Table 1.
Baseline physiological parameters in the different in vivo experimental groups.
Figure 1.
NO synthase blockade increases mean arterial pressure (MAP), while decreases heart rate (HR) and