196 Transplant Kidney Outcomes in Patients with Thrombotic Microangiopathy, Switched to Co-Stimulation Blocking Agent (Belatacept)

Key Points The use of terminal complement blockade is compatible with virus-specific T-cell (VST) expansion and clinical effectiveness. VST and complement-blocking agent concurrent therapy may be safely used in patients with thrombotic microangiopathy and viral infections.

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The hemolytic uremic syndrome. Renal cortical thrombotic microangiopathy

Archives of Internal Medicine ◽

10.1001/archinte.126.5.816 ◽

1970 ◽

Vol 126 (5) ◽

pp. 816-822 ◽

Cited By ~ 6

Author(s):

D. Hammond

Keyword(s):

Hemolytic Uremic Syndrome ◽

Thrombotic Microangiopathy ◽

Uremic Syndrome

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Blood will find its way. Retrograde perfusion of a transplant- kidney via a femoro- femoral crossover bypass

VASA ◽

10.1024/0301-1526/a000316 ◽

2013 ◽

Vol 42 (6) ◽

pp. 453-456 ◽

Cited By ~ 1

Author(s):

Jurgen Knuth ◽

Dirk Wenzel ◽

Axel Goßmann ◽

Marko Aleksic

Keyword(s):

Retrograde Perfusion ◽

Transplant Kidney ◽

Crossover Bypass

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Contribution of Adrenaline to the Fibrinolytic Activity Evoked by E. Coli Endotoxin in the Rat

Thrombosis and Haemostasis ◽

10.1055/s-0038-1665254 ◽

1983 ◽

Vol 50 (02) ◽

pp. 557-559 ◽

Cited By ~ 3

Author(s):

J F Fracasso ◽

A M Rothschild

Keyword(s):

Fatty Acid ◽

Adrenal Gland ◽

Intravenous Injection ◽

Fibrinolytic Activity ◽

Blocking Agent ◽

E Coli ◽

Adrenergic Blocking

SummaryIntravenous injection of E. coli endotoxin (ETX), of adrenaline (AD) or of carbamylcholine (CBCH), caused fibrinolytic activity (FA), directly detectable on plasminogen-rich fibrin plates, to appear in the plasma of the rat. Adrenodemedul- lation abolished responses to ETX or CBCH, but enhanced those to AD. Rats given ETX exhibited marked hypotension, followed by a compensatory phase of normotension abolished by adrenodemedullation and significantly attenuated by phenoxy- benzamine, an a-adrenergic blocking agent which however failed to block FA caused by either ETX or AD. Aspirin, but not indomethacin, inhibited FA evoked by ETX, AD or CBCH. These results suggest that FA evoked by ETX in the rat is caused by AD released from the adrenal gland and does involve the fatty acid cyclooxygenase system.

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PROPRANOLOL-BLOCKADE OF VASOPRESSIN INDUCED INCREASE IN PLASMA PROGESTERONE IN EARLY HUMAN PREGNANCY

Acta Endocrinologica ◽

10.1530/acta.0.0660283 ◽

1971 ◽

Vol 66 (2) ◽

pp. 283-288 ◽

Cited By ~ 4

Author(s):

Petter Fylling

Keyword(s):

Cyclic Amp ◽

Uterine Cervix ◽

Adenosine Monophosphate ◽

First Trimester ◽

Blocking Agent ◽

Simultaneous Administration ◽

Plasma Progesterone ◽

Human Pregnancy ◽

Peripheral Plasma ◽

Early Human

ABSTRACT Following continuous dilation of the uterine cervix or intravenous infusion of vasopressin during the first trimester of human pregnancy, a marked increase in the peripheral plasma progesterone levels was observed. This effect was blocked by simultaneous administration of propranolol (Inderal®), a β-blocking agent. It is suggested that both these stimulating and inhibiting effects might be related to 3′, 5′-adenosine monophosphate (cyclic AMP). The results indicate the existence of β-receptors in steroid producing tissues.

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ADRENERGIC CONTROL MECHANISM FOR ACTH SECRETION IN MAN

Acta Endocrinologica ◽

10.1530/acta.0.0740263 ◽

1973 ◽

Vol 74 (2) ◽

pp. 263-270 ◽

Cited By ~ 50

Author(s):

Yoshikatsu Nakai ◽

Hiroo Imura ◽

Teruya Yoshimi ◽

Shigeru Matsukura

Keyword(s):

Intravenous Infusion ◽

Human Subjects ◽

Blocking Agent ◽

Inhibitory Effect ◽

Plasma Acth ◽

Acth Secretion ◽

Glucose Levels ◽

Alpha Receptors ◽

Normal Human ◽

Adrenergic Blocking

ABSTRACT In order to determine if an adrenergic mechanism is involved in the secretion of corticotrophin (ACTH), the effect of adrenergic-blocking or -stimulating agent on plasma ACTH, cortisol and glucose levels was studied in normal human subjects. The intravenous infusion of methoxamine, an alpha adrenergic-stimulating agent, caused a rise in plasma ACTH and cortisol. This increase in plasma ACTH and cortisol was significantly inhibited by the simultaneous administration of phentolamine, an alpha adrenergic-blocking agent, in combination with methoxamine. The intravenous infusion of propranolol, a beta adrenergic-blocking agent, caused no significant change in plasma ACTH and cortisol, although it enhanced the plasma ACTH response to insulin-induced hypoglycaemia. On the other hand, alpha adrenergicblockade by intravenous infusion of phentolamine significantly suppressed the plasma ACTH response to insulin-induced hypoglycaemia. These studies suggest a stimulatory effect of alpha receptors and a possible inhibitory effect of beta receptors on ACTH secretion in man.

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