دورية أكاديمية

Autoregulation of blood flow drives early hypotension in a rat model of systemic inflammation induced by bacterial lipopolysaccharide.

التفاصيل البيبلوغرافية
العنوان: Autoregulation of blood flow drives early hypotension in a rat model of systemic inflammation induced by bacterial lipopolysaccharide.
المؤلفون: Moretti EH; Departamento de Imunologia, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Av. Prof. Lineu Prestes, 1730, Sao Paulo, SP 05508-000, Brazil., Rodrigues AC; Instituto Internacional de Neurociencias Edmond e Lily Safra, Instituto de Ensino e Pesquisa Alberto Santos Dumont, Macaiba, RN 59288-899, Brazil., Marques BV; Departamento de Farmacologia, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, SP 05508-000, Brazil., Totola LT; Departamento de Fisiologia e Biofisica, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, SP 05508-000, Brazil., Ferreira CB; Departamento de Farmacologia, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, SP 05508-000, Brazil.; Department of Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213-2548, USA., Brito CF; Departamento de Imunologia, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Av. Prof. Lineu Prestes, 1730, Sao Paulo, SP 05508-000, Brazil., Matos CM; Departamento de Imunologia, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Av. Prof. Lineu Prestes, 1730, Sao Paulo, SP 05508-000, Brazil., da Silva FA; Departamento de Fisiologia e Biofisica, Instituto de Ciencias Biologias, Universidade Federal de Minas Gerais, Belo Horizonte, MG 31270-901, Brazil., Santos RAS; Departamento de Fisiologia e Biofisica, Instituto de Ciencias Biologias, Universidade Federal de Minas Gerais, Belo Horizonte, MG 31270-901, Brazil., Lopes LB; Departamento de Farmacologia, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, SP 05508-000, Brazil., Moreira TS; Departamento de Fisiologia e Biofisica, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, SP 05508-000, Brazil., Akamine EH; Departamento de Farmacologia, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, SP 05508-000, Brazil., Baccala LA; Departamento de Engenharia de Telecomunicacoes e Controle, Escola Politecnica, Universidade de Sao Paulo, Sao Paulo, SP 05508-900, Brazil., Fujita A; Departamento de Estatistica, Instituto de Matematica e Estatistica, Universidade de Sao Paulo, Sao Paulo, SP 05508-090, Brazil., Steiner AA; Departamento de Imunologia, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Av. Prof. Lineu Prestes, 1730, Sao Paulo, SP 05508-000, Brazil.
المصدر: PNAS nexus [PNAS Nexus] 2023 Jan 21; Vol. 2 (2), pp. pgad014. Date of Electronic Publication: 2023 Jan 21 (Print Publication: 2023).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Oxford University Press on behalf of the National Academy of Sciences Country of Publication: England NLM ID: 9918367777906676 Publication Model: eCollection Cited Medium: Internet ISSN: 2752-6542 (Electronic) Linking ISSN: 27526542 NLM ISO Abbreviation: PNAS Nexus Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [Oxford] : Oxford University Press on behalf of the National Academy of Sciences, [2022]-
مستخلص: Uncontrolled vasodilation is known to account for hypotension in the advanced stages of sepsis and other systemic inflammatory conditions, but the mechanisms of hypotension in earlier stages of such conditions are not clear. By monitoring hemodynamics with the highest temporal resolution in unanesthetized rats, in combination with ex-vivo assessment of vascular function, we found that early development of hypotension following injection of bacterial lipopolysaccharide is brought about by a fall in vascular resistance when arterioles are still fully responsive to vasoactive agents. This approach further uncovered that the early development of hypotension stabilized blood flow. We thus hypothesized that prioritization of the local mechanisms of blood flow regulation (tissue autoregulation) over the brain-driven mechanisms of pressure regulation (baroreflex) underscored the early development of hypotension in this model. Consistent with this hypothesis, an assessment of squared coherence and partial-directed coherence revealed that, at the onset of hypotension, the flow-pressure relationship was strengthened at frequencies (<0.2 Hz) known to be associated with autoregulation. The autoregulatory escape to phenylephrine-induced vasoconstriction, another proxy of autoregulation, was also strengthened in this phase. The competitive demand that drives prioritization of flow over pressure regulation could be edema-associated hypovolemia, as this became detectable at the onset of hypotension. Accordingly, blood transfusion aimed at preventing hypovolemia brought the autoregulation proxies back to normal and prevented the fall in vascular resistance. This novel hypothesis opens a new avenue of investigation into the mechanisms that can drive hypotension in systemic inflammation.
(© The Author(s) 2023. Published by Oxford University Press on behalf of National Academy of Sciences.)
