Endogenous and exogenous catecholamines in critical care medicine

Chernow, Bart; Rainey, Thomas G.; Lake, C. Raymond

doi:10.1097/00003246-198206000-00019

Cited by 122 publications

(41 citation statements)

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“…Two hours after the beginning of LPS infusion, the diminished pressor and carotid, mesenteric and hindquarters vasoconstrictor effects of methoxamine are consistent with reports of vascular hyporeactivity to a variety of vasoconstrictor agents in other rat models (Fink et al, 1985;Schaller et al, 1985;Guc et al, 1990;Hollenberg et al, 1993) and in man (Chernow et al, 1982). It is generally agreed that NOmediated mechanisms are involved (see Moncada et al, 1991) and, if so, it is interesting that not all vascular beds responded uniformly and that the pattern of hyporesponsiveness changed with time during LPS infusion (see below).…”

Section: Discussionsupporting

confidence: 88%

“…Additionally, there are i.e., a raised cardiac output with marked peripheral vasodilareports of reduced responses to vasodilators such as acetyltation (see Parrillo, 1993). In man, this hyperdynamic state choline (Altura et al, 1985;Young et al, 1991; and the subsequent development of septic shock is often 1991 ;Parker & Adams, 1993), salbutamol (Guc et al, 1991) associated with reduced pressor responsiveness to vasoconand bradykinin (Altura et al, 1985;Guc et al, 1991) in strictors (Chernow et al, 1982), which may be related to different animal models of septic shock, although the induction of the calcium-independent form of nitric oxide mechanisms underlying these abnormalities are not entirely synthase (iNOS) (see Moncada et al, 1991). clear.…”

Section: Introductionmentioning

confidence: 99%

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Regional haemodynamic responses to acetylcholine, methoxamine, salbutamol and bradykinin during lipopolysaccharide infusion in conscious rats

Waller

Gardiner

Bennett

1994

British J Pharmacology

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1 The aim of the study was to assess the regional haemodynamic responsiveness to vasoconstrictor and vasodilator challenges during continuous 24 h infusion of lipopolysaccharide (LPS) in conscious Long Evans rats.2 Rats were chronically instrumented for the measurement of regional haemodynamics (either internal and common carotid or renal, superior mesenteric and hindquarters) and received 3 min of infusions of acetylcholine (22 nmol min-'), methoxamine (120 nmol min-'), salbutamol (0.83 nmol min-') and bradykinin (14.4 nmol min-') at 2, 6 and 24 h after the start of saline or LPS (150 ;g kg-' h-') infusion (rats with carotid probes received only acetylcholine and methoxamine). 3 During infusion of LPS there was a changing haemodynamic profile. After 2 h, there was a modest hypotension and vasodilatation in the internal carotid, renal and hindquarters vascular beds. After 6 h, arterial blood pressure had returned to baseline, there was still vasodilatation in the renal vascular bed but vasoconstriction in the internal and common carotids and the hindquarters. After 24 h, there was hypotension, tachycardia and generalized vasodilatation. 4 Acetylcholine caused a fall in blood pressure, tachycardia and hyperaemic vasodilatation in the carotid and renal vascular beds. Throughout the infusion of LPS, the carotid vasodilator response was enhanced after 2 h, reduced after 6 h and enhanced again after 24 h, whereas the renal vasodilator response to acetylcholine was either reduced (6 h) or absent (2 and 24 h); at this juncture the hypotensive response to acetylcholine was also enhanced and the tachycardia was reduced. 5 Methoxamine caused a rise in blood pressure, a fall in heart rate, and vasoconstriction in all the vascular beds monitored. During infusion of LPS, the pressor response to methoxamine was consistently reduced as were the vasoconstrictor responses in the carotid and mesenteric vascular beds, whereas the renal and hindquarters vasoconstrictor responses to methoxamine were only significantly reduced at some time points (renal 6 h, hindquarters 2 and 6 h).6 Salbutamol caused hypotension, tachycardia and hyperaemic vasodilatation, particularly in the hindquarters vascular bed. Throughout the infusion of LPS, the cardiovascular responses to salbutamol were substantially attenuated.7 Bradykinin caused hypotension, tachycardia and hyperaemic vasodilatation in the renal, mesenteric and hindquarters vascular beds. During the infusion of LPS, the hypotensive response to bradykinin was consistently augmented, and the tachycardia was consistently reduced, but the regional haemodynamic profile changed with time. Thus, after 2 h, the mesenteric vasodilator response was augmented and the hindquarters vasodilator response was reduced; after 6 h, the mesenteric vasodilator response appeared normal, but the renal and hindquarters vasodilator responses were reduced; after 24 h, the hindquarters vasodilator response was markedly augmented and the renal response had changed to a vasoconstriction.8 The present findings indica...

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Regional haemodynamic responses to acetylcholine, methoxamine, salbutamol and bradykinin during lipopolysaccharide infusion in conscious rats

Waller

Gardiner

Bennett

1994

British J Pharmacology

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“…Ve dřeni nadledvin, která je funkčně ganglionem sympatického systému, dochází k uvolňování noradrenalinu a adrenalinu do krevního oběhu. V těžkém šoku se zvýší plasmatická koncentrace noradrenalinu 10x a adrenalinu až 50x (49). U pacientů v těžkém stresu se z kůry nadlevin uvolní až 10ti násobné množství kortizolu (odpovídá asi 300mg hydrocortisonu za den) (50).…”

Section: Rozdíly V Metabolismu Glukózy Kriticky Nemocnýchunclassified

The Central Role of Glucose in Metabolism and Nutrition of Critically Ill Patients

Skořepa¹,

Sobotka²,

Fortunato³

et al. 2017

Mil. Med. Sci. Lett.

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“…The reduction in peripheral vascular resistance is thought to be a key factor responsible for the death of patients with septic shock (Groeneveld et al, 1986;Parrillo, 1985). However, these septic patients experience adrenergic unresponsiveness despite elevated circulating levels of catecholamines (Chernow et al, 1982).…”

Section: Vascular Hyporesponsiveness To Vasocontractile Stimulimentioning

confidence: 99%

Vascular biology in sepsis: pathophysiological and therapeutic significance of vascular dysfunction

Matsuda

Hattori

2007

J Smooth Muscle Res

116

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Sepsis is the leading cause of mortality in critically ill patients. In this pathological syndrome, septic shock and sequential multiple organ failure correlate with poor outcome. The pathophysiology of sepsis with acute organ dysfunction involves a highly complex, integrated response that includes activation of number of cell types, inflammatory mediators, and the hemostatic system. Central to this process may be alterations in vascular functions. This review article provides a growing body of evidence for the potential impact of vascular dysfunction on sepsis pathophysiology with a major emphasis on the endothelium. Furthermore, the role of apoptotic signaling molecules in the mechanisms underlying endothelial cell injury and death during sepsis and its potential value as a target for sepsis therapy will be discussed, which may help in the assessment of ongoing therapeutic strategies.

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Endogenous and exogenous catecholamines in critical care medicine

Cited by 122 publications

References 0 publications

Regional haemodynamic responses to acetylcholine, methoxamine, salbutamol and bradykinin during lipopolysaccharide infusion in conscious rats

Regional haemodynamic responses to acetylcholine, methoxamine, salbutamol and bradykinin during lipopolysaccharide infusion in conscious rats

The Central Role of Glucose in Metabolism and Nutrition of Critically Ill Patients

Vascular biology in sepsis: pathophysiological and therapeutic significance of vascular dysfunction

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