1992
DOI: 10.1007/bf01706478
|View full text |Cite
|
Sign up to set email alerts
|

Recurrent episodes of Gram-negative bacteremia or endotoxemia change reactivity of pre- and post-capillary pulmonary segments to Angiotensin or free radicals

Abstract: Abnormal lung vascular reactivity after SEPSIS or ENDOTOXIN is evident on challenge, the two agents used here detecting site specific changes.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1

Citation Types

0
3
0

Year Published

2000
2000
2021
2021

Publication Types

Select...
4

Relationship

0
4

Authors

Journals

citations
Cited by 4 publications
(3 citation statements)
references
References 22 publications
0
3
0
Order By: Relevance
“…Endotoxin is more likely to cause the spasm of small blood vessels, thereby causing microcirculation disorders. 29 The smaller urine output of patients with abdominal sepsis also indicated a poorer prognosis, which can be mutually confirmed by their higher ICU mortality rate.…”
Section: Discussionmentioning
confidence: 90%
“…Endotoxin is more likely to cause the spasm of small blood vessels, thereby causing microcirculation disorders. 29 The smaller urine output of patients with abdominal sepsis also indicated a poorer prognosis, which can be mutually confirmed by their higher ICU mortality rate.…”
Section: Discussionmentioning
confidence: 90%
“…To examine the effects of PDE5 inhibition in the absence and presence of inhaled NO in ALI, we studied pulmonary vasodilatory response patterns of zaprinast and sildenafil and their ability to improve responsiveness to inhaled NO isolated-perfused lungs from rats pre-treated with endotoxin. Prior studies have demonstrated that although rats are relatively resistant to endotoxin, administration of LPS produces interstitial and alveolar edema, thickening of lung microvascular walls, and leukocyte adherence and infiltration [21,22]. Although zaprinast and sildenafil showed different patterns of pulmonary vasodilation both augmented the response to inhaled NO.…”
Section: Figmentioning
confidence: 99%
“…In rabbit cardiac myocytes, angiotensin II and endotoxin have synergistic effects on the activation of nitric oxide and cyclic GMP pathways to induce dose-dependent impairment of contractile functions (42). In mice and rats, endotoxin also alters the vascular reactivity to angiotensin II (13,22), and the blood pressure response to exogenous angiotensin II is significantly diminished (4). It has been shown that angiotensin II type 1 receptor expression is markedly downregulated in septic rats, an effect that could be reproduced in vitro by administration of nitric oxide as well as by a combination of proinflammatory cytokines to rat renal mesangial cells (4).…”
Section: G253 Blood Flow Regulation: Dobutamine and Endotoxinmentioning
confidence: 99%