References: Shock. 2007 Jul;28(1):71-7. (PMID: 17510599)
Am J Physiol. 1981 Aug;241(2):G143-9. (PMID: 7270691)
Crit Care. 2013 Oct 16;17(5):R238. (PMID: 24131656)
Am J Physiol Regul Integr Comp Physiol. 2000 Jan;278(1):R60-5. (PMID: 10644622)
Clin Physiol Funct Imaging. 2016 Nov;36(6):490-496. (PMID: 26017052)
Am J Physiol. 1979 Aug;237(2):H174-7. (PMID: 464109)
Eur J Neurosci. 2006 Jun;23(12):3359-67. (PMID: 16820025)
Am J Physiol. 1991 Feb;260(2 Pt 2):H305-18. (PMID: 1671735)
Am J Physiol. 1987 Jan;252(1 Pt 2):H118-24. (PMID: 3812706)
Crit Care Med. 2004 Jan;32(1):175-83. (PMID: 14707577)
JAMA. 2016 Feb 23;315(8):801-10. (PMID: 26903338)
Circ Res. 1969 May;24(5):599-605. (PMID: 4306062)
Jpn J Pharmacol. 2000 Mar;82(3):261-4. (PMID: 10887957)
Curr Opin Crit Care. 2018 Aug;24(4):292-299. (PMID: 29846206)
Physiol Rev. 2015 Apr;95(2):405-511. (PMID: 25834230)
Eur J Pharmacol. 1999 May 28;373(1):41-9. (PMID: 10408250)
Crit Care Med. 2013 May;41(5):1167-74. (PMID: 23442987)
Adv Physiol Educ. 2011 Mar;35(1):5-15. (PMID: 21385995)
Eur J Pharmacol. 1996 Aug 8;309(2):175-82. (PMID: 8874136)
Chest. 2013 Feb 1;143(2):364-370. (PMID: 22910834)
Intensive Care Med Exp. 2015 Dec;3(1):49. (PMID: 26215813)
Br J Pharmacol. 1996 Jul;118(5):1218-22. (PMID: 8818346)
Crit Care. 2018 Feb 27;22(1):52. (PMID: 29486781)
Am J Physiol Heart Circ Physiol. 2007 Jan;292(1):H432-8. (PMID: 16963612)
Shock. 2002 Jan;17(1):55-60. (PMID: 11795670)
Circ Res. 1976 May;38(5):379-85. (PMID: 1269076)
ERJ Open Res. 2021 Aug 02;7(3):. (PMID: 34350288)
Circ Res. 1964 Aug;15:SUPPL:39-47. (PMID: 14206319)
Nat Rev Neurosci. 2006 May;7(5):335-46. (PMID: 16760914)
Physiol Rep. 2017 Feb;5(4):. (PMID: 28242823)
Shock. 2014 Jun;41(6):546-53. (PMID: 24569508)
N Engl J Med. 2001 Aug 23;345(8):588-95. (PMID: 11529214)
Crit Care. 2012 Oct 04;16(5):R181. (PMID: 23036135)
Crit Care Med. 2019 Mar;47(3):436-448. (PMID: 30516567)
Am J Physiol. 1987 Oct;253(4 Pt 2):H728-36. (PMID: 2889369)
Intensive Care Med. 2004 Apr;30(4):580-8. (PMID: 14997295)
Shock. 2001 Dec;16(6):466-72. (PMID: 11770046)
Crit Care. 2008;12(3):R63. (PMID: 18457586)
J Pharmacol Exp Ther. 2003 Aug;306(2):538-45. (PMID: 12730359)
Lancet. 2020 Jan 18;395(10219):200-211. (PMID: 31954465)
N Engl J Med. 2020 Jan 9;382(2):163-178. (PMID: 31914243)
J Trauma. 1999 Oct;47(4):706-12. (PMID: 10528605)
Circ Res. 1977 Jul;41(1):19-26. (PMID: 862138)
Biol Cybern. 2001 Jun;84(6):463-74. (PMID: 11417058)
Front Physiol. 2019 Oct 17;10:1329. (PMID: 31749708)
JAMA. 2016 Sep 27;316(12):1298-309. (PMID: 27673307)
Br J Pharmacol. 1993 Mar;108(3):786-92. (PMID: 7682137)
Am J Physiol Regul Integr Comp Physiol. 2012 Dec;303(11):R1127-35. (PMID: 23076874)
Dig Dis Sci. 1982 Aug;27(8):675-9. (PMID: 7094790)
J Hypertens. 2008 Jun;26(6):1127-37. (PMID: 18475150)
Proc Natl Acad Sci U S A. 2016 Nov 22;113(47):13289-13294. (PMID: 27834220)
Crit Care. 2013 Jul 12;17(4):R139. (PMID: 23849307)
J Physiol. 2006 Nov 15;577(Pt 1):369-86. (PMID: 16901945)
Br J Pharmacol. 2022 Jun;179(12):3061-3077. (PMID: 34978069)
Crit Care Med. 2017 Mar;45(3):486-552. (PMID: 28098591)
J Physiol. 2014 Sep 1;592(17):3901-16. (PMID: 24951620)
Crit Care Med. 2012 Jun;40(6):1873-8. (PMID: 22610190)
PLoS One. 2013;8(2):e56331. (PMID: 23457552)
فهرسة مساهمة: Keywords: blood pressure; critical care; endotoxic shock; perfusion; septic shock; vascular function; vasoplegia
تواريخ الأحداث: Date Created: 20230306 Latest Revision: 20230307
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC9982072
DOI: 10.1093/pnasnexus/pgad014
PMID: 36874271
قاعدة البيانات: MEDLINE
الوصف
تدمد:2752-6542
DOI:10.1093/pnasnexus/pgad014