Endothelin and vasopressin influence splanchnic blood flow distribution during and after cardiopulmonary bypass

Bomberg, Hagen; Bierbach, Benjamin; Flache, Stephan; Wagner, Isabell; Gläser, L; Groesdonk, Heinrich V.; Menger, Michael D.; Schäfers, Hans Joachim

doi:10.1016/j.jtcvs.2012.03.014

Cited by 28 publications

(32 citation statements)

References 25 publications

(55 reference statements)

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“…We assume that in this experiment, vasopressin induced the vasoconstriction within the gastric tissue via arginine vasopressin receptor 1A interaction (AVPR1A) [26]. This finding is in contrast to our previous results demonstrating a protective effect of vasopressin administration on the small bowel microcirculation [7]. …”

Section: Discussionmentioning

confidence: 63%

“…In order to avoid the effects of catecholamines on α- and β-receptors, we chose vasopressin as vasopressor in this experiment. Previously, we have found that the administration of vasopressin diminishes the CPB-induced elevation of endothelin-1 (ET-1) and its receptor subtype A (ET A ), thus preventing CPB-induced jejunal mucosal ischemia [7]. Therefore, in the current study, we investigated whether a similar mechanism is also present in the gastric mucosa, considering that the endothelin system is involved in gastric mucosal ischemia [12].…”

Section: Introductionmentioning

confidence: 97%

“…Gastric ischemia has also been observed during and after CPB [5,6]; thus, a common pathogenetic mechanism can be hypothesized. Impairment of the microcirculation during CPB has been found in different organs, such as the pancreas, kidney and small bowel [5,7]. The underlying mechanisms are discussed controversially and are not fully understood [8].…”

Section: Introductionmentioning

confidence: 99%

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Vasopressin Aggravates Cardiopulmonary Bypass-Induced Gastric Mucosal Ischemia

Bomberg

Bierbach²,

Flache³

et al. 2014

Eur Surg Res

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Background/Aim: Upper gastrointestinal bleeding (UGIB) is one of the most frequent gastrointestinal complications after cardiac surgery with cardiopulmonary bypass (CPB). Endothelin expression and microcirculatory dysfunction have been shown to be involved in UGIB. The aim of this study was to analyze the effect of vasopressin during CPB on the gastric mucosal microcirculation and the involvement of the endothelin system. Methods: Eighteen pigs were randomized into three groups (n = 6 each): group I = sham, group II = CPB (1-hour CPB) and group III = CPB + vasopressin (1-hour CPB and vasopressin administration during CPB to maintain baseline arterial pressure). All animals were observed for a further 90 min after termination of CPB. Systemic hemodynamics as well as blood flow and oxygen saturation of the gastric mucosa were measured continuously. At the end of the experiment, the gastric mucosal expressions of endothelin-1 (ET-1) and its receptor subtypes A (ET_A) and B (ET_B) were determined by polymerase chain reaction. Gastric mucosal injury, apoptotic cell death and leukocytic infiltration were determined by histology and immunohistochemical analyses of cleaved caspase-3 and myeloperoxidase. Results: CPB decreased gastric microvascular perfusion, which was associated with an increased expression of ET-1 and ET_A. Vasopressin aggravated the CPB-associated malperfusion, whereas it completely abrogated the upregulation of ET-1 and ET_A. Interestingly, vasopressin did not induce gastric mucosal morphologic injury, leukocytic infiltration or apoptotic cell death. Conclusion: Vasopressin aggravates CPB-associated microvascular malperfusion of the gastric mucosa but does not induce gastric mucosal injury.

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Section: Discussionmentioning

confidence: 63%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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Vasopressin Aggravates Cardiopulmonary Bypass-Induced Gastric Mucosal Ischemia

Bomberg

Bierbach²,

Flache³

et al. 2014

Eur Surg Res

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“…They theorized that the mechanism behind this phenomenon lies in vasopressin's interaction with arginine vasopressin receptor 1a 18 . However, the same group has shown vasopressin to protect against the impairment of jejunal microcirculatory flow seen with cardiopulmonary bypass through the upregulation of endothelin 19 …”

Section: Enteric Effects Of Pressorsmentioning

confidence: 99%

Feeding the Postoperative Patient on Vasopressor Support

Bruns

Kozar

2015

Nut in Clin Prac

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Initiating enteral nutrition in the postoperative patient can be challenging. Postoperative ileus and bowel edema, bowel anastomosis, and intra-abdominal pathology contribute to the reluctance and inability to achieve adequate nutrition in this patient population. The addition of vasopressors confounds the difficulties. Clinical data are sparse but suggest that most postoperative patients requiring vasopressor therapy can be safely initiated and advanced on enteral nutrition. Consideration of the vasopressor agent being utilized and its dose is imperative, as are individual patient characteristics. Temporal changes in the dosage should be closely monitored, as increasing doses may reflect worsening clinical status that can be due to intestinal ischemia. Well-designed prospective trials are clearly necessary to address this controversial topic.

