Endothelial dependent dilation in pial arterioles after crosslinked hemoglobin transfusion

Y. Asano, John A Ulatowski, Raymond C Koehler, R. J. Travstman, E. Bucci

Research output: Contribution to journalArticle

Abstract

Plasma-based hemoglobin may provide a more effective sink for NO than red cell-based hemoglobin. We tested the hypothesis that cell-free hemoglobin transfusion impairs dilation to acetylcholine (Ach) in pial arterioles with tight endothelial junctions. Exchange transfusion of approximately 5-7 g of crosslink! hemoglobin in 8 pentobarbital-anesthetized cats resulted in a decrease in hematocrit (30±1 to 18±1%; ±SE), an increase in arterial pressure (112±4 to 138±6 mmHg), and a decrease in diameter in small (2550 urn; 11±3%), medium (50-100 jim; 9±1%) and large (>100 iaa); 8±3%) arterioles. Topical Ach (SxlO'M) increased diameter by 31±4, 21±3 and 22±6%, respectively. The corresponding increases in 7 time controls cats at 33% hematocrit (38±10, 21±4, 19±4%), and in 6 albumin transfused cats at 18% hematocrit (20±4, 17±4, 13±5%) were similar to those in hemoglobin transfused cats. Likewise, size-dependent dilation to the NO donor SIN-1 (10-6M) in the hemoglobin group (23 ±4,16±3,9±2%) was similar to that in the control group (19±3, 12±2, 9±3%) and in the albumin group(23±4,18±4,7±1%). TopicalL-nitroarginine(3×104M) attenuated Ach but not SIN-1 dilation in all groups. We conclude that crosslinked hemoglobin transfusion does not impair dilation to Ach or SIN-1. Close contact of cell-free hemoglobin with the luminal endothelial glycocalyx does not appear to substantially impair abluminal diffusion of NO or a nitrosothiol to the smooth muscle.

Original languageEnglish (US)
JournalFASEB Journal
Volume10
Issue number3
StatePublished - 1996

Fingerprint

Arterioles
Dilatation
hemoglobin
Hemoglobins
acetylcholine
Acetylcholine
Cats
Hematocrit
cats
hematocrit
albumins
Albumins
Molsidomine
Glycocalyx
pentobarbital
arterioles
Tight Junctions
Nitroarginine
cells
Pentobarbital

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

Endothelial dependent dilation in pial arterioles after crosslinked hemoglobin transfusion. / Asano, Y.; Ulatowski, John A; Koehler, Raymond C; Travstman, R. J.; Bucci, E.

In: FASEB Journal, Vol. 10, No. 3, 1996.

Research output: Contribution to journalArticle

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abstract = "Plasma-based hemoglobin may provide a more effective sink for NO than red cell-based hemoglobin. We tested the hypothesis that cell-free hemoglobin transfusion impairs dilation to acetylcholine (Ach) in pial arterioles with tight endothelial junctions. Exchange transfusion of approximately 5-7 g of crosslink! hemoglobin in 8 pentobarbital-anesthetized cats resulted in a decrease in hematocrit (30±1 to 18±1{\%}; ±SE), an increase in arterial pressure (112±4 to 138±6 mmHg), and a decrease in diameter in small (2550 urn; 11±3{\%}), medium (50-100 jim; 9±1{\%}) and large (>100 iaa); 8±3{\%}) arterioles. Topical Ach (SxlO'M) increased diameter by 31±4, 21±3 and 22±6{\%}, respectively. The corresponding increases in 7 time controls cats at 33{\%} hematocrit (38±10, 21±4, 19±4{\%}), and in 6 albumin transfused cats at 18{\%} hematocrit (20±4, 17±4, 13±5{\%}) were similar to those in hemoglobin transfused cats. Likewise, size-dependent dilation to the NO donor SIN-1 (10-6M) in the hemoglobin group (23 ±4,16±3,9±2{\%}) was similar to that in the control group (19±3, 12±2, 9±3{\%}) and in the albumin group(23±4,18±4,7±1{\%}). TopicalL-nitroarginine(3×104M) attenuated Ach but not SIN-1 dilation in all groups. We conclude that crosslinked hemoglobin transfusion does not impair dilation to Ach or SIN-1. Close contact of cell-free hemoglobin with the luminal endothelial glycocalyx does not appear to substantially impair abluminal diffusion of NO or a nitrosothiol to the smooth muscle.",
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