Blood loss is accompanied by severe physiological changes that influence various organ systems. It is believed to result due to bleeding, also known as haemorrhaging. Haemorrhage may become risky or even fatal when it causes hypovolemia (low blood volume) or hypotension (low blood pressure). When moderate blood loss occurs, the immediate physiological change that is expected to occur is the maintenance of homeostasis by the baroreceptor reflex and renal and endocrine responses such as the renin-angiotensin – aldosterone system (RAAS). Both these processes are accomplished through a cascade of events.
Baroreceptors are meant for detecting the pressure of blood flowing through them and informing the central nervous system through messages to increase or decrease the total peripheral resistance and cardiac output. Hence, the regulation of heart rate and blood pressure is under the body’s homeostatic mechanism of the baroreflex or baroreceptor reflex. It is thought to provide a negative feedback loop in which an elevated blood pressure reflexively facilitates blood pressure to decrease.
Similarly, decreased blood pressure would depress the baroreflex, causing blood pressure to rise. This ensures the distension of the carotid and aortic sinuses and the baroreceptor activation. Therefore, the baroreceptors are better regarded as stretch-sensitive mechanoreceptors. The larger the stretch, the more rapid would be the baroreceptor fire action potential. The ultimate result of the baroreceptor activation is the inhibition of the sympathetic nervous system and activation of the parasympathetic nervous system.
The coupling action of these two branches of the autonomic nervous system has opposing effects on blood pressure. Sympathetic activation causes an elevation of total peripheral resistance and cardiac output via increased heart rate which enables increase blood pressure. While parasympathetic activation leads to a decreased cardiac output via decreased heart rate, resulting in a tendency to decrease blood pressure.
Similarly, the inhibition versus activation of these two branches would result in maximized blood pressure reduction, and depressed heart rate and contractility, respectively. The activation versus inhibition allows the baroreflex to elevate blood pressure.
Previously, it was reported that the sudden blood loss of moderate degree would cause a fall in blood pressure, which is compensated to a certain extent by baroreceptor mediated rise in heart rate and vasoconstriction (Gupta & Fahim, 2005). These workers studied the regulation of cardiovascular functions on increasing severity of blood loss in the absence of any therapeutic intervention to elucidate the mechanisms involved in the recovery of blood pressure under such conditions. Their findings suggested that 20% of blood loss is compensated by the baroreflex.
Hartikainen et al. (1990) investigated the role of aortic baroreceptors during slow haemorrhage, in particular the mechanisms by which baroreceptors would respond to hypovolaemia in the absence of hypotension and the manner in which haemodynamic information would be encoded in the aortic nerve discharge. Their results indicated that during non-hypotensive haemorrhage, aortic baroreceptor discharge is reduced by constriction and stiffening of aortic smooth muscle and direct effects of the compensatory mechanisms on the baroreceptors. They described that the reduced sensitivity would render the baroreceptors capable of responding to hypovolaemia prior to the onset of hypotension.
In another earlier report, it was described that dogs with heart failure would exhibit reduced sensitivity of aortic baroreceptors but preserved baroreflex control of renal nerve activity (Dibner-Dunlap & Thames, 1989). This report has indicated that reduced baroreceptor sensitivity with preservation of baroreflex control of sympathetic nerve activity may contribute to the sympathoexcitatory state known to exist in heart failure.
Therefore, these findings may strengthen the connection between baroreceptor flex and physiological responses through the channel of the autonomous nervous system.
Next, it is also reasonable to connect this part of the description with the renin-angiotensin – aldosterone system (RAAS) that maintains homeostasis through the renal and endocrine responses following a moderate blood loss.
The renin-angiotensin-aldosterone system (RAAS) is a hormone system that regulates blood pressure and water (fluid) balance. Whenever blood pressure gets lowered, the kidneys secrete renin which flows into the blood and stimulates the production of angiotensin. The function of angiotensin is to constrict blood vessels that lead to increased blood pressure.
Generally, RAAS is thought to get activated when there is a loss of blood volume or a drop in blood pressure as seen in haemorrhage. So, renin plays a vital role in converting angiotensinogen into angiotensin I which is later converted to the key product, angiotensin II by the angiotensin-converting enzyme (ACE). This conversion is vital for angiotensin I to exert its physiological effect on the body.
Angiotensin II constricts glomerular arterioles that result in increased arteriolar resistance raising systemic arterial blood pressure and decreasing the blood flow. But, in order to keep the blood pressure high Angiotensin II constricts efferent arterioles, which would force blood to build up in the glomerulus, increasing glomerular pressure. The glomerular filtration rate (GFR) would be finally maintained, and blood filtration could continue regardless of lowered overall kidney blood flow. Thus Angiotensin II increases blood pressure by contracting arterial muscles.
Secondly, angiotensin also stimulates the secretion of the hormone aldosterone from the adrenal cortex. Aldosterone facilitates the tubules of the kidneys to retain sodium and water. This would increase the volume of fluid in the body, which also increases blood pressure. Blood pressure will get elevated largely if the RAAS is too active. Individuals with moderate blood loss may also be prone to thirst. This may be due to RAAS induced aldosterone action on the central nervous system.
Further, it is also reasonable to consider the influence of RAAS on acute haemorrhage for a better understanding of the physiological responses. Earlier workers studied the effect of acute haemorrhage on hemodynamics and the RAAS in eight anaesthetized dogs (Michailov et al., 1987).
Their findings demonstrated that the high sensitivity and prompt activation of RAAS are required for the blood loss and further described that RAAS is involved in regulating the mechanisms of hemodynamics during acute graded haemorrhage (Michailov et al., 1987). There were previously some discrepancies regarding the role of prostaglandins and renin-angiotensin systems on blood pressure and renal function. To this end, their interactions were studied in conscious rabbits following mild or moderate haemorrhage (Golub et al., 1981).
It was revealed that experimental inhibition of prostaglandin lowered basal plasma renin levels (PRA) levels but that the renin response to haemorrhage and renin-angiotensin converting enzyme inhibitor was not prevented, suggesting that prostaglandins do not play a major role in this effect. They described that the magnitude of the hemorrhagic stress would influence the renal responses to inhibition of the prostaglandin or renin-angiotensin systems in the conscious rabbit.
Paul et al. (2006) emphasized the role of RAAS in the light of its new functional components and pathways. They highlighted that the inhibitors of the RAAS such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin (ANG) II receptor blockers have become important clinical tools in the treatment of cardiovascular and renal diseases such as hypertension, heart failure, and diabetic nephropathy.
Finally, the other physiological response that is reported to occur following the moderate blood loss is through the “retro-stress-relaxation” mechanism of cardiac muscle. But as the literature is sparsely available, this description is confined to highlighting only two well-known mechanisms. Therefore, the research findings have not only provided insightful information on the physiological responses but also indicated their future implications for clinical research.
References:
- Gupta, R.K., & Fahim, M. (2005). Regulation of cardiovascular functions during acute blood loss. Indian J Physiol Pharmacol, 49, 213-9.
- Hartikainen, J., Ahonen, E, Nevalainen,T., Sikanen, A, Hakumäki, M.(1990). Haemodynamic information encoded in the aortic baroreceptor discharge during haemorrhage. Acta Physiol Scand, 140, 181-9.
- Dibner-Dunlap, M.E and Thames, M.D. (1989). Baroreflex control of renal sympathetic nerve activity is preserved in heart failure despite reduced arterial baroreceptor sensitivity. Circ Res. 65, 1526-35.
- Michailov, M.L., Schad, H., Dahlheim, H., Jacob, I.C., Brechtelsbauer, H. (1987). Renin-angiotensin system responses of acute graded hemorrhage in dogs. Circ Shock, 21, 217-24.
- Golub, M.S., Berger, M.E., Sambhi, M.P., Eggena, P. (1981). Prostaglandin and angiotensin converting enzyme inhibition: effect on blood pressure, renin activity and renal function in hemorrhaged conscious rabbits. Clin Exp Hypertens, 3, 477-95.
- Paul, M., Poyan Mehr, A., Kreutz, R. (2006). Physiology of local renin-angiotensin systems. Physiol Rev, 86,747-803.
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