Effects of endotoxin on distribution of cardiac output in unanesthetized rabbits

Wyler, F; Jm, Neutze; Am, Rudolph

doi:10.1152/ajplegacy.1970.219.1.246

Cited by 49 publications

(10 citation statements)

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“…The regional vascular responses in the present experiments under prolonged moderate hypoxia are comparable to those seen after a reduced cardiac output from hemorrhage or endotoxic shock [11,14,24,31]. This is not surprising since the cardiovascular adjustments, i.e., the balance between enhanced adrenergic activity and local flow regulation, serve to divert blood predominately from the kidneys in order to provide a greater blood supply to the vital organs represented by the brain, the heart and possibly also by the skeletal muscle.…”

Section: Discussionsupporting

confidence: 74%

Effects of Hypoxia on Distribution of Cardiac Output and Organ Blood Flow in the Rabbit

Wyler¹

1975

Cardiology

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The hemodynamic responses of various vascular beds in the systemic circulation to prolonged moderate hypoxia were studied in the rabbit using the radioactive microsphere method. Although cardiac output remained unchanged, there was a redistribution of blood flow in which blood was mainly diverted from the kidneys to provide greater supply to heart, brain and skeletal muscle. These regional adjustments are similar to those seen after low cardiac output due to hemorrhage or endotoxic shock.

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Section: Discussionsupporting

confidence: 74%

Effects of Hypoxia on Distribution of Cardiac Output and Organ Blood Flow in the Rabbit

Wyler¹

1975

Cardiology

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“…Indeed, Wyler et al reported that a high-dose bolus injection of LPS produces a rapid cardiovascular collapse and early death. 17 Basically, a prolonged infusion of a low dose of bacteria limits the appearance of the cardiovascular collapse in small or large animals.…”

Section: Discussionmentioning

confidence: 99%

Validation of a Pseudomonas aeruginosa porcine model of septic shock

Rimmelé

Assadi

Benatir

et al. 2006

Journal of Infection

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“…The evidence from the present experiments suggests that the increased sympathetic discharge maintains myocardial contractility (increased dP/dt max at the same LVEDP) well into the shock period but that output is reduced because of the lowered venous return. Although there is some disagreement in the literature (see Introduction), some recent evidence appears to demonstrate that endotoxin does have a direct myocardial depressant effect (Solis & Downing, 1966;Wyler, Neutze & Rudolph, 1970). In vivo, this appears to be balanced by the effect of released catecholamines; if the myocardial effects of catecholamines are prevented by 8-adrenoceptor blockade, at least in the early stage of shock, myocardial contractility is not maintained and the animals die in right ventricular failure.…”

Section: Discussionmentioning

confidence: 99%

Myocardial and circulatory effects of E. coli endotoxin; modification of responses to catecholamines

Parratt

1973

British J Pharmacology

129

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Summary1. The predominant acute effect of E. coli endotoxin in anaesthetized, ventilated cats was pulmonary hypertension resulting from a 8-12 fold increase in pulmonary vascular resistance. This was followed by decreases in left ventricular (LV) and systemic arterial pressures and in LV dP/dt max. Recovery occurred within 2-4 min and was dependent upon increased sympathetic drive; recovery did not occur in cats treated with the f3-adrenoceptor blocking drug alprenolol. 2. The pulmonary vasoconstriction was reduced in cats given compound 48/80 and evidence is presented that it results primarily from histamine release. 3. Over the 2-3 h period following endotoxin injection, systemic arterial pressure tended to decrease and heart rate and myocardial metabolic heat production to increase. Myocardial blood flow and LV dP/dt remained fairly stable until the terminal stages of shock. 4. The predominant delayed effects of E. coli endotoxin in cats were a markedly reduced stroke volume, an increase in peripheral vascular resistance and a severe metabolic acidosis (arterial base excess-20 mEq/litre). Arterial pO2 and pCO2 were not significantly affected. It is concluded that myocardial contractility is maintained at this time through the release of catecholamines and that endotoxin itself depresses contractility. 5. The effects of adrenaline and noradrenaline infusions on systolic and diastolic blood pressures, heart rate, cardiac output, myocardial blood flow and LV dP/dt max were markedly reduced in the period 2-3 h after endotoxin. In a few animals some recovery of the response to noradrenaline occurred and was associated with a general circulatory improvement and a reduced metabolic acidosis.

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Effects of endotoxin on distribution of cardiac output in unanesthetized rabbits

Cited by 49 publications

References 0 publications

Effects of Hypoxia on Distribution of Cardiac Output and Organ Blood Flow in the Rabbit

Effects of Hypoxia on Distribution of Cardiac Output and Organ Blood Flow in the Rabbit

Validation of a Pseudomonas aeruginosa porcine model of septic shock

Myocardial and circulatory effects of E. coli endotoxin; modification of responses to catecholamines

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