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angiotensin/krvarenje
Veza se sprema u međuspremnik
Stranica 1 iz 1155 rezultatima
Acute Bradykinin Receptor Blockade During Hemorrhagic Shock in Mice Prevents the Worsening Hypotensive Effect of Angiotensin-Converting Enzyme Inhibitor.
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Angiotensin-converting enzyme inhibitors are associated with deleterious hypotension during anesthesia and shock. Because the pharmacologic effects of angiotensin-converting enzyme inhibitors are partly mediated by increased bradykinin B2 receptor activation, this study aimed to determine the impact
Prior use of angiotensin-converting enzyme inhibitors does not affect outcome in patients with intracerebral hemorrhage.
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OBJECTIVE
Angiotensin-converting enzyme inhibitors (ACEI) exert protective effects in patients with stroke but their effects remain unknown in patients with intracerebral hemorrhage (ICH).
METHODS
We recruited consecutive patients with acute ICH and analysed pre-admission demographic variables and
Action of angiotensin II on renal blood flow and function during hemorrhagic shock.
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The purpose of this study was to evaluate during hemorrhagic hypotension and shock the effect of angiotensin II on renal blood flow, glomerular filtration rate, and sodium and potassium excretions, and to determine its role in the development of irreversible hemorrhagic shock. Anesthetized dogs were
Cardiovascular, sympathetic, and renin-angiotensin system responses to hemorrhage in vasopressin-deficient rats.
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To determine if the subnormal blood pressure recovery after hemorrhage in Brattleboro rats is due to secondary abnormalities in the renin-angiotensin or sympathetic nervous systems, we measured the hemodynamic, catecholamine, and renin activity responses to moderate acute hemorrhage in anesthetized
Angiotensin II antagonists and gastrointestinal bleeding in left ventricular assist devices: A systematic review and meta-analysis
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Gastrointestinal bleeding (GIB) especially from arteriovenous malformations (AVM) remains one of the devastating complications following continuous-flow left ventricular device (CF-LVAD) implantation. Blockade of angiotensin II pathway using angiotensin-converting enzyme inhibitors
Effect of [1-Sar,8-Thr]-angiotensin II on the hyperglycemic response to hemorrhage in adrenodemedullated and guanethidine-treated rats.
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The present experiments were designed to further investigate the action of an angiotensin II antagonist on the hyperglycemic response to hemorrhage (1.2 ml/100 g b.wt./2 min). The animals were divided into 3 experimental groups; (1) sham-operated animals submitted to intravenous administration of
Impact of the renin-angiotensin system on cerebral perfusion following subarachnoid haemorrhage in the rat.
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1. This study investigated the effects of blocking the AT1 angiotensin receptors with irbesartan, either peripherally or centrally, on systemic blood pressure, intracranial pressure and cerebral perfusion pressure following experimental subarachnoid haemorrhage (SAH) in urethane-anaesthetized rats.
Deterioration of metabolic coronary regulation in hemorrhagic shock. Role of hypoxia and the renin-angiotensin system.
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The effect of hypoxia and the renin-angiotensin system on metabolic coronary regulation in hemorrhagic shock was studied in 22 anesthetized open-chest dogs. Left circumflex coronary blood flow was measured with an electromagnetic flowmeter. Dogs were ventilated with room air (n = 8) or 100% oxygen
Effect of bilateral nephrectomy on the recovery of blood pressure after acute hemorrhage in rats: role of renin-angiotensin system.
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The effect of bilateral nephrectomy, and administration of an inhibitor of angiotensin converting enzyme, on the recovery of arterial blood pressure after hemorrhage (loss of 1% of b.wt), was studied in male Sprague-Dawley rats. Neither manoeuver significantly affected the recovery of blood pressure
Modulation of jejunal ion and water absorption by endogenous angiotensin after hemorrhage.
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In the pentobarbital sodium-anesthetized rat, hemorrhage of blood equivalent to 1% body weight (18.4% blood volume) increases plasma renin activity and plasma aldosterone concentration and also markedly elevates jejunal ion and water absorption. Infusion of angiotensin II (AII) also stimulates
The effect of angiotensin AT1 receptor blockade in the brain on the maintenance of blood pressure during haemorrhage in sheep.
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The effect of systemic or intracerebroventricular (ICV) infusion of the angiotensin AT1 receptor antagonist losartan on blood pressure during hypotensive haemorrhage was investigated in five conscious sheep. Mean arterial pressure (MAP) was measured during haemorrhage (15 mL kg-1 body wt). Losartan
Oxytocin release after bleeding in rat: the role of sympathetic and renin-angiotensin system.
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The aim of this experiment was to compare the role of renin-angiotensin and sympathetic nervous system in post-haemorrhagic mechanism of oxytocin release. Oxytocin content in venous dialysates was determined by radioimmunoassay. In control rats the release of oxytocin into dialysates did not change
Beneficial effect of renin-angiotensin system for maintaining blood pressure control following subarachnoid haemorrhage.
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Subarachnoid haemorrhage is a serious condition often accompanied by delayed cerebral ischaemia. Earlier reports have provided evidence suggesting a role for angiotensin II in the development of cerebral vasospasm following subarachnoid bleeding. We sought to examine the influence of angiotensin II
Role of renin-angiotensin system in response to hemorrhage in fetal sheep.
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During fetal life, the autonomic nervous system is not fully mature, and it is likely that hormonal mechanisms play an important role in controlling cardiovascular function. In chronically instrumented fetal sheep, hemorrhage increased plasma renin activity and plasma angiotensin concentration
A role for angiotensin II in the activation of extracellular signal-regulated kinases in the liver during hemorrhagic shock.
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Hemorrhagic shock (HS) is a complex process that initiates a global stress response. However, the earliest signaling pathways responsible for initiating this response remain unidentified. We have investigated the involvement of the extracellular signal-regulated kinases (ERK 1/2; also known as
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