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“…1 In fact, the present publication is just the last addition to a very well-defined scientific excursus the authors have developed in the last years. 2,3 It should be emphasized that despite the fact that NOMI carries a heavy burden of mortality, its existence stays poorly acknowledged, and, as an obvious consequence, NOMI often remains unrecognized and untreated.…”

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confidence: 99%

Perioperative endothelin-1 levels: Searching for the hidden fingerprint of nonocclusive mesenteric ischemia

D’Ancona

Kische

İnce

2015

The Journal of Thoracic and Cardiovascular Surgery

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We commend the Saarland University Medical Centre group for its consistent effort in trying to identify the biological basis and the eventual biomarkers of nonocclusive mesenteric ischemia (NOMI) in patients undergoing cardiac surgery. 1 In fact, the present publication is just the last addition to a very well-defined scientific excursus the authors have developed in the last years. 2,3 It should be emphasized that despite the fact that NOMI carries a heavy burden of mortality, its existence stays poorly acknowledged, and, as an obvious consequence, NOMI often remains unrecognized and untreated.First, in the present study, 1 the authors report a 9% rate of NOMI, based on angiographic and clinical evaluation. This finding underlines the fact that in environments ''tuned up'' for diagnosis and treatment, NOMI occurrence is significantly high when compared with other morbidities often encountered in the perioperative phases of cardiac surgery. It is even more striking that when left untreated, NOMI has a mortality rate of more than 20%. As a consequence, misdiagnosis and mistreatment of this occurrence may increase to 2% the overall mortality rate after cardiac surgery on cardiopulmonary bypass. Per se, this is an important message to the readers.Second, we should reflect on the present tools available for NOMI diagnosis. Postoperative visceral angiography cannot be accepted, because of its invasiveness, as a standard for diagnosis. For this reason, in the near future, we should aim at ''less-invasive'' tools, including endothelin (ET)-1 sampling. In this context, we should review critically review the authors' findings. 1 Their receiver operating characteristic (ROC) analyses of preoperative ET-1 serum levels and the occurrence of NOMI revealed an optimal cutoff value of 11.7 pg/mL with a sensitivity of 44% and a specificity of 85%. ROC analyses of postoperative ET-1 serum levels showed an optimal cutoff value of 14.5 pg/mL with a sensitivity of 51% and a specificity of 94%. Such a test sensitivity implies that if we were to make our diagnosis just on the basis of ET-1 sampling, we would fail to correctly diagnose NOMI in at least 1 of 2 patients (false-negative). Of note, even in the authors' practice, 1 ''ET-1 is not presently used as a routine stratification tool due to the fact, that this is not a routine laboratory value and therefore cannot be provided in daily care.'' Third, although we understand that Groesdonk and colleagues 1 are scientifically trying to identify a specific and independent determinant for NOMI, some realistic caution should be advised. ET-1 could be just one of the many markers and mediators increasing after cardiopulmonary bypass and being involved in the ischemic-reperfusion cascade. In this context, the same group recently proposed that there is also an association between serum procalcitonin levels and NOMI. 4 In the same observational cohort study of 865 patients undergoing elective cardiac surgery, ROC analyses showed that elevated serum procalcitonin levels accurately predicted the...

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Endothelin and vasopressin influence splanchnic blood flow distribution during and after cardiopulmonary bypass

Abstract: Cardiopulmonary bypass leads to microvascular impairment of jejunal microcirculation, which is associated with the upregulation of endothelin-1 and endothelin subtype A. The administration of vasopressin minimizes these cardiopulmonary bypass-associated alterations.

Cited by 28 publications

References 25 publications

Vasopressin Aggravates Cardiopulmonary Bypass-Induced Gastric Mucosal Ischemia

Vasopressin Aggravates Cardiopulmonary Bypass-Induced Gastric Mucosal Ischemia

Feeding the Postoperative Patient on Vasopressor Support

Perioperative endothelin-1 levels: Searching for the hidden fingerprint of nonocclusive mesenteric ischemia

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