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Volume 4, Issue 3, Pages 197-204 (September 1997) Mechanism of circulatory shock induced by monoclonal antibody against neutrophils Ichiro Shiraishi, Eisuke F Sato, Manabu Nishikawa, Fujiro Sendo, Masayasu Inoue Pathophysiology Volume 4, Issue 3, Pages 197-204 (September 1997) DOI: 10.1016/S0928-4680(97)00020-5

Fig. 1 Effect of monoclonal antibody on the number of circulating PMN. Under urethane anesthesia (1 g/kg, i.p.), 500 μl/kg of either RP3 (○), RP1 (▵), or X63 (□) were administered intravenously. At the indicated times, 100 μl of blood samples were collected from the left femoral vein and the number of circulating PMN was calculated. Results are given as means±S.D. derived from three animals. Pathophysiology 1997 4, 197-204DOI: (10.1016/S0928-4680(97)00020-5)

Fig. 2 Effect of monoclonal antibody on the blood pressure. Under urethane anesthesia, the blood pressure was monitored continuously at the left femoral artery. At the indicated times (arrows), 500 μl/kg of either X63 (A), RP3 (B) or RP1 (C) were administered intravenously. Pathophysiology 1997 4, 197-204DOI: (10.1016/S0928-4680(97)00020-5)

Fig. 3 Effect of monoclonal antibody on the mean arterial pressure. Under urethane anesthesia, various doses of RP3 (○) or RP1 (▵) were administered intravenously. Changes in the mean arterial pressure were measured 10 min after administration. Values show the means±S.D. derived from three animals. Pathophysiology 1997 4, 197-204DOI: (10.1016/S0928-4680(97)00020-5)

Fig. 4 Effect of RP3 on MPO activity in various tissues. Under urethane anesthesia, 500 μl/kg RP3 was administered intravenously. At the indicated times, lung (•), spleen (□) and intestine (▵) were excised and MPO activity in these tissues was determined. Results are given as means±S.D. derived from three animals. Pathophysiology 1997 4, 197-204DOI: (10.1016/S0928-4680(97)00020-5)

Fig. 5 Effect of intermittent administration of RP3 on blood pressure. At the indicated times (arrow), varying doses of RP3 (50–500 μl/kg) were intravenously administered to the rat and their blood pressure was monitored continuously (A). The circulating PMN were depleted by intraperitoneal administration of 5 ml/kg RP3 (B). A total of 500 μl/kg RP3 was injected intravenously (arrow) 6 h after this treatment. Pretreatment by RP3 decreased the number of circulating PMN to less than 100 cells/mm3. Other conditions were the same as in Fig. 2. Pathophysiology 1997 4, 197-204DOI: (10.1016/S0928-4680(97)00020-5)

Fig. 6 Effect of PMN on the blood pressure. Control animals were intravenously injected with either 108 PMN (A) or their homogenate (B). The circulating PMN were depleted by intraperitoneal administration of 5 ml/kg RP3 (C, D, E); pretreatment by RP3 decreased the number of the circulating PMN to less than 100 cells/mm3. At 6 h after treatment, either 107 (C) or 108 (D) PMN were injected intravenously. Supernatant of RP3-treated PMN were also injected intravenously (E). Arrows show the time of administration. Pathophysiology 1997 4, 197-204DOI: (10.1016/S0928-4680(97)00020-5)

Fig. 7 Effect of SM-SOD on RP3-induced hypotension. Before (A) or after (B) administration of 10 mg/kg SM-SOD, 500 μl/kg RP3 was injected intravenously. Other conditions were the same as in Fig. 2. Pathophysiology 1997 4, 197-204DOI: (10.1016/S0928-4680(97)00020-5)

Fig. 8 Effect of NO synthase inhibitor on RP3-induced hypotension. Animals were intravenously injected with 500 μl/kg of RP3 before (A) or after (B) administration of 2 mg/kg LNNA. Other conditions were the same as in Fig. 2. Pathophysiology 1997 4, 197-204DOI: (10.1016/S0928-4680(97)00020-5)

Fig. 9 Effect of RP3 on the aortic levels of cGMP and cAMP. Under urethane anesthesia, 500 μl/kg of RP3 was administered intravenously. At the indicated times, the thoracic aorta was excised from the rat and the levels of cGMP (•) and cAMP (×) were determined. Results are given as means±S.D. derived from three animals. Pathophysiology 1997 4, 197-204DOI: (10.1016/S0928-4680(97)00020-5)

Fig. 10 Effect of RP3 on plasma levels of nitrate and nitrite. Under urethane anesthesia, animals were intravenously administered 500 μl/kg of either RP3 or X63. After 10 min, blood samples were obtained into heparinized tubes, centrifuged at 3000 rpm for 10 min. Plasma samples were determined for nitrate+nitrite as described in the text. Results are given as means±S.D. derived from three animals. Pathophysiology 1997 4, 197-204DOI: (10.1016/S0928-4680(97)00020-5)

Fig. 11 Effect of PAF antagonist on RP3-induced hypotension. Before or after intravenous administration of 25 μg/kg TCV309, 500 μl/kg RP3 was injected intravenously (A, B). The same dose of TCV309 was also administered before (C) or after (D) administration of 2 μg/kg PAF. The same dose of PAF was also administered in animals whose PMN were depleted by RP3 (E). Other conditions were the same as in Fig. 2. Pathophysiology 1997 4, 197-204DOI: (10.1016/S0928-4680(97)00020-5)