title: Cerebral influences of sodium and angiotensin II on cardiovascular function in hypotensive hemorrhage.
abstract: During progressive blood loss several mechanisms act in concert to compensate for the reduced intravascular volume with the overall aim to provide sufficient blood supply to vital organs. The hemodynamic responses in this situation follow a characteristic course of events in conscious individuals with an initial phase of largely maintained blood pressure and tachycardia followed by an abrupt fall in pressure, accompanied by bradycardia and widespread inhibition of sympathetic nervous activity when 20-30% of the blood volume is lost. Our research has focussed on Na+ and angiotensin II effects on the brain for the cardiovascular compensatory mechanisms in response to hypotensive hemorrhage in sheep. We have found that intracerebroventricular infusion of hypertonic NaCl solution improves the tolerance to blood loss, i.e., increases the amount of blood loss needed to induce hypotension. Inhalation anesthesia abolished this effect of the infusion. Similarly, corresponding infusions of angiotensin II also increased the resistance to blood loss in conscious animals only, although accompanied by different hemodynamic compensatory mechanisms. The effects of intracerebroventricular hypertonic NaCl infusion on cardiovascular compensation during hemorrhage are similar to those achieved with treatment of hemorrhagic shock with intravenous infusions of small volumes of hypertonic NaCl solutions. We therefore suggest that a substantial part of the beneficial effect of that treatment is mediated via direct effects of the hypernatremia on the brain. These observations also illustrate the need for further elucidation of more possible influences on autonomic functions by increased Na+ concentration which, together with hypovolemia, is a hallmark of dehydration.
authors.affiliation: Karolinska Institutet, Department of Physiology and Pharmacology, S-171 77 Stockholm, Sweden. Mats.Rundgren@ki.se
authors.forename: Mats
authors.initials: M
authors.lastname: Rundgren
authors.forename: Robert
authors.initials: R
authors.lastname: Frithiof
authors.forename: Hans
authors.initials: H
authors.lastname: Hjelmqvist
authors.forename: Johan E
authors.initials: JE
authors.lastname: Ullman
authors.forename: Stefan
authors.initials: S
authors.lastname: Eriksson
mesh_terms: D000222:Adaptation, Physiological; D000804:Angiotensin II / Q000008:administration & dosage / Q000378:metabolism*; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001921:Brain / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D007022:Hypotension / Q000209:etiology / Q000378:metabolism*; D007276:Injections, Intraventricular; D009434:Neural Pathways / Q000502:physiology; D012756:Sheep; D012771:Shock, Hemorrhagic / Q000150:complications / Q000378:metabolism*; D012964:Sodium / Q000008:administration & dosage / Q000378:metabolism*; D014882:Water-Electrolyte Balance / Q000502:physiology
chemical_list: D000804:Angiotensin II; D012964:Sodium