Figure 1
Figure 1. Injection of RB6-8C5 causes specific depletion of neutrophils and decreases blood pressure and vascular tone in Balb/C mice, in an iNOS-dependent manner. (A) Induction of neutropenia following intraperitoneal injection of RB6-8C5. RB6-8C5 was administered by intraperitoneal injection, 150 μg on day 0 and 300 μg on days 2, 4, and 6. Differential counts were performed on whole blood (n = 3, mean ± SEM). ***P < .001 vs day 0 using one-way analysis of variance (ANOVA) and Dunnett posthoc test analysis. (B) Control antibody does not cause neutropenia. Differential counts were performed on whole blood from mice administered either RB6-8C5 or GL113, following 3 days of neutropenia. (C) Depletion of neutrophils causes progressive hypotension. Blood pressures were measured daily by tail-cuff plethysmography, in mice administered either RB6-8C5 or an equal dose of GL113 intraperitoneal (n ≥ 15 for RB6-8C5 and n ≥ 10 for GL113, mean ± SEM). ***P < .001, *P < .05 versus day 0 using one-way ANOVA and Dunnett posthoc test analysis. (D) Thoracic aortae from neutropenic mice display reduced vasoconstriction responses. PE-induced constriction dose-response curves were constructed in thoracic aortae from control mice and mice depleted of neutrophils for 3 days using myography (n ≥ 4, mean ± SEM). ***P < .001 vs control using 2-way ANOVA. (E) L-NAME restores constriction to control levels in aortae from neutropenic mice. Dose-responses curves to PE were determined in thoracic aortae from control mice and mice depleted of neutrophils for 3 days in the presence or absence of 300 μM L-NAME (n ≥ 4, mean ± SEM). ***P < .001, neutropenic plus L-NAME versus neutropenic using 2-way ANOVA. (F) Acetylcholine relaxation is normal in aortae from neutropenic mice. Relaxation dose-response curves to ACh in PE-preconstricted aortae from control and neutropenic mice (day 3) were constructed (n ≥ 4, mean ± SEM). (G) 1400W restores constriction to control levels in aortae from neutropenic mice. PE-induced constriction responses in aortae from control and neutropenic mice (day 3) in the presence or absence of 10 μM 1400W were constructed (n ≥ 4, mean ± SEM). ***P < .001, neutropenic plus 1400W versus neutropenic using 2-way ANOVA.

Injection of RB6-8C5 causes specific depletion of neutrophils and decreases blood pressure and vascular tone in Balb/C mice, in an iNOS-dependent manner. (A) Induction of neutropenia following intraperitoneal injection of RB6-8C5. RB6-8C5 was administered by intraperitoneal injection, 150 μg on day 0 and 300 μg on days 2, 4, and 6. Differential counts were performed on whole blood (n = 3, mean ± SEM). ***P < .001 vs day 0 using one-way analysis of variance (ANOVA) and Dunnett posthoc test analysis. (B) Control antibody does not cause neutropenia. Differential counts were performed on whole blood from mice administered either RB6-8C5 or GL113, following 3 days of neutropenia. (C) Depletion of neutrophils causes progressive hypotension. Blood pressures were measured daily by tail-cuff plethysmography, in mice administered either RB6-8C5 or an equal dose of GL113 intraperitoneal (n ≥ 15 for RB6-8C5 and n ≥ 10 for GL113, mean ± SEM). ***P < .001, *P < .05 versus day 0 using one-way ANOVA and Dunnett posthoc test analysis. (D) Thoracic aortae from neutropenic mice display reduced vasoconstriction responses. PE-induced constriction dose-response curves were constructed in thoracic aortae from control mice and mice depleted of neutrophils for 3 days using myography (n ≥ 4, mean ± SEM). ***P < .001 vs control using 2-way ANOVA. (E) L-NAME restores constriction to control levels in aortae from neutropenic mice. Dose-responses curves to PE were determined in thoracic aortae from control mice and mice depleted of neutrophils for 3 days in the presence or absence of 300 μM L-NAME (n ≥ 4, mean ± SEM). ***P < .001, neutropenic plus L-NAME versus neutropenic using 2-way ANOVA. (F) Acetylcholine relaxation is normal in aortae from neutropenic mice. Relaxation dose-response curves to ACh in PE-preconstricted aortae from control and neutropenic mice (day 3) were constructed (n ≥ 4, mean ± SEM). (G) 1400W restores constriction to control levels in aortae from neutropenic mice. PE-induced constriction responses in aortae from control and neutropenic mice (day 3) in the presence or absence of 10 μM 1400W were constructed (n ≥ 4, mean ± SEM). ***P < .001, neutropenic plus 1400W versus neutropenic using 2-way ANOVA.

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