Central angiotensinergic system and hypertonic resuscitation from severe hemorrhage

Velasco, Irineu Tadeu; Baena, Renato Corrêa; Silva, M. Rocha e; Loureiro, M.I

doi:10.1152/ajpheart.1990.259.6.h1752

Cited by 13 publications

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“…These findings suggest that the hypernatremia during hypertonic saline resuscitation is detected by osmotic or sodium sensors in the lamina terminalis, which, via an angiotensinergic link possibly to the paraventricular nucleus of the hypothalamus, leads to stimulation of CSNA and inhibition of RSNA, for which there must be an inhibitory synapse in the pathway (18). Activation of such pathways by hypertonic saline in hemorrhage is supported by the finding that blocking cerebral AT 1 receptors attenuates the improvement in systemic hemodynamics after resuscitation with hypertonic saline (9,31). The areas of the brain thought to be involved in the initiation of the decompensatory phase, such as the rostral ventrolateral medulla, the ventrolateral periaqueductal gray, and the caudal midline medulla (4,14,23), may also be affected by the hypertonic saline.…”

Section: Discussionmentioning

confidence: 97%

Hypertonic sodium resuscitation after hemorrhage improves hemodynamic function by stimulating cardiac, but not renal, sympathetic nerve activity

Frithiof

Ramchandra

Hood

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Frithiof R, Ramchandra R, Hood SG, May CN. Hypertonic sodium resuscitation after hemorrhage improves hemodynamic function by stimulating cardiac, but not renal, sympathetic nerve activity. Am J Physiol Heart Circ Physiol 300: H685-H692, 2011. First published December 10, 2010 doi:10.1152/ajpheart.00930.2010.-Small volume hypertonic saline resuscitation can be beneficial for treating hemorrhagic shock, but the mechanism remains poorly defined. We investigated the effects of hemorrhagic resuscitation with hypertonic saline on cardiac (CSNA) and renal sympathetic nerve activity (RSNA) and the resulting cardiovascular consequences. Studies were performed on conscious sheep instrumented with cardiac (n ϭ 7) and renal (n ϭ 6) sympathetic nerve recording electrodes and a pulmonary artery flow probe. Hemorrhage (20 ml/kg over 20 min) caused hypotension and tachycardia followed by bradycardia, reduced cardiac output, and abolition of CSNA and RSNA. Resuscitation with intravenous hypertonic saline (1.2 mol/l at 2 ml/kg) caused rapid, dramatic increases in mean arterial pressure, heart rate, and CSNA, but had no effect on RSNA. In contrast, isotonic saline resuscitation (12 ml/kg) had a much delayed and smaller effect on CSNA, less effect on mean arterial pressure, no effect on heart rate, but stimulated RSNA, although the plasma volume expansion was similar. Intracarotid infusion of hypertonic saline (1 ml/min bilaterally, n ϭ 5) caused similar changes to intravenous administration, indicating a cerebral component to the effects of hypertonic saline. In further experiments, contractility (maximum change in pressure over time), heart rate, and cardiac output increased significantly more with intravenous hypertonic saline (2 ml/kg) than with Gelofusine (6 ml/kg) after hemorrhage; the effects of hypertonic saline were attenuated by the ␤-receptor antagonist propranolol (n ϭ 6). These results demonstrate a novel neural mechanism for the effects of hypertonic saline resuscitation, comprising cerebral stimulation of CSNA by sodium chloride to improve cardiac output by increasing cardiac contractility and rate and inhibition of RSNA. brain; sodium chloride; sheep; conscious; saline; shock SEVERE HEMORRHAGE IS A LEADING cause of death and morbidity (30). Hypertonic saline solutions are frequently used for resuscitation in states of shock, having beneficial cardiovascular effects comprising improved cardiac output (CO), blood pressure, and regional blood flows (32) and leading to prompt restoration of oxygen delivery. Plasma volume expansion, caused by cellular dehydration via an osmotic gradient, partly accounts for these effects. There is, however, evidence that hypertonic saline has important additional actions to increase cardiac function, as similar increases in plasma volume by other fluids cause less improvement in CO (2). Studies investigating the direct effects of elevated osmolality/sodium levels on the heart have rendered inconclusive results, showing increased, decreased, or no effect on cardiac performance (5,10,13,2...

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Section: Discussionmentioning

confidence: 97%

Hypertonic sodium resuscitation after hemorrhage improves hemodynamic function by stimulating cardiac, but not renal, sympathetic nerve activity

Frithiof

Ramchandra

Hood

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…We know for sure that systemic administration of prostaglandin synthesis inhibitors, antihistaminergic agents, beta-adrenergic blockers, and serotonin antagonists does not interfere with hyperosmotic saline effects in experimental hemorrhagic shock (Lopes et al, 1981). We also know that alpha-adrenergic, angiotensin and vasopressin antagonists reduce the beneficial effects of hypertonic solutions in hemorrhagic shock (Kosoglou et al, 1986;Velasco et al, 1990;Giusti-Paiva et al, 2007). It seems there is no single pattern that explains the responses to hypertonic saline infusion in hemorrhagic shock.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular adjustments induced by hypertonic saline in hemorrhagic rats: Involvement of carotid body chemoreceptors

Pedrino

Rossi

Schoorlemmer

et al. 2011

Autonomic Neuroscience

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The peripheral hyperosmolarity elicited by intravenous infusion of hypertonic saline brings potential benefits to the treatment of hemorrhage. The neural mechanisms involved in these beneficial effects remain unknown. The present study examines the role of carotid chemoreceptors in cardiovascular responses induced by hypertonic saline after hypovolemic hemorrhage in rats. Male Wistar rats (300-400 g) were anesthetized with thiopental, and instrumented for recording of mean arterial pressure. Arterial pressure was reduced to 60 mm Hg by withdrawal of arterial blood over 10 min, and maintained at this level for 60 min by withdrawal or infusion of blood. In control rats (n = 8) with intact chemoreceptors, the subsequent intravenous infusion of hypertonic saline (3M NaCl, 1.8 ml kg(-1) body weight, in 2 min) restored blood pressure (pressure increased from 61 ± 4 to 118 ± 5 mm Hg). In experimental rats (n = 8), the carotid body arteries were tied, 30 min after the beginning of the hypotensive phase, leaving the carotid chemoreceptors ischemic. In these rats, hypertonic saline failed to restore blood pressure (pressure increased from 55 ± 1 to 70 ± 6 mm Hg). These findings suggest that the restoration of blood pressure after hypovolemic hemorrhage induced by hypertonic saline depends on intact carotid chemoreceptors.

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“…Centrally administered Ang II also increases blood pressure and this effect is especially important in hypovolemic conditions (12,15,16,19,(29)(30)(31). Intracerebroventricular injections of renin-angiotensin system antagonists decrease blood pressure in spontaneously hypertensive and normotensive rats (9,17,19,20,32,33).…”

Section: Discussionmentioning

confidence: 99%

Central injection of captopril inhibits the blood pressure response to intracerebroventricular choline

Isbil-Buyukcoskun

Gulec

Ozluk

et al. 2001

Braz J Med Biol Res

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In the present study, we investigated the involvement of the brain renin-angiotensin system in the effects of central cholinergic stimulation on blood pressure in conscious, freely moving normotensive rats. In the first step, we determined the effects of intracerebroventricular (icv) choline (50, 100 and 150 µg) on blood pressure. Choline increased blood pressure in a dose-dependent manner. In order to investigate the effects of brain renin-angiotensin system blockade on blood pressure increase induced by choline (150 µg, icv), an angiotensin-converting enzyme inhibitor, captopril (25 and 50 µg, icv), was administered 3 min before choline. Twenty-five µg captopril did not block the pressor effect of choline, while 50 µg captopril blocked it significantly. Our results suggest that the central renin-angiotensin system may participate in the increase in blood pressure induced by icv choline in normotensive rats. CorrespondenceN.

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Central angiotensinergic system and hypertonic resuscitation from severe hemorrhage

Cited by 13 publications

References 0 publications

Hypertonic sodium resuscitation after hemorrhage improves hemodynamic function by stimulating cardiac, but not renal, sympathetic nerve activity

Hypertonic sodium resuscitation after hemorrhage improves hemodynamic function by stimulating cardiac, but not renal, sympathetic nerve activity

Cardiovascular adjustments induced by hypertonic saline in hemorrhagic rats: Involvement of carotid body chemoreceptors

Central injection of captopril inhibits the blood pressure response to intracerebroventricular choline

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