Cardiovascular Effect of Cuneiform Nucleus During Hemorrhagic Hypotension
Related Experiment Video
Updated: Dec 8, 2025

Standardized Hemorrhagic Shock Induction Guided by Cerebral Oximetry and Extended Hemodynamic Monitoring in Pigs
Published on: May 21, 2019
Reza Mohebbati1, Mahmoud Hosseini2, Majid Khazaei1
1Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Insights
Blockading the Cuneiform nucleus (CnF) with cobalt chloride (CoCl2) significantly reduced hypotension and tachycardia during hemorrhage (HEM). This suggests the CnF plays a key role in cardiovascular regulation during blood loss.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
Background:
- The precise mechanisms behind cardiovascular responses to hemorrhage remain unclear.
- The Cuneiform nucleus (CnF) is implicated in cardiovascular regulation.
- This study investigates the role of the CnF in cardiovascular responses during hemorrhage (HEM).
Purpose of the Study:
- To evaluate the cardiovascular effects of the Cuneiform nucleus (CnF) during hemorrhage (HEM).
Main Methods:
- Animals were divided into Vehicle, HEM, Cobalt chloride (CoCl2), CoCl2+saline, and CoCl2+HEM groups.
- Femoral artery catheterization was used to record blood pressure and induce HEM via blood withdrawal.
- CoCl2 or saline was microinjected into the CnF, and cardiovascular parameters (SBP, MAP, HR) were analyzed.
Main Results:
- Hemorrhage (HEM) significantly decreased systolic blood pressure (SBP) and mean arterial pressure (MAP), while increasing heart rate (HR).
- Microinjection of CoCl2 into the CnF before HEM significantly attenuated the reduction in SBP and MAP, and also reduced tachycardia.
- CoCl2 alone did not significantly alter baseline cardiovascular parameters.
Conclusions:
- Blockade of the Cuneiform nucleus (CnF) using CoCl2 significantly mitigates hypotension and tachycardia induced by hemorrhage (HEM).
- These findings highlight the involvement of the CnF in cardiovascular regulation during HEM.
- The CnF represents a potential therapeutic target for managing cardiovascular dysfunction during hemorrhage.
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 (Δ) 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 ΔSBP and ΔMAP and augmented ΔHR than the vehicle group. CoCl2 did not significantly affect basic ΔSBP, ΔMAP, and ΔHR compared with the vehicle group. However, injection of CoCl2 into the CnF before HEM (CoCl2+HEM group) significantly decreased ΔSBP, ΔMAP, 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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