Endotoxaemic myocardial dysfunction: the role of coronary driving pressure in subendocardial perfusion
Carregando...
Citações na Scopus
6
Tipo de produção
article
Data de publicação
2015
Título da Revista
ISSN da Revista
Título do Volume
Editora
AUSTRALASIAN MED PUBL CO LTD
Citação
CRITICAL CARE AND RESUSCITATION, v.17, n.1, p.12-22, 2015
Resumo
Objective: To investigate the role of coronary driving pressure (CDP) in myocardial microcirculatory blood flow during sepsis. We hypothesised that in septic shock there is an impaired autoregulation of microcirculation, and blood flow is totally dependent on CDP. We analysed the effect of lipopolysaccharide (LPS)-induced shock on myocardial microcirculation, separating subendocardial and epicardial areas. We then studied the effect of CDP increases using noradrenaline (NOR) or metaraminol (Aramine [ARA]) on myocardial microcirculation and function, and we analysed the effect of volume infusion on CDP and myocardial function. Design and setting: Endotoxaemia was induced in male Wistar rats by an intraperitoneal injection of LPS 10 mg/kg. Animals were divided into a control (CT) group, an LPS-injected group, and an LPS-injected group treated with saline fluid, NOR or ARA. Main outcome measures: Ninety minutes later, a haemodynamic evaluation was performed. NOR or ARA were used to manage the mean arterial pressure (MAP) and CDP, and we inserted a catheter into the left ventricle to measure cardiac parameters. To measure blood flow in the myocardium and other organs, microspheres were introduced into the left ventricle using an infusion pump. Results: After LPS treatment, left ventricular (LV) systolic function (dP/dt max) and diastolic function (dP/dt min) decreased by 34% and 15%, respectively, and load-independent indices (LV contractility in ejection phase and dP/dt max divided by end-diastolic volume) were reduced. The CDP was also reduced (by 58%) in the endotoxaemic rats. Myocardial blood flow was reduced (by 80%) in animals with an MAP <= 65 mmHg. NOR increased the CDP (LPS; 38 mmHg [SEM, 2 mmHg]; LPS+NOR, 59 mmHg [SEM, 3 mmHg]) and microcirculatory perfusion (LPS, 2 mL/min/g tissue [SEM, 0.6 mL/min/g]; LPS+NOR, 6.2 mL/min/g [SEM, 0.8 mL/min/g]). ARA was also effective in improve microcirculation but saline volume infusion was ineffective in improving CDP or myocardial function. CDP showed a significant correlation with subendocardial blood flow. Conclusions: Myocardial blood flow in the LV subendocardium and the right ventricle decreases in endotoxaemic rats. Increasing CDP improves myocardial blood flow and function. Thus, in endotoxaemia, microcirculatory blood flow is pressure dependent, suggesting that it may be beneficial to treat patients with sepsis using a higher CDP.
Palavras-chave
Referências
- Asfar P, 2014, NEW ENGL J MED, V370, P1583, DOI 10.1056/NEJMoa1312173
- Ashruf JF, 2013, CURR OPIN CRIT CARE, V19, P381, DOI 10.1097/MCC.0b013e328364d7c8
- Bateman RM, 2005, CRIT CARE, V9, pS27, DOI 10.1186/cc3756
- Bonow RO, 2012, BRAUNWALDS HEART DIS, V1
- Cannon TR, 1998, BRIT J PHARMACOL, V123, P637, DOI 10.1038/sj.bjp.0701650
- Chirinos JA, 2009, HYPERTENSION, V54, P558, DOI 10.1161/HYPERTENSIONAHA.109.131870
- CUNNION RE, 1986, CIRCULATION, V73, P637
- Davani EY, 2006, CARDIOVASC RES, V72, P134, DOI 10.1016/j.cardiores.2006.06.029
- Dellinger RP, 2013, CRIT CARE MED, V41, P580, DOI 10.1097/CCM.0b013e31827e83af
- DHAINAUT JF, 1987, CRIT CARE MED, V15, P148, DOI 10.1097/00003246-198702000-00014
- Dubin A, 2009, CRIT CARE, V13, DOI 10.1186/cc7922
- Grandel U, 2000, CIRCULATION, V102, P2758
- Guido MC, 2007, CLIN EXP PHARMACOL P, V34, P1165, DOI 10.1111/j.1440-1681.2007.04689.x
- HAKKINEN JP, 1995, CARDIOVASC RES, V29, P74, DOI 10.1016/S0008-6363(96)88549-X
- Hiller KH, 1997, J MOL CELL CARDIOL, V29, P3115, DOI 10.1006/jmcc.1997.0538
- Ichinose F, 2007, CIRC RES, V100, P130, DOI 10.1161/01.RES.0000253888.09574.7a
- Ince C, 1999, CRIT CARE MED, V27, P1369, DOI 10.1097/00003246-199907000-00031
- Kumar A, 1996, J EXP MED, V183, P949, DOI 10.1084/jem.183.3.949
- Lorigados Clara Batista, 2010, Endocrine Metabolic & Immune Disorders-Drug Targets, V10, P274
- Merx MW, 2005, CIRCULATION, V112, P117, DOI 10.1161/CIRCULATIONAHA.104.502195
- Morelli A, 2005, INTENS CARE MED, V31, P638, DOI 10.1007/s00134-005-2619-z
- Munt B, 1998, CRIT CARE MED, V26, P1829
- Nogueira AC, 2008, SHOCK, V29, P342
- Pacher P, 2008, NAT PROTOC, V3, P1422, DOI 10.1038/nprot.2008.138
- PARKER MM, 1990, CHEST, V97, P126, DOI 10.1378/chest.97.1.126
- Prinzen FW, 2000, CARDIOVASC RES, V45, P13, DOI 10.1016/S0008-6363(99)00252-7
- Rigamonti F, 2013, CRIT CARE MED, V41, P2484, DOI 10.1097/CCM.0b013e3182982ac3
- Rimoldi O, 2006, J NUCL MED, V47, P163
- Rivers E, 2001, NEW ENGL J MED, V345, P1368, DOI 10.1056/NEJMoa010307
- Russell JA, 2014, NEW ENGL J MED, V370, P1649, DOI 10.1056/NEJMe1402066
- STAHL TJ, 1990, AM J PHYSIOL, V258, pH625
- Thooft A, 2011, CRIT CARE, V15, DOI 10.1186/cc10462
- Tokunaga C, 2007, CRIT CARE MED, V35, P1341, DOI 10.1097/01.CCM.0000260242.77637.57
- Trzeciak S, 2008, ACAD EMERG MED, V15, P399, DOI 10.1111/j.1553-2712.2008.00109.x
Coleções
Artigos e Materiais de Revistas Científicas - FM/MCM
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - HC/IOT
Artigos e Materiais de Revistas Científicas - LIM/51
Artigos e Materiais de Revistas Científicas - ODS/03
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - HC/IOT
Artigos e Materiais de Revistas Científicas - LIM/51
Artigos e Materiais de Revistas Científicas - ODS/03