Cardiac output in bacterial shock

Weil, Max Harry; Nishijima, Hirotaka

doi:10.1016/0002-9343(78)90444-8

Cited by 86 publications

(23 citation statements)

References 15 publications

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“…It is widely accepted that low systemic vascular resistance and increased cardiac output (CO) are observed during septic shock (hyperdynamic state) [11]. However, in the present study, fluid replacement was moderate (20 ml·kg -1 ·h -1 ) and this resulted in a hypodynamic model during continuous infusion of endotoxin via the portal vein.…”

Section: Discussionmentioning

confidence: 57%

Effects of olprinone on hepatosplanchnic circulation and mitochondrial oxidation in a porcine model of endotoxemia

et al. 2005

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Section: Discussionmentioning

confidence: 57%

Effects of olprinone on hepatosplanchnic circulation and mitochondrial oxidation in a porcine model of endotoxemia

et al. 2005

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“…Animals with intact prostaglandin synthesis had a 25% fall in MAP (126-94 mm Hg), which was completely abolished by prior treatment with indomethacin or meclofenemate. One important factor in the hypotension following endotoxin was the reduction in CO, an observation noted in previous studies (1,(35)(36)(37)(38). However, the similar depression of cardiac function in groups I and II yet maintenance of MAP in group II indicates that another factor was operant.…”

Section: Discussionmentioning

confidence: 72%

Dissociation of systemic and renal effects in endotoxemia. Prostaglandin inhibition uncovers an important role of renal nerves.

Henrich¹,

Hamasaki²,

Said³

et al. 1982

J. Clin. Invest.

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A B S T R A C T To elucidate the mechanisms responsible for systemic and renal hemodynamic changes in early endotoxemia, the roles of prostaglandins (PG) and renal nerves were investigated. Endotoxin (E, 3 ag/kg i.v.) was given to two groups of anesthetized dogs that had undergone unilateral renal denervation: Group I (n = 9) E only; Group II (n = 11) E + indomethacin (10 mg/kg i.v.) or meclofenamate (5 mg/kg i.v.). A third group of dogs (Group III, n = 5) received indomethacin (10 mg/kg i.v.) only. 1 h after E in group I dogs, mean arterial pressure (MAP) decreased from 126 to 94 mm Hg (P < 0.001), and prostacyclin (6-keto-Fla metabolite, PGI2) increased (from 0.64 to 2.08 ng/ml, P < 0.005). Glomerular filtration rate (GFR) and renal blood flow (RBF) declined comparably both in innervated and denervated kidneys. In marked contrast, group II dogs had a stable MAP (136-144 mm Hg, NS) and no increase in PGI2 levels. Plasma renin activity (0.7-2.5 ng/ml per h, P < 0.005) increased, and renin secretion was greater in innervated compared with denervated kidneys (255 vs. 74 U/min, P < 0.01) in these PG-inhibited dogs. In addition, denervated kidneys in group II dogs had a greater GFR (42 vs. 34 ml/min, P < 0.01) and RBF (241 vs. 182 ml/min, P < 0.01) than innervated kid- renin activity or PGI2 during the study. These results suggest that PGI2 mediates the systemic hypotension of early endotoxemia in the PG-intact animal. Moreover, PG inhibition uncovers an important effect of E to increase efferent renal nerve activity with a consequent decline in GFR and RBF independent of changes in MAP. Finally, the results demonstrate that renal nerves are important stimuli to renin secretion in early endotoxemia via pathways that are PG-independent.

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“…The hyperdynamic circulation may be further accentuated by a further decrease in R V related to hemodilution and decreased blood viscosity (not shown in figure). This classical hyperdynamic (high CO/low SVR) hemodynamic picture of established septic shock typically does not manifest without fluid resuscitation (39)(40)(41)(42). However, even a modest degree of fluid resuscitation may be sufficient to allow the permissive effects of the decreased R v to be expressed as increased CO.…”

Section: Distributive Shockmentioning

confidence: 99%