Role of Muscle Microvasculature during Hyperdynamic and Hypodynamic Phases of Endotoxin Shock in Decerebrate Rats

Hm, Cryer; Rn, Garrison; Pd, Harris

doi:10.1097/00005373-198803000-00006

Cited by 21 publications

(18 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, our recent study in skeletal muscle provided evidence against edema as the cause (38). Despite the changes in arteriolar diameter and reactivity shown by Cryer and co-workers (10,11), it is important to note that our observed loss of functional capillaries appeared to involve individual capillaries. Thus, random individual capillaries seemed to be affected as opposed to a bed of capillaries related to a single arteriole or venule.…”

Section: Methodscontrasting

confidence: 65%

“…Previous studies, which have used in vivo microscopy techniques to study changes in the microcirculation with sepsis, have examined the arterioles and venules rather than the capillaries which are the primary exchange vessels for waste products and metabolites, including oxygen. For example, Cryer and co-workers (10,11 ) have shown that during the hyperdynamic state after an acute infusion of either live Escherichia coli bacteria or endotoxin, first and second order arterioles constrict, while third and fourth order arterioles dilate and venular diameters remain unchanged. Baker and co-workers (12,13) reported that infusing endotoxin restricts red blood cell (RBC) flow by causing arteriolar constriction and increased RBC transit time relative to plasma transit time.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Microvascular perfusion is impaired in a rat model of normotensive sepsis.

Lam¹,

Tyml²,

Martin³

et al. 1994

J. Clin. Invest.

334

208

View full text Add to dashboard Cite

We hypothesized that normotensive sepsis affects the ability of the microcirculation to appropriately regulate microregional red blood cell (RBC) flux. An extensor digitorum longus muscle preparation for intravital study was used to compare the distribution of RBC flux and the functional hyperemic response in SHAM rats and rats made septic by cecal ligation and perforation (CLP). Using intravital microscopy, we found that sepsis was associated with a 36% reduction in perfused capillary density (from 35.3±+1.5 to 22.5±1.0 capillaries/mm of test line) and a 265% increase in stopped-flow capillaries (from 0.9±0.2 to 3.3±0.4 capillaries/mm); the spatial distribution of perfused capillaries was also 72% more heterogeneous. Mean intercapillary distance (ICD) increased 30% (from 25.7±0.8 to 33.5±1.6 ,um), and the proportion of capillary pairs with intercapillary distances > 33.8 ,um (the 75th percentile of ICDsHAM) was greater with sepsis. Mean capillary RBC velocity increased 17% in CLP rats (391 vs 333 ,um/s). Laser Doppler flowmetry was used to assess the functional hyperemic response of the extensor digitorum longus muscle before and after a period of maximal twitch contraction designed to increase oxygen demand. RBC flux was 36% lower in the CLP rats at rest. After contraction, RBC flux increased in both SHAM and CLP rats; however, the relative increase was less in the CLP group. We concluded that sepsis affects the ability of the skeletal muscle microcirculation to appropriately distribute RBC flux and to respond to increases in oxygen need. (J. Clin. Invest. 1994. 94

show abstract

Section: Methodscontrasting

confidence: 65%

Section: Introductionmentioning

confidence: 99%

Microvascular perfusion is impaired in a rat model of normotensive sepsis.

Lam¹,

Tyml²,

Martin³

et al. 1994

J. Clin. Invest.

334

208

View full text Add to dashboard Cite

show abstract

“…Recently, Cryer et al (9,10) found that during septic shock in the rat, large arterioles constricted and small terminal arterioles dilated. These studies showed that changes in the microvascular network might be responsible for some of the hemodynamic alterations found in sepsis, but did not provide any information about the potential role of TNF in these morphological alterations.…”

Section: Resultsmentioning

confidence: 99%

“…An important aspect of these hemodynamic disorders concerns the changes occurring in the microcirculatory network, where several mechanisms of pressure regulation are located. Recent studies have shown that septic shock induced by endotoxin or E. coli may affect arteriolar diameter by constricting large arterioles and dilating small terminal arterioles (9,10). However, it is not known whether TNF is involved in these morphological alterations of the microcirculatory network.…”

Section: Introductionmentioning

confidence: 99%

Acute effects of tumor necrosis factor on the microcirculation in rat cremaster muscle.

Vicaut

Hou²,

Payen³

et al. 1991

J. Clin. Invest.

View full text Add to dashboard Cite

The acute effects of TNF on the microcirculation were studied by in vivo microscopy in rat cremaster muscle. The changes in arteriolar diameter after topical administration of recombinant TNF (rTNF; i0-O-104 ng/ml) were studied in second-, third-, and fourth-order arterioles (A2-A4) whose mean diameters under control conditions were 64.3, 30.7, and 14.8 ,um, respectively. rTNF induced a concentration-dependent vasodilation whose amplitude was largest for the smallest arterioles. At the highest concentration tested, arteriolar diameter increased by 21, 29, and 41% of control diameter for the A2, A3, and A4 arterioles, respectively. Indomethacin or mefenamic acid, two structurally different prostaglandin synthesis inhibitors, markedly inhibited the degree of vasodilation induced by rTNF in the three arteriolar orders. As regards the effect of rTNF on vasoconstriction in response to norepinephrine, vasoconstriction was greatest for the smallest arterioles, and did not change 10 min after rTNF administration for any ofthe three arteriolar orders. We conclude that (a) rTNF has a direct vasodilatory effect which is greatest in the smallest arterioles, (b) this vasodilation is at least partly mediated by prostaglandins, and (c) administration of rTNF in itself does not acutely alter the response of the arterioles to vasopressive drugs. (J. Clin. Invest.

show abstract

“…Ce phénomène contribue à l'altération de la microvascularisation des villosités intestinales [7]. Cependant, au niveau des muscles crémastériens [8] et du diaphragme [9], la réponse artériolaire aux sepsis est diff érente en fonction de la taille des vaisseaux : les artérioles de gros diamètres se vasoconstrictent alors que les artérioles de petit diamètre se vasodilatent. Au niveau de la micro vascularisation hépatique, on observe une vasodilatation des deux tiers des sinusoïdes périportales et centrolobulaires, et des veinules centrales et portales, alors que la microcirculation restante est en état de vasoconstriction [10].…”

Section: La Micro Vascularisation : Système Fonctionnel De Distributiunclassified