Intravenous infusions of highly concentrated NaCl (2,400 mosmol/l; infused volume 4 ml/kg; equivalent to 10% of shed blood), given to lightly anesthetized dogs in severe hemorrhagic shock, rapidly restore blood pressure and acid base equilibrium toward normality. No appreciable plasma volume expansion occurs for at least 12 h, indicating that fluid shift into the vascular bed plays no essential role in this response. Initial effects wee sustained indefinitely; long term survival was 100%, compared to 0% for a similar group of controls treated with saline. Hemodynamic analysis of the effects of hyperosmotic NaCl showed that these infusions substantially increase mean and pulse arterial pressure, cardiac output and mesenteric flow, whereas heart rate was slightly diminished. These effects immediately follow infusions with no tendency to dissipate with time (6-h observation). We conclude that hyperosmotic NaCl infusions increase the dynamic efficiency of the circulatory system, enabling it to adequately handle oxygen supply and metabolite clearance, despite a critical reduction of blood volume.

Abstract-Brain pathways controlling arterial pressure are distributed throughout the neuraxis and are organized in topographically selective networks. In this brief review, we will focus on the medulla oblongata. The nucleus tractus solitarius (NTS) is the primary site of cardiorespiratory reflex integration. It is well accepted that lesions or other perturbations in the NTS can result in elevations of arterial pressure (AP), with many of the associated features so commonly found in humans. However, recent studies have shown 2 distinct subpopulations of neurons within the NTS that can influence AP in opposite ways. Commissural NTS neurons located on the midline may contribute to maintenance of hypertension in spontaneously hypertensive rats (SHR), because small lesions in this area result in a very significant reduction in AP. Also involved in this blood pressure regulation network are 2 distinct regions of the ventrolateral medulla: caudal (CVLM) and rostral (RVLM). Neurons in CVLM are thought to receive baroreceptor input and to relay rostrally to control the activity of the RVLM. Projections from CVLM to RVLM are inhibitory, and a lack of their activity may contribute to development of hypertension. The RVLM is critical to the tonic and reflexive regulation of AP. In different experimental models of hypertension, RVLM neurons receive significantly more excitatory inputs. This results in enhanced sympathetic neuronal activity, which is essential for the development and maintenance of the hypertension. Key Words: brain Ⅲ chemoreceptors Ⅲ homeostasis Ⅲ hypertension, experimental Ⅲ sympathetic nervous system Ⅲ nitric oxide Ⅲ angiotensin Ⅲ sympathectomy E ssential hypertension is one of the most common disorders affecting human health. That the sympathetic nervous system participates in control of arterial pressure is indisputable; the controversy regards its role in the pathogenesis of human hypertension. Over the past decade, there has been an increasing awareness that the central nervous system (CNS) has a critical role in the development and maintenance of elevated arterial pressure. Presently, it seems clear that in both clinical and experimental hypertension, an increased vascular resistance to flow is an essential ingredient of the disorder. We could say, narrowing down the problem, that the disagreement rests on the answer to a simple question: which comes first, the neural or the humoral factor? Certainly this controversy is not going to finish here, but our purpose is to show how recent experimental data have put a re-emphasis on the neural factor and, by consequence, on the sympathetic nervous system, in particular the medulla oblongata.Re-emphasis is indeed the correct word, because in the 1930s the treatment for serious hypertension was mainly surgical, not clinical, and the approach was interruption of the splanchnic nerves. By the beginning of the 1940s, 2 approaches had been developed to remove the sympathetic chain, one by Keith Grimson 1 and another, less radical, by Reginald Smithwick. 2 These s...

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The aim of the present study was to examine the participation of the rostral ventrolateral medulla (RVLM) in the maintenance of hypertension in rats submitted to the renovascular Goldblatt (two-kidney, one clip) procedure. We inhibited or stimulated this area with the use of drugs such as glycine, L-glutamate, or kynurenic acid. (1) Bilateral microinjection of glycine (100 nmol, 200 nL, n = 13) into the RVLM of hypertensive rats produced a decrease in mean arterial blood pressure (MAP) from 177.2 +/- 29.3 to 102.3 +/- 20.9 mm Hg (P < .05), which was similar to the decrease produced by intravenous administration of hexamethonium. The inhibition of RVLM with glycine in normotensive rats produced a decrease in MAP from 106 +/- 17.1 to 59.7 +/- 7.3 mm Hg (P < .05, n = 9). (2) An impressive increase in MAP from 153.3 +/- 16.3 to 228 +/- 34.9 mm Hg (P < .05) occurred in hypertensive rats after microinjection of L-glutamate (50 nmol, 200 nL, n = 6) into the RVLM. The same procedure caused a significant but less intense increase in MAP from 105 +/- 13.8 to 148.3 +/- 24.9 mm Hg in normotensive rats (P < .05, n = 6). (3) A decrease in MAP from 151.6 +/- 25.3 to 96.8 +/- 22.5 mm Hg occurred in hypertensive rats after microinjection of the broad-spectrum glutamate antagonist kynurenic acid (4 nmol, 200 nL, n = 6) into the RVLM, whereas the same procedure did not change MAP in normotensive animals (n = 6). Heart rate was not significantly affected in any group.(ABSTRACT TRUNCATED AT 250 WORDS)

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