The Pathogenesis of Vasodilatory Shock

Landry, Donald W.; Oliver, Juan A.

doi:10.1056/nejmra002709

Cited by 959 publications

(727 citation statements)

References 73 publications

Supporting

Mentioning

666

Contrasting

Unclassified

Order By: Relevance

“…Vasopressin (Table 3) depletion is believed to play a causative role in sepsis-induced vasodilatory shock [47]. In a mixed population with catecholamine-resistant vasodilatory shock, additional low-dose arginine vasopressin (AVP) was associated with an increment of pCO 2 g-a over time, but lower than NE alone [48].…”

Section: Vasopressorsmentioning

confidence: 99%

The role of vasoactive agents in the resuscitation of microvascular perfusion and tissue oxygenation in critically ill patients

Boerma

İnce

2012

Applied Physiology in Intensive Care Medicine 2

View full text Add to dashboard Cite

show abstract

Section: Vasopressorsmentioning

confidence: 99%

The role of vasoactive agents in the resuscitation of microvascular perfusion and tissue oxygenation in critically ill patients

Boerma

İnce

2012

Applied Physiology in Intensive Care Medicine 2

View full text Add to dashboard Cite

show abstract

“…The endothelium was removed by gently rubbing the intimal surface with a sterile cotton pad. Approximately 3Â3-mm sections were placed with the intimal side down into 28-cm 2 Petri dishes. Dulbecco's Modified Eagle's Medium (DMEM) containing fetal bovine serum (10%), penicillin (100 U ml À1 ), streptomycin (100 mg ml À1 ) and amphotericin-B (250 ng ml À1 , all from Life Technologies, Ta Èby, Sweden) was added to cover the tissue without disturbing the orientation of the explants.…”

Section: Cell Culturementioning

confidence: 99%

“…Lipopolysaccharide induce dilation of the blood vessels, which contributes to the hypotension during septic shock (2). This dilation is in part the result of an LPS-induced increase of the production of nitric oxide (NO) in the blood vessel wall, which relaxes the vascular smooth muscle cells (3).…”

mentioning

confidence: 99%

Effects of human cathelicidin antimicrobial peptide LL‐37 on lipopolysaccharide‐induced nitric oxide release from rat aorta in vitro

Ciornei

Egesten

Bodelsson

2003

Acta Anaesthesiol Scand

View full text Add to dashboard Cite

Background: Lipopolysaccharides (LPS), released by Gram‐negative bacteria, cause vascular expression of inducible nitric oxide synthase (iNOS) leading to nitric oxide (NO) production and septic shock. Human cathelicidin antimicrobial peptide (LL‐37) can bind and neutralize LPS. We wanted to study whether LL‐37 affects LPS or interleukin‐1β (IL‐1β)‐induced production, release and function of NO in intact rat aorta rings and cultured rat aorta smooth muscle cells.Methods: Isolated segments of thoracic aorta and cultured cells were incubated in the presence of LPS, LL‐37, LPS + IL‐37, IL‐1β, IL‐1β + IL‐37 or in medium alone. Smooth muscle contraction in response to phenylephrine and accumulation of the sdegradation products of NO, nitrate and nitrite, were measured on aorta segments. Levels of iNOS were assessed by Western blot and cytotoxic effects were detected by measurement of DNA fragmentation in cultured cells. Number of viable cells were determined after Trypan blue treatment.Results: Both LPS and IL‐1β reduced contractility in response to phenylephrine and increased NO production as well as iNOS expression. LL‐37 inhibited the LPS depression of vascular contractility induced only by LPS. LL‐37 reduced both the LPS‐ and IL‐1β‐induced NO production and iNOS expression. LL‐37 at high concentrations induced DNA fragmentation and decreased the number of living cells.Conclusion: IL‐37 reduces NO production induced by LPS and IL‐1β. The reduction does not seem to result only from neutralization of LPS but also from a cytotoxic effect, possibly via induction of apoptosis.

show abstract

“…In septic shock, despite appropriate fluid resuscitation and noradrenaline administration, the following factors can create difficulty in maintaining hemodynamics: (i) difficulty in controlling peripheral vascular resistance accompanying vasodilatation (relative hypovolemic shock)119 and (ii) cardiac dysfunction associated with SIMD (cardiogenic shock) 113, 114. These pathologies can be distinguished relatively easily through echocardiography.…”

Section: Introductionmentioning

confidence: 99%

The Japanese Clinical Practice Guidelines for Management of Sepsis and Septic Shock 2016 (J‐SSCG 2016)

Nishida

Ogura

Egi

et al. 2018

Acute Medicine & Surgery

157

View full text Add to dashboard Cite

Background and PurposeThe Japanese Clinical Practice Guidelines for Management of Sepsis and Septic Shock 2016 (J‐SSCG 2016), a Japanese‐specific set of clinical practice guidelines for sepsis and septic shock created jointly by the Japanese Society of Intensive Care Medicine and the Japanese Association for Acute Medicine, was first released in February 2017 in Japanese. An English‐language version of these guidelines was created based on the contents of the original Japanese‐language version.MethodsMembers of the Japanese Society of Intensive Care Medicine and the Japanese Association for Acute Medicine were selected and organized into 19 committee members and 52 working group members. The guidelines were prepared in accordance with the Medical Information Network Distribution Service (Minds) creation procedures. The Academic Guidelines Promotion Team was organized to oversee and provide academic support to the respective activities allocated to each Guideline Creation Team. To improve quality assurance and workflow transparency, a mutual peer review system was established, and discussions within each team were open to the public. Public comments were collected once after the initial formulation of a clinical question (CQ), and twice during the review of the final draft. Recommendations were determined to have been adopted after obtaining support from a two‐thirds (>66.6%) majority vote of each of the 19 committee members.ResultsA total of 87 CQs were selected among 19 clinical areas, including pediatric topics and several other important areas not covered in the first edition of the Japanese guidelines (J‐SSCG 2012). The approval rate obtained through committee voting, in addition to ratings of the strengths of the recommendation and its supporting evidence were also added to each recommendation statement. We conducted meta‐analyses for 29 CQs. Thirty seven CQs contained recommendations in the form of an expert consensus due to insufficient evidence. No recommendations were provided for 5 CQs.ConclusionsBased on the evidence gathered, we were able to formulate Japanese‐specific clinical practice guidelines that are tailored to the Japanese context in a highly transparent manner. These guidelines can easily be used not only by specialists, but also by non‐specialists, general clinicians, nurses, pharmacists, clinical engineers, and other healthcare professionals.

show abstract

The Pathogenesis of Vasodilatory Shock

Cited by 959 publications

References 73 publications

The role of vasoactive agents in the resuscitation of microvascular perfusion and tissue oxygenation in critically ill patients

The role of vasoactive agents in the resuscitation of microvascular perfusion and tissue oxygenation in critically ill patients

Effects of human cathelicidin antimicrobial peptide LL‐37 on lipopolysaccharide‐induced nitric oxide release from rat aorta in vitro

The Japanese Clinical Practice Guidelines for Management of Sepsis and Septic Shock 2016 (J‐SSCG 2016)

Contact Info

Product

Resources

About