Defense reaction alters the response to blood loss in the conscious rabbit

By: James C. Schadt and Eileen M. Hasser (Am J Physiol Regulatory Integrative Comp Physiol
280: R985–R993, 2001.)

When blood loss occurs, mammals respond to this in two different phases. The first phase is a sympathoexcitatory phase where sympathetic nerve activity (SNA) and blood pressure (BP) increase to compensate. This occurs through the baroreflex, which senses the changes. The second phase of blood loss is the sympathoinhibitory phase, where BP and SNA fall below critical levels and not able to compensate for the blood loss. The purpose of the study is examine the response to blood loss when the defense reaction (fight or flight, i.e. increase BP, HR, and skeletal muscle blood flow) is activated. The study hypothesized that exposure to air jet would lower the rabbits ability to maintain BP during blood loss.

31 rabbits are used in this study. To start the sensory stimulation, air or no stimulation occurred (sham). To induce blood loss, blood was removed at a rate of 8-9 ml/min. The end point of hemorrhage was 5ml after BP reached 40 mmHg. Blood was reinfused at the end of the experiment.

Following the experiments, results showed that air increased BP and HR in both groups. Pressor responses caused an increase in hindquarters blood flow and decrease in mesenteric blood flow. Also, there was a decrease, followed by an increase of renal flow, combined with an increase in cardiac output. In the presence of air, rabbits were better able to defend BP. A greater blood loss was needed to cause a decrease in mean arterial pressure and HR.

The results of the study showed that air jet stimulation extended defense of arterial BP. This was the opposite of what was hypothesized. When a hemorrhage occurs, it usually coincides with stress responses. The data showed that as stressors become greater, it tends to defend the BP more during hemorrhage. Of course, there is still a critical point where the inhibitory phase kicks in and the body cannot compensate any longer. The mechanism by which stressors defend BP is not known. My guess would be an increase in NE and EPI due to the activation of the sympathetic nervous system causes vasoconstriction to occur at a longer rate. Could be more neurotransmitter release or slower breakdown.

This study shows how vital the sympathetic nervous system is to sustaining BP during hemorrhage. The contribution is already high, but when stressors are introduced, it gets even greater. In our lab, we study the SNA that the RVLM contributes too. We can also use the process of blood loss to see how the RVLM compensates to keep BP and HR from falling.

-Tsetse Fly