Blockade of Sympathetic Vasoconstriction in the Treatment of Shock

Nickerson, Mark; Gourzis, James T.

doi:10.1097/00005373-196207000-00008

Cited by 52 publications

(9 citation statements)

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“…There appears to be no reason to assume that reduced lactacidemia in these animals was related to the absence of sympathetically mediated va soconstriction [15] since phenoxybenzamine-premedication fails to affect shock-induced lactacidosis [10]. The present experiments corroborate previous observations suggesting that lactic acidosis in shock is related to the metabolic consequences of sympathetic overactivity [10].…”

Section: Effect Of Hemorrhage On Bretylium-medicated Sheepsupporting

confidence: 84%

“…

Hemorrhagic hypotension is a powerful stimulus to sympathetic activi ty and the resulting excessive norepinephrine (NE) secretion is considered to account for the tissue injury that supposedly underlines the progressive failure of the circulation despite restoration of the blood volume [3,15,20]. Since, surprisingly, no previous attempt was made to assess the effect of selective suppression of NE production in shock, we premedicated our bled animals with bretylium tosylate, an agent known to block selectively NE release [1],

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mentioning

confidence: 99%

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Course of Hemorrhagic Shock After Blockade of Norepinephrine Release

Halmagyi¹,

Neering²,

Varga³

1970

Eur Surg Res

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Section: Effect Of Hemorrhage On Bretylium-medicated Sheepsupporting

confidence: 84%

“…

Methods

…”

mentioning

confidence: 99%

Course of Hemorrhagic Shock After Blockade of Norepinephrine Release

Halmagyi¹,

Neering²,

Varga³

1970

Eur Surg Res

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“…This would indicate that drugs which increase tissue perfusion (providing myocardial contractility is maintained), for example a-adrenoceptor blocking agents, might improve survival in endotoxic shock. There is some evidence that this is indeed so (Longerbeam, Liilehei, Scott & Rosenberg, 1962;Nickerson & Gourzis, 1962;Phillips & Vick, 1971).…”

Section: Discussionmentioning

confidence: 98%

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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“…The increase in venous resistance and rise in small vein pressure which occur also during adrenergic stimulation may be detrimental because they increase capillary filtration, reduce intravascular volume, and increase hematocrit (2)(3)(4)(5). In certain vascular beds (6,7) and particularly in hemorrhagic or endotoxin shock (8,9) venous constriction may be relatively greater than arteriolar constriction during adrenergic stimulation.…”

Section: Introductionmentioning

confidence: 99%

Vascular responses after alpha adrenergic receptor blockade

Abboud

Schmid²,

Eckstein³

1968

J. Clin. Invest.

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A B S T R A C T Experiments were done to test the hypothesis that alpha receptor blockers antagonize more effectively venous than arterial responses to norepinephrine in man.Systemic arterial blood pressure, venous pressure in the forearm, blood flow through the forearm, and the volume of the forearm at a venous pressure of 30 mm Hg were measured using pressure transducers and a mercury strain-gauge plethysmograph. Infusions of norepinephrine into the brachial artery reduced forearm blood flow and venous distensibility without changing arterial pressure. After intraarterial infusion of phentolamine the decrease in venous distensibility during administration of norepinephrine was blocked almost completely whereas the decrease in blood flow through the forearm was not altered.The results indicate that alpha adrenergic receptor blockade can antagonize constriction of capacitance vessels more effectively than constriction of resistance vessels.

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Blockade of Sympathetic Vasoconstriction in the Treatment of Shock

Cited by 52 publications

References 0 publications

Course of Hemorrhagic Shock After Blockade of Norepinephrine Release

Course of Hemorrhagic Shock After Blockade of Norepinephrine Release

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

Vascular responses after alpha adrenergic receptor blockade

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