Endotoxin-induced alterations in contractility of isolated blood vessels from sheep

Nelson, Sharon H.; Steward, Roberta; Traber, L. D.; Traber, Daniel L.

doi:10.1152/ajpheart.1991.260.6.h1790

Cited by 12 publications

(15 citation statements)

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“…This difference could lead to hypocontractile response to histamine in mesenteric but not in pulmonary arteries. Our findings may provide a basis for the results of past investigations that iNOS induction-associated vascular hypocontractility was not observed in the pulmonary circulation (Nelson et al, 1991;Suba et al, 1992;Spath et al, 1994;Fullerton et al, 1995) despite the presence of iNOS mRNA in pulmonary vessels in vivo LPS (Griffiths et al, 1995).…”

Section: Vascular Hyporesponsiveness To Vasocontractile Stimulisupporting

confidence: 75%

Vascular biology in sepsis: pathophysiological and therapeutic significance of vascular dysfunction

Matsuda

Hattori

2007

J Smooth Muscle Res

116

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Sepsis is the leading cause of mortality in critically ill patients. In this pathological syndrome, septic shock and sequential multiple organ failure correlate with poor outcome. The pathophysiology of sepsis with acute organ dysfunction involves a highly complex, integrated response that includes activation of number of cell types, inflammatory mediators, and the hemostatic system. Central to this process may be alterations in vascular functions. This review article provides a growing body of evidence for the potential impact of vascular dysfunction on sepsis pathophysiology with a major emphasis on the endothelium. Furthermore, the role of apoptotic signaling molecules in the mechanisms underlying endothelial cell injury and death during sepsis and its potential value as a target for sepsis therapy will be discussed, which may help in the assessment of ongoing therapeutic strategies.

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Section: Vascular Hyporesponsiveness To Vasocontractile Stimulisupporting

confidence: 75%

Vascular biology in sepsis: pathophysiological and therapeutic significance of vascular dysfunction

Matsuda

Hattori

2007

J Smooth Muscle Res

116

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“…Our results suggest that in vivo treatment with LPS leads to iNOS upregulation and vascular hypocontractility in mesenteric but less in pulmonary vessels. This finding may provide a basis for the results of past investigations that iNOS inductionassociated vascular hypocontractility was not observed in the pulmonary circulation (Nelson et al, 1991;Suba et al, 1992;Spath et al, 1994;Fullerton et al, 1995) despite the presence of iNOS mRNA in pulmonary vessels after in vivo LPS (Griffiths et al, 1995).…”

Section: Discussionsupporting

confidence: 64%

Contractions to Histamine in Pulmonary and Mesenteric Arteries from Endotoxemic Rabbits: Modulation by Vascular Expressions of Inducible Nitric-Oxide Synthase and Histamine H₁-Receptors

Matsuda¹,

Hattori²,

Zhang³

et al. 2003

J Pharmacol Exp Ther

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The inducible isoform of nitric-oxide synthase (iNOS) is highly expressed after induction of endotoxemia and contributes to vascular hypocontractility in endotoxemia. Circulating levels of histamine are elevated in animal models of sepsis and in patients with septic shock. This study assessed whether the vascular effects of histamine play a significant role in the pathophysiology of endotoxemic shock despite the hyporesponsiveness to vasoconstrictors associated with iNOS up-regulation. Rabbits were rendered endotoxemic by lipopolysaccharide (LPS; 100 g/kg, i.v.). In mesenteric arteries taken from animals at 6 h of LPS administration, the contractile response to histamine was significantly impaired but histamine-evoked contractions in pulmonary arteries were unchanged. Western blot revealed a drastic increase in iNOS expression in mesenteric vessels after LPS, but endotoxin-induced iNOS increase was not so marked in pulmonary vessels. On the other hand, expression of endothelial nitric-oxide synthase was suppressed under LPS challenge in both types of vessels. In the presence of N G -nitro-L-arginine or (S)-ethylisothiourea used for iNOS inhibition, histamine-evoked contractions of endotoxemic pulmonary and mesenteric vessels were significantly enhanced. This was possibly associated with a dramatic increase in H 1 -receptor expression at the gene and protein levels, as determined by Northern blot and immunoblot analyses. Furthermore, we found that LPS-induced endotoxemia caused prominent increases in production of histamine through induction of histidine decarboxylase in tissues, including blood vessels. From these results, we propose that histamine may contribute to the development of endotoxin-induced pulmonary hypertension.

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“…However, the dose of NA needed to achieve the desired increase in MAP was significantly higher in the septic phase (see Figure 2). These results are in accordance with in vitro experiments using isolated vessel rings harvested from healthy and septic sheep [13]. In a previous investigation, we found fading vasoconstrictive properties when NA was given continuously during a prolonged course of sepsis (48 h) [7].…”

Section: Discussionsupporting

confidence: 91%

Noradrenaline and Nω-monomethyl-L-arginine (L-NMMA): effects on haemodynamics and regional blood flow in healthy and septic sheep

et al. 2000

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This prospective, non-randomized, controlled experimental study looks at the effects of N(omega)-monomethyl-L-arginine (L-NMMA) on haemodynamics, oxygen transport and regional blood flow in healthy and septic sheep, and compares these effects with those of noradrenaline (NA; norepinephrine). All sheep were chronically instrumented. Six sheep received L-NMMA (7 mg.kg(-1).h(-1)), six sheep received NA, and seven sheep received the carrier alone (0.9% NaCl). The NA dosage was continuously and individually adjusted to achieve the same increase in blood pressure as observed in matched sheep of the L-NMMA group (non-septic phase). Treatment was discontinued after 3 h. Sepsis was initiated and maintained by a continuous infusion of live Pseudomonas aeruginosa. After 24 h of sepsis, the sheep were again challenged over a treatment period of 3 h with their previously assigned drug (septic phase). During the non-septic phase of the experiment, NA and L-NMMA both caused an increase in mean arterial pressure (MAP) through vasoconstriction. Ater 24 h of sepsis, all sheep developed a hyperdynamic circulatory state. While L-NMMA caused an increase in MAP through intense vasoconstriction, NA caused MAP to increase through a further elevation of the cardiac index. The NA dosage needed was significantly higher in the septic phase compared with the non-septic phase, reflecting a reduced vascular responsiveness to catecholamines during sepsis. Renal blood flow remained unchanged during either treatment in both the non-septic and the septic phases. Nevertheless, urine output increased during NA treatment in both the non-septic and the septic phases, while L-NMMA caused urine output to increase only under septic conditions.

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Endotoxin-induced alterations in contractility of isolated blood vessels from sheep

Cited by 12 publications

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Vascular biology in sepsis: pathophysiological and therapeutic significance of vascular dysfunction

Vascular biology in sepsis: pathophysiological and therapeutic significance of vascular dysfunction

Contractions to Histamine in Pulmonary and Mesenteric Arteries from Endotoxemic Rabbits: Modulation by Vascular Expressions of Inducible Nitric-Oxide Synthase and Histamine H₁-Receptors

Noradrenaline and Nω-monomethyl-L-arginine (L-NMMA): effects on haemodynamics and regional blood flow in healthy and septic sheep

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Endotoxin-induced alterations in contractility of isolated blood vessels from sheep

Cited by 12 publications

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Vascular biology in sepsis: pathophysiological and therapeutic significance of vascular dysfunction

Vascular biology in sepsis: pathophysiological and therapeutic significance of vascular dysfunction

Contractions to Histamine in Pulmonary and Mesenteric Arteries from Endotoxemic Rabbits: Modulation by Vascular Expressions of Inducible Nitric-Oxide Synthase and Histamine H1-Receptors

Noradrenaline and Nω-monomethyl-L-arginine (L-NMMA): effects on haemodynamics and regional blood flow in healthy and septic sheep

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Contractions to Histamine in Pulmonary and Mesenteric Arteries from Endotoxemic Rabbits: Modulation by Vascular Expressions of Inducible Nitric-Oxide Synthase and Histamine H₁-Receptors