Introduction: The underlying mechanism responsible for the cardiovascular response to hemorrhage (HEM) is still unknown; however, several brain areas, such as the cuneiform nucleus (CnF) have shown to be involved. In this study, the cardiovascular effect of the CnF during HEM was evaluated.
Methods: The animals were divided into the following groups: 1. Vehicle; 2. HEM; 3. Cobalt chloride (CoCl2); 4. CoCl2+saline; and 5. CoCl2+HEM. Catheterization of the left and right femoral artery was performed to record blood pressure and blood withdrawal, respectively. Saline and CoCl2 were microinjected into the CnF nucleus, and then blood withdrawal was done for HEM induction. Cardiovascular regulation throughout the experiments was recorded and changes (∆) in the Systolic Blood Pressure (SBP), Mean Arterial Pressure (MAP) and Heart Rate (HR) were calculated over time and compared with those treated with saline and HEM, using repeated-measures ANOVA. 
Results: HEM significantly reduced ∆SBP and ∆MAP and augmented ∆HR than the vehicle group. CoCl2 did not significantly affect basic ∆SBP, ∆MAP, and ∆HR compared with the vehicle group. However, injection of CoCl2 into the CnF before HEM (CoCl2+HEM group) significantly decreased ∆SBP, ∆MAP, and tachycardia, induced by HEM. 
Conclusion: Our results indicated that blockade of the CnF by CoCl2 significantly reduced the hypotension and tachycardia, induced by HEM indicating the involvement of CnF in cardiovascular regulation during HEM. 

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