A person recovered from a moderate degree of haemorrhagic shock. The participating physiological mechanisms in this recovery process are proposed in following statements.

A. The decrease in arterial pressure after haemorrhage causes inhibition of sympatic-vasoconstrictor system.

B. After haemorrhage, angiotensin II level in blood is increased which causes increased re-absorption of Na⁺ in renal tubules.

C. The increased secretion of vasopressin after haemorrhage increases water.

D. After haemorrhage, reduced secretion of epinephrine and nor-epinephrine from adrenal medulla induces decreased peripheral resistance.

E. In haemorrhage, central nervous system ischemic response elicits sympatic inhibition.

Choose one of following combinations with both correct statements.

The correct answer is Option 2 i.e. B and C

Explanation:-

A. The decrease in arterial pressure after hemorrhage causes inhibition of sympathetic-vasoconstrictor system.

• Incorrect. The decrease in arterial pressure after hemorrhage would actually stimulate the sympathetic-vasoconstrictor system, leading to vasoconstriction in an attempt to increase arterial pressure and maintain perfusion of vital organs.

B. After hemorrhage, the angiotensin II level in blood is increased which causes increased re-absorption of Na⁺ in renal tubules.

• Correct. Hemorrhage leads to a reduction in blood volume and blood pressure, which can stimulate the renin-angiotensin-aldosterone system. The increased production of angiotensin II promotes renal reabsorption of Na⁺, helping to retain water (via osmosis) and increase blood volume.

C. The increased secretion of vasopressin after hemorrhage increases water reabsorption in the kidneys.

• Correct. Vasopressin (antidiuretic hormone or ADH) secretion increases in response to a decrease in blood volume or blood pressure to enhance water reabsorption in the kidneys, effectively concentrating the urine and expanding the circulating blood volume.

D. After hemorrhage, the reduced secretion of epinephrine and norepinephrine from the adrenal medulla induces decreased peripheral resistance.

• Incorrect. The opposite occurs; after hemorrhage, there's an increased secretion of epinephrine and norepinephrine from the adrenal medulla, which contributes to increasing peripheral resistance (via vasoconstriction) and cardiac output, as part of the body's compensatory response to maintain blood pressure and perfusion.

E. In hemorrhage, the central nervous system ischemic response elicits sympathetic inhibition.

• Incorrect. The central nervous system ischemic response, triggered by significantly reduced cerebral perfusion, actually results in a potent activation (not inhibition) of the sympathetic nervous system to maximize blood flow to critical organs, particularly the brain and heart, by increasing heart rate, contractility, and peripheral vasoconstriction.

Additional InformationB. Angiotensin II and Renal Reabsorption of Sodium
Following hemorrhage, the body experiences a decline in blood volume and blood pressure. This reduction is sensed by the juxtaglomerular cells of the kidneys, which respond by releasing renin into the bloodstream. Renin acts on angiotensinogen (produced by the liver) to produce angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE), primarily in the capillaries of the lungs.Angiotensin II has several crucial effects aimed at restoring blood volume and pressure:

• Vasoconstriction: It directly causes constriction of small arteries (arterioles), increasing systemic vascular resistance and blood pressure.
• Stimulation of Aldosterone Secretion: Angiotensin II stimulates the adrenal cortex to release aldosterone, a hormone that increases sodium reabsorption in the distal nephrons of the kidneys. As sodium is reabsorbed, water follows (due to osmotic forces), leading to increased retention of water, expanding blood volume, and improving circulatory status.
• Thirst Stimulation: Angiotensin II can stimulate the thirst center in the brain, prompting water intake to further aid in restoring blood volume.

C. Increased secretion of Vasopressin (Antidiuretic Hormone, ADH)
Vasopressin plays a pivotal role in the body’s response to hemorrhage. Its primary functions include:

• Water Reabsorption in the Kidneys: Vasopressin increases the permeability of the kidney's collecting ducts to water, enhancing water reabsorption back into the bloodstream, which helps to concentrate the urine and minimize water loss, thereby conserving blood volume.
• Vasoconstriction: At high concentrations, vasopressin can cause vasoconstriction, which also helps in increasing blood pressure.
• Vasopressin is released in response to increased plasma osmolality (such as would be caused by the loss of blood volume), as well as low blood pressure sensed by baroreceptors. Its secretion following hemorrhage supports the body's efforts to conserve water and reinforce blood volume, while also contributing to the restoration of vascular tone.

Conclusion:

The body's response to hemorrhagic shock involves intricate physiological mechanisms aimed at compensating for the loss of blood volume and restoring hemodynamic stability. These mechanisms include hormonal responses that reabsorb water, retain sodium, and increase vascular resistance. Angiotensin II and vasopressin are key players in these compensatory responses, orchestrating renal adjustments, stimulating thirst, and contributing to vasoconstriction to support the recovery process. Such integrated bodily responses are critical for survival in the face of acute blood loss. Therefore, the correct combination of statements regarding the recovery from hemorrhagic shock is: B and C.