Lesion of the anteroventral third ventricle region impairs the recovery of arterial pressure induced by hypertonic saline in rats submitted to hemorrhagic shock

Barbosa, Silas Pereira; Camargo, Luiz Antônio de Arruda; Saad, Wilson Abrão; Renzi, Antonio; Luca, Laurival A. De; Menani, José Vanderlei

doi:10.1016/0006-8993(92)91434-g

Cited by 15 publications

(6 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Hypernatremia activate various neuronal reflex mechanisms for homeostasis restoration in severe hemorrhagic cases [ 9 – 11 , 33 , 37 ]. Some authors demonstrated that sinoaortic denervation abolishes the renal vasodilation induced by hypernatremia unlike bilateral vagotomy (removal of cardiopulmonary receptors) that does not alter this response [ 38 , 39 ].…”

Section: Discussionmentioning

confidence: 99%

Median Preoptic Nucleus Mediates the Cardiovascular Recovery Induced by Hypertonic Saline in Hemorrhagic Shock

Amaral

Naves

Ferreira-Neto

et al. 2014

The Scientific World Journal

View full text Add to dashboard Cite

Changes in plasma osmolarity, through central and peripheral osmoreceptors, activate the median preoptic nucleus (MnPO) that modulates autonomic and neuroendocrine adjustments. The present study sought to determine the participation of MnPO in the cardiovascular recovery induced by hypertonic saline infusion (HSI) in rats submitted to hemorrhagic shock. The recordings of mean arterial pressure (MAP) and renal vascular conductance (RVC) were carried out on male Wistar rats (250–300 g). Hemorrhagic shock was induced by blood withdrawal over 20 min until the MAP values of approximately 60 mmHg were attained. The nanoinjection (100 nL) of GABAA agonist (Muscimol 4 mM; experimental group (EXP)) or isotonic saline (NaCl 150 mM; control (CONT)) into MnPO was performed 2 min prior to intravenous overload of sodium through HSI (3 M NaCl, 1.8 mL/kg, b.wt.). Hemorrhagic shock reduced the MAP in control (62 ± 1.1 mmHg) and EXP (61 ± 0.4 mmHg) equipotently. The inhibition of MnPO impaired MAP (CONT: 104 ± 4.2 versus EXP: 60 ± 6.2 mmHg) and RVC (CONT: 6.4 ± 11.4 versus EXP: -53.5 ± 10.0) recovery 10 min after HSI. The overall results in this study demonstrated, for the first time, that the MnPO plays an essential role in the HSI induced resuscitation during hypovolemic hemorrhagic shock.

show abstract

Section: Discussionmentioning

confidence: 99%

Median Preoptic Nucleus Mediates the Cardiovascular Recovery Induced by Hypertonic Saline in Hemorrhagic Shock

Amaral

Naves

Ferreira-Neto

et al. 2014

The Scientific World Journal

View full text Add to dashboard Cite

show abstract

“…It would seem feasible that the administration of H-saline leads to exaggerated vasoconstrictor efficacy of neurogenic-derived catecholamines and relevant circulating factors. Lesions of the anteroventral region of the third ventricle (AV3V) impair the recovery of MAP induced by H-saline (7.5% NaCl, 4 ml/kg) in HEM rats (Barbosa et al, 1990, 1992). As such, it is likely that the beneficial actions of H-saline in our study also involved changes in the activities of AV3V neurons that control neurogenic outflow and the release of hormones regulating vascular tone and fluid/salt balance such as angiotensin II and arginine vasopressin (see Barbosa et al, 1990, 1992).…”

Section: Discussionmentioning

confidence: 99%

“…Lesions of the anteroventral region of the third ventricle (AV3V) impair the recovery of MAP induced by H-saline (7.5% NaCl, 4 ml/kg) in HEM rats (Barbosa et al, 1990, 1992). As such, it is likely that the beneficial actions of H-saline in our study also involved changes in the activities of AV3V neurons that control neurogenic outflow and the release of hormones regulating vascular tone and fluid/salt balance such as angiotensin II and arginine vasopressin (see Barbosa et al, 1990, 1992). It should be mentioned that systemic injections of γ 2 -melanocyte-stimulating hormone (γ 2 -MSH) elicits equivalent increases in resistance in the renal, mesenteric and hindquarter vascular beds of pentobarbital-anesthetized rats (Whalen et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

“…There is considerable information as to effects of small volumes of isotonic saline (I-saline) and H-saline on MAP, CO and TPR in low CO-induced hypotension during HEM (Brooks, 1935; Nakayama et al, 1984; Smith et al, 1985; Maningas et al, 1986; Traveso et al, 1987; Hannon et al, 1989; Barbosa et al, 1990, 1992). However, although the changes in systemic vascular resistances during HEM in animals have received attention (see Liu et al, 2003; Whalen et al, 2007), nothing is known about the changes in systemic resistances elicited by administration of I-saline or H-saline in these rats.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Hemodynamic responses elicited by systemic injections of isotonic and hypertonic saline in hemorrhaged rats

Whalen

Johnson

Lewis

2014

Microvascular Research

View full text Add to dashboard Cite

Purpose The objectives of this study were (i) to characterize the hemodynamic responses caused by controlled hemorrhage (HEM) in pentobarbital-anesthetized rats, and (ii) to determine the responses elicited by systemic bolus injections of isotonic saline (0.15 M) or hypertonic saline (3 M) given 5 min after completion of HEM. Results Controlled HEM (4.3 ± 0.2 ml/rat at 1.5 ml/ min) resulted in a pronounced and sustained fall in mean arterial blood pressure (MAP) to about 40 mmHg. The fall in MAP was associated with a reduction in hindquarter vascular resistance (HQR) but no changes in renal (RR) or mesenteric (MR) vascular resistances. Systemic injections of isotonic saline (96–212 µmol/kg iv, in 250–550 µl) did not produce immediate responses but promoted the recovery of MAP to levels below pre-HEM values. Systemic injections of hypertonic saline (750–3000 µmol/kg, i.v., in 250–550 µl) produced immediate and pronounced falls in MAP, RR, MR and especially HQR of 30–120 sec in duration. However, hypertonic saline prompted a full recovery of MAP, HQR and RR to pre-HEM levels and an increase in MR to levels above pre-HEM values. Conclusions This study demonstrates that (i) HEM induced a pronounced fall in MAP which likely involved a fall in cardiac output and HQR, (ii) isotonic saline did not fully normalize MAP, and (iii) hypertonic saline produced dramatic initial responses, and promoted normalization of MAP probably by restoring blood volume and cardiac output through sequestration of fluid from intracellular compartments.

show abstract

“…The effects are mediated by central osmoreceptors and a cascade of neurotransmitters including angiotensin [36, 37]. There is evidence that brain lesions of osmosensitivity regions reduce the endocrine and cardiovascular responses to osmotic stimulation [38, 39]. There is also evidence that osmotic pathways involve the renin angiotensin system [40, 41].…”

Section: Discussionmentioning

confidence: 99%

Rapid Neurosecretory and Cardiovascular Response to Osmotic Stimulation in Conscious Mice

Chen¹,

Morris²,

Key³

et al. 2004

Neuroendocrinology

View full text Add to dashboard Cite

Experiments were performed to evaluate the neuroendocrine and cardiovascular effects of osmotic stimulation in mice. Hypertonic saline (HS) was administered centrally or via the blood stream to conscious mice during measurement of blood pressure (BP), heart rate (HR) and plasma vasopressin (VP) and oxytocin (OT). A test of hypovolemia on VP secretion was also performed. Chronic carotid arterial cannulas were inserted for blood sampling, cardiovascular monitoring and vascular injections. Intracerebroventricular (ICV) cannulas were used for central injections. Vascular injection of HS (30 µl, 3.4 M NaCl) caused rapid and transient increases in plasma VP and OT. Plasma VP increased from 5.6 ± 0.9 to 10.0 ± 1.0 pg/ml, while plasma OT increased from 1.5 ± 0.6 to 8.6 ± 2.4 pg/ml at the earliest time point, immediately after ICV injection. ICV osmotic stimulation produced a rapid and sustained increase in plasma VP, with no change in OT. Plasma VP levels were increased from basal levels of 5.1 ± 1.5 to 13.1 ± 4.6, 11.4 ± 1.5, 12.6 ± 1.7 pg/ml at 0, 1 and 5 min after injection, respectively. ICV HS also increased plasma corticosterone. BP was increased by both vascular and central osmotic stimulation. Vascular HS increased BP immediately (Δ15.3 ± 1.7 mm Hg, 0 min) and transiently (Δ–3.9 ± 4.6 mm Hg, 5 min) while central HS produced a sustained increase in BP (Δ10 ± 1.4 and Δ9.8 ± 1.9 mm Hg, 0 and 5 min). Osmotic stimulation produced no significant changes in HR. Acute hemorrhage (∼10% decrease in blood volume) increased plasma VP (4.9 ± 1.0 vs. 8.4 ± 2.2 pg/ml). These results show the pattern of endocrine and cardiovascular responses to osmotic stimulation in conscious mice. They demonstrate that (1) there are extremely rapid changes in plasma VP and OT; (2) plasma OT is increased only after peripheral vascular hypertonic injection, and (3) central and peripheral osmotic stimulations are associated with pressor responses.

show abstract

Lesion of the anteroventral third ventricle region impairs the recovery of arterial pressure induced by hypertonic saline in rats submitted to hemorrhagic shock

Cited by 15 publications

References 19 publications

Median Preoptic Nucleus Mediates the Cardiovascular Recovery Induced by Hypertonic Saline in Hemorrhagic Shock

Median Preoptic Nucleus Mediates the Cardiovascular Recovery Induced by Hypertonic Saline in Hemorrhagic Shock

Hemodynamic responses elicited by systemic injections of isotonic and hypertonic saline in hemorrhaged rats

Rapid Neurosecretory and Cardiovascular Response to Osmotic Stimulation in Conscious Mice

Contact Info

Product

Resources

About