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Mohebbati R, Hosseini M, Khazaei M, Khajavirad A, Shafei M N. The Effects of Inactivation of Pedunculopontine Tegmental Nucleus by Cobalt (II) Chloride on Cardiovascular Responses in Hemorrhagic Hypotensive Rats. BCN 2019; 10 (3) :235-244
URL: http://bcn.iums.ac.ir/article-1-1081-fa.html

Introduction: Based on the evidence, the Pedunculopontine Tegmental nucleus (PPT) is involved in cardiovascular function regulation. In this study, the probable role of PPT on cardiovascular parameters in the hypotension induced by Hemorrhage (HEM) was evaluated. 
Methods: The study rats were divided up into 5 groups: 1. Control (Saline); 2. Cobalt(II) chloride (CoCl2); 3. HEM; 4. Saline+HEM; and 5. CoCl2+HEM. Their right and left femoral arteries were cannulated for recording the cardiovascular responses and blood withdrawal, respectively. Saline and CoCl2 were microinjected into the PPT using the stereotaxic apparatus. Maximum changes of Systolic Blood Pressure (SBP), Mean Arterial Pressure (MAP), and the Heart Rate (HR) after the microinjection of CoCl2 in normal and Hemorrhage conditions were recorded. Changes of SBP, MAP, and HR were calculated over time at 5-min intervals and compared with those of the control and HEM groups using repeated measures ANOVA. The Independent sample t-test was used to compare the changes in cardiovascular parameters between the control and HEM groups at 0 and 20 min after Hemorrhage. 
Results: The changes in SBP, MAP, and HR in the CoCl2 group were not significantly different from those in the control group. In the HEM group, the SBP and MAP changes significantly decreased (P<0.001) and HR changes significantly increased (P<0.001) compared to those parameters in the control group. In the CoCl2+HEM group, SBP and MAP changes were significantly attenuated compared to those in the HEM group (P<0.05) and HR changes induced by Hemorrhage decreased compared to that in the HEM group (P<0.01).
Conclusion: Our results indicate that the PPT has no effects on normal cardiovascular parameters. However, it could modulate cardiovascular responses induced by Hemorrhage.