Drug therapy of shock

Nickerson, Mark

doi:10.1007/978-3-662-22403-8_30

Cited by 20 publications

(24 citation statements)

References 34 publications

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confidence: 99%

The Origin of the Decline in the Vasopressor Response to Infused Noradrenaline in the Pithed Rat

Gillespie¹,

Muir²

1967

British Journal of Pharmacology and Chemotherapy

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In several species, including man, the continuous infusion of noradrenaline always results in an eventual steady decline from the initial pressor level (Nickerson, 1962;Rosenthale & Dipalma, 1963;Beyth & Gutman, 1965). This reduction in response is usually attributed to desensitization or tachyphylaxis. Our interest in this phenomenon arose during attempts to modify that preparation of the anaesthetized rat described by Straughan (1958) as an assay method for acetylcholine. To overcome the large reflex depressor artefact which accompanies any intravenous injection in this preparation, the rat was pithed and the normal neurally maintained vascular tone mimicked by infusing noradrenaline continuously in amounts sufficient to raise the blood pressure to about 120 mm Hg. A highly sensitive and artefact-free preparation in which the effect of 0.25 ng of acetylcholine could be recognized was obtained. However, within 5 10 min of beginning the infusion both the blood pressure and the sensitivity to acetylcholine began to fall. Two points seemed of interest. First, if this were due to desensitization to noradrenaline, it was not specific for one substance. Secondly, although the noradrenaline infused was limited to that required to match the neurally released transmitter in restoring the blood pressure to normal levels, desensitization still occurred. Previous investigations of this phenomenon have employed animals with an intact vasoconstrictor outflow in which the infused noradrenaline raised the blood pressure above normal.The present paper reports the results of an investigation into the causes of these changes. The literature contains few reports which allow the contribution of the peripheral vascular smooth muscle to the fall in blood pressure to be separated from that of the heart. To do this, a modification of the technique of Bygdeman (1963) was used, in which the isolated vascular bed of one lower limb was perfused in situ with the animal's own arterial blood. The perfusion pressure gave a measure of the response of the vascular smooth muscle uncomplicated by cardiac efficiency. The blood pressure response of the whole animal, excluding the perfused limb, gave an integrated picture of both the peripheral vascular response and the ability of the heart to maintain its output in face of any increase in peripheral resistance. * Henry Head Fellow.

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The Origin of the Decline in the Vasopressor Response to Infused Noradrenaline in the Pithed Rat

Gillespie¹,

Muir²

1967

British Journal of Pharmacology and Chemotherapy

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“…Using rat pleural polymorphonuclear leukocytes as a model , we found that inhibition of arachidonic acid metabolism was observed only when atropine, anisodamine and scopolamine were used at millimolar concentrations and the incubation period was extended to 30 min (unpublished data). In comparison, aladrenoceptor blockade was exerted by micromolar concentrations ofanisodamine, which can be clinically achieved and, like other adrenoceptor antagonists (Nickerson, 1962), be effective in maintaining the competence of microcirculation. On the other hand, anisodine is far too weak as an adrenoceptor antagonist for it to be likely that this property makes an important contribution to its clinical usefulness in shock.…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, atropine-like agents have long been known to possess adrenergic antagonistic properties (Bussell, 1940;Burn & Dutta, 1948;Fleckenstein, 1952;Furchgott, 1955); recent studies have confirmed these observations and characterized these agents as specific xl-adrenoceptor antagonists (Abraham et al, 1981;Cantor et al, 1983). a-Adrenoceptor antagonism can be beneficial in circulatory shock (Nickerson, 1962). However, whether or not anisodamine and anisodine possess adrenergic inhibiting activities is not known.…”

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Adrenoceptor blocking properties of atropine‐like agents anisodamine and anisodine on brain and cardiovascular tissues of rats

Varma

Yue

1986

British J Pharmacology

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1 The cholinoceptor antagonists anisodamine and anisodine are widely used in the People's Republic of China for the management of acute circulatory shock but the mechanism of their beneficial effects is not fully known; we therefore investigated if these agents possessed adrenoceptor blocking properties. 2 The antagonistic effect of anisodamine and anisodine against the specific binding of the a,-adrenoceptor ligand [3H]-WB-4101 to cardiac and brain tissue membrane preparations and against the effects of phenylephrine on isolated aortic strips and left atria of rats were compared with classical muscarinic receptor and adrenoceptor blocking agents. 3 Both anisodamine and anisodine possessed a,-adrenoceptor blocking properties; the order of potency of various agents in displacing the binding of [3H1-WB-4101 to receptors and in antagonizing the effects of phenylephrine on aortic strips and left atria was: prazosin > atropine > anisodamine > scopolamine > anisodine. 4 It is concluded that both anisodamine and to a lesser extent anisodine possess a,-adrenoceptor blocking properties; this antagonistic activity of anisodamine may contribute to its salutary effects on the microcirculation. However, it is unlikely that anisodine produces a significant adrenoceptor blockade in the clinically used dose-range.

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“…Significant increases in the survival rate of animals subjected to various types of shock have been demonstrated and discussed using many different drugs and procedures to induce vasodilation (12). For example, dibenzyline, which is an adrenergic blocking agant, was found to prevent death of animals in a state of shock.…”

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confidence: 99%

Effect of Dopa on the Catecholamine Content of Dog Heart After Hemorrhagic Hypotension

Hashimoto

Lydtin

1965

Japanese Journal of Pharmacology

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It has been noted that there is evidence of myocardial failure following the reinfusion of blood into animals after hemorrhagic hypotension (1-3). Glaviano and Coleman have shown in rabbits that the norepinephrine content of the left ventricle was markedly decreased and its epinephrine content increased after hemorrhagic hypotension. They suggested that myocardial failure after hemorrhagic hypotension could be due to norepinephrine depletion in the heart (4). Gomerz and Hamilton (5, 6) were unable to show cardiac failure immediately after the hypotensive period, but 40 to 120 minutes later the heart showed signs of damage if the blood pressure was kept at a normotensive level. Therefore, it seemed advisable to investigate the successive changes in the catecholamine content of the heart after subjection to hemorrhagic hypotension and also to study the effect of DOPA infusion on the myocardial catecholamine content after hemorrhagic hypotension.It is well known that there is a marked increase in the release of epinephrine and norepinephrine from the sympathoadrenal system during hemorrhagic hypotension (7-9). This may play an important role in producing vasoconstriction, causing irreversible tissue damage and then deterioration of cardiac efficiency (10, 11). Therefore, it is understandable that adrenergic blocking agents protect animals from the fatal outcome caused by hemorrhagic hypotension.The present experiments were also designed to determine if pretreatment with dibenzyline had an effect on myocardial catecholamine synthesis and/or storage in the heart after hemorrhagic hypotension, and further if this compound protected the tissues from damages in shock. METHODSFifty-two mongrel dogs of both sexes, weighing 13 to 20 kg, were used. They were anesthetized with 5 mg/kg morphine followed by 20 mg/kg sodium pentobarbital. The right femoral artery and vein were canulated for bleeding and retransfusion. Pressures Present address :

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Drug therapy of shock

Cited by 20 publications

References 34 publications

The Origin of the Decline in the Vasopressor Response to Infused Noradrenaline in the Pithed Rat

The Origin of the Decline in the Vasopressor Response to Infused Noradrenaline in the Pithed Rat

Adrenoceptor blocking properties of atropine‐like agents anisodamine and anisodine on brain and cardiovascular tissues of rats

Effect of Dopa on the Catecholamine Content of Dog Heart After Hemorrhagic Hypotension

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