Abstract
Introduction: Platelet-neutrophil (P-PMN) interactions may contribute to impaired microvascular blood flow in severe sepsis (S). We examined whether blocking adhesive molecules mediating P-PMN interactions attenuates S induced P-PMN interactions. Methods: P's, PMN's, and normal platelet poor plasma (NPPP) were isolated from 12 normal subjects. Platelet poor plasma was isolated from 12 patients with S (SPPP). Blocking monoclonal antibodies (mAb) were added to desired cell lines after incubation with SPPP and before coincubation of PMN and P. The following mAb's were used: anti-CD41 recognizes the P complex GPIIb-IIIa; anti-CD62P blocks P-selectin on P; anti-CD11a/LFA blocks ICAM 2 on PMN; anti-CD11b and anti-CD18 block receptors on PMN. Cell suspensions were infused at 1 ml/m through 5 u pore filters and the maximal point of the pressure time curve, Pi (mm Hg), was recorded. P-PMN interactions were assessed using fluorecscein conjugated mAb to activated CD63 P receptors. The mean intensity of mAb fluorescence (MF) of the PMN subgroup was used as an index of P-PMN adhesion. Data are expressed as mean ± SE,*p
| Original language | English (US) |
|---|---|
| Journal | Critical Care Medicine |
| Volume | 27 |
| Issue number | 12 SUPPL. |
| State | Published - 1999 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine
Cite this
Mechanisms of platelet-neutrophil interactions in sepsis. / Adler, Darryl; Kirschenbaum, Linda A.; Astiz, Mark E.; Saha, Dhanonjoy C.; Rackow, Eric C.
In: Critical Care Medicine, Vol. 27, No. 12 SUPPL., 1999.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Mechanisms of platelet-neutrophil interactions in sepsis
AU - Adler, Darryl
AU - Kirschenbaum, Linda A.
AU - Astiz, Mark E.
AU - Saha, Dhanonjoy C.
AU - Rackow, Eric C.
PY - 1999
Y1 - 1999
N2 - Introduction: Platelet-neutrophil (P-PMN) interactions may contribute to impaired microvascular blood flow in severe sepsis (S). We examined whether blocking adhesive molecules mediating P-PMN interactions attenuates S induced P-PMN interactions. Methods: P's, PMN's, and normal platelet poor plasma (NPPP) were isolated from 12 normal subjects. Platelet poor plasma was isolated from 12 patients with S (SPPP). Blocking monoclonal antibodies (mAb) were added to desired cell lines after incubation with SPPP and before coincubation of PMN and P. The following mAb's were used: anti-CD41 recognizes the P complex GPIIb-IIIa; anti-CD62P blocks P-selectin on P; anti-CD11a/LFA blocks ICAM 2 on PMN; anti-CD11b and anti-CD18 block receptors on PMN. Cell suspensions were infused at 1 ml/m through 5 u pore filters and the maximal point of the pressure time curve, Pi (mm Hg), was recorded. P-PMN interactions were assessed using fluorecscein conjugated mAb to activated CD63 P receptors. The mean intensity of mAb fluorescence (MF) of the PMN subgroup was used as an index of P-PMN adhesion. Data are expressed as mean ± SE,*p
AB - Introduction: Platelet-neutrophil (P-PMN) interactions may contribute to impaired microvascular blood flow in severe sepsis (S). We examined whether blocking adhesive molecules mediating P-PMN interactions attenuates S induced P-PMN interactions. Methods: P's, PMN's, and normal platelet poor plasma (NPPP) were isolated from 12 normal subjects. Platelet poor plasma was isolated from 12 patients with S (SPPP). Blocking monoclonal antibodies (mAb) were added to desired cell lines after incubation with SPPP and before coincubation of PMN and P. The following mAb's were used: anti-CD41 recognizes the P complex GPIIb-IIIa; anti-CD62P blocks P-selectin on P; anti-CD11a/LFA blocks ICAM 2 on PMN; anti-CD11b and anti-CD18 block receptors on PMN. Cell suspensions were infused at 1 ml/m through 5 u pore filters and the maximal point of the pressure time curve, Pi (mm Hg), was recorded. P-PMN interactions were assessed using fluorecscein conjugated mAb to activated CD63 P receptors. The mean intensity of mAb fluorescence (MF) of the PMN subgroup was used as an index of P-PMN adhesion. Data are expressed as mean ± SE,*p
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M3 - Article
VL - 27
JO - Critical Care Medicine
JF - Critical Care Medicine
SN - 0090-3493
IS - 12 SUPPL.
ER -