diseases, acutely upregulates IGF-1R expression in the lung. This led us to suspect that reduction of IGF-1R levels in lung tissue could prevent deleterious effects of oxygen exposure.

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Section: Methodsmentioning

confidence: 99%

Deficiency in type 1 insulin-like growth factor receptor in mice protects against oxygen-induced lung injury

et al. 2005

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“…EB extravasation was the method selected in the present study to examine regional capillary permeability, and it has been validated previously (30). Endothelial resistance is organ-and/or tissue dependent and is associated with blood redistribution (4).…”

Section: Effects On Capillary Permeabilitymentioning

confidence: 99%

Comparative effects of vasopressin, norepinephrine, and l-canavanine, a selective inhibitor of inducible nitric oxide synthase, in endotoxic shock

Lévy

Vallée²,

Lauzier³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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. Comparative effects of vasopressin, norepinephrine, and L-canavanine, a selective inhibitor of inducible nitric oxide synthase, in endotoxic shock. Am J Physiol Heart Circ Physiol 287: H209 -H215, 2004. First published February 26, 2004 10.1152/ajpheart.00946.2003, a standard of care, AVP, an alternative candidate, and L-canavanine (LC), a selective inhibitor of inducible nitric oxide synthase, were compared for efficacy and innocuousness on global and regional hemodynamics, plasmatic and tissue lactate-to-pyruvate ratio (L/P), tissue high-energy phosphates, renal function, and tissue capillary permeability in a rat model of endotoxic normokinetic shock. Mean arterial pressure (MAP) decreased (ϳ35%) but aortic blood flow increased during endotoxin infusion (P Ͻ 0.05 vs. control). Additionally, there was a decrease in mesenteric (MBF) and renal (RBF) blood flows along with regional-to-systemic ratio (P Ͻ 0.05 vs. control). All tested drugs restored MAP to basal levels but slightly decreased abdominal aortic flow; however, RBF and MBF remained unchanged. Endotoxin significantly decreased diuresis and inulin clearance (ϳ3-to 4-fold), whereas AVP or LC attenuated this drop (P Ͻ 0.05 vs. control). In contrast, NE did not improve endotoxininduced renal dysfunction. Endotoxin induced gut and lung hyperpermeability (P Ͻ 0.05 vs. control). Endotoxin-induced gut hyperpermeability was inhibited by AVP, LC, and NE. Endotoxin-induced lung hyperpermeability was further worsened by NE (ϳ2-fold increase) but not AVP infusion (P Ͻ 0.05 vs. endotoxin). LC significantly improved endotoxin-induced pulmonary hyperpermeability. Endotoxin increased renal lactate and decreased renal ATP. NE did not change renal lactate or renal ATP. AVP and LC decreased renal lactate and normalized renal ATP. Finally, endotoxin was associated with increased lactate levels and L/P (ϳ2-and 1.5-fold increases vs. control, respectively), whereas AVP and LC, but not NE, normalized both parameters after endotoxin challenge. These results suggest that, in a short-term endotoxic shock model, AVP improves systemic hemodynamics without side effects and has particular beneficial effects on renal function. septic shock; vascular permeability; renal function THE HUMAN RESPONSE to septic challenge usually includes increased cardiac output, decreased peripheral resistance, low arterial pressure, and increased vascular permeability. AVP, also known as "the" antidiuretic hormone (ADH), is an emerging alternative candidate for management of redistributive shock (7). Indeed, AVP exhibits strong vasoconstrictor effects through stimulation of the V1 receptor leading to arterial pressure improvement (28). Moreover, low concentrations of exogenous AVP mediate vasodilatation in coronary, cerebral, and pulmonary arterial circulation (20). The recognized effects of AVP on renal function are complex and include association of an antidiuretic effect through stimulation of V2 receptors, an increase of diuresis/natriuresis through V1 receptors by efferent arteriolar vasoconstric...

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“…Like P. falciparum-parasitized erythrocytes, both P. yoelii-and P. berghei-parasitized erythrocytes sequester by adhering to brain microvasculature (15,21). P. berghei-infected mice also exhibit respiratory distress with lactic acidosis, anemia, and nephritis, indicating that these mice also exhibit other clinical manifestations of severe falciparum malaria (37).…”

mentioning

confidence: 99%

Inhibition of Platelet Adherence to Brain Microvasculature Protects against SeverePlasmodium bergheiMalaria

Sun¹,

Chang²,

Li³

et al. 2003

Infect Immun

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Some patients with Plasmodium falciparum infections develop cerebral malaria, acute respiratory distress, and shock and ultimately die even though drug therapy has eliminated the parasite from the blood, suggesting that a systemic inflammatory response contributes to malarial pathogenesis. Plasmodium berghei-infected mice are a well-recognized model of severe malaria (experimental severe malaria [ESM]), and infected mice exhibit a systemic inflammatory response. Because platelets are proposed to contribute to ESM and other systemic inflammatory responses, we determined whether platelet adherence contributes to experimental malarial pathogenesis. Indeed, a significant (P < 0.005) increase in the number of rolling and adherent platelets was observed by intravital microscopy in brain venules of P. berghei-infected mice compared with the number in uninfected controls. P-selectin-or ICAM-1-deficient mice exhibit increased survival after P. berghei infection. We observed a significant (P < 0.0001) reduction in the morbidity of mice injected with anti-CD41 (␣ IIb or gpIIb) monoclonal antibody on day 1 of P. berghei infection compared with the morbidity of infected controls injected with rat immunoglobulin G. Additionally, platelet rolling and adhesion in brain venules were reduced in P. berghei mice lacking either P-selectin or ICAM-1 or when the platelets were coated with anti-CD41 monoclonal antibody. Unlike other inflammatory conditions, we did not detect platelet-leukocyte interactions during P. berghei malaria. Because (i) leukocyte adhesion is not markedly altered in the absence of P-selectin or ICAM-1 and (ii) CD41 is not an adhesion molecule for parasitized erythrocytes, these findings support the hypothesis that inhibition of platelet adhesion to the brain microvasculature protects against development of malarial pathogenesis.

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Assessing Vascular Permeability during Experimental Cerebral Malaria by a Radiolabeled Monoclonal Antibody Technique

Cited by 42 publications

References 32 publications

Deficiency in type 1 insulin-like growth factor receptor in mice protects against oxygen-induced lung injury

Deficiency in type 1 insulin-like growth factor receptor in mice protects against oxygen-induced lung injury

Comparative effects of vasopressin, norepinephrine, and l-canavanine, a selective inhibitor of inducible nitric oxide synthase, in endotoxic shock

Inhibition of Platelet Adherence to Brain Microvasculature Protects against SeverePlasmodium bergheiMalaria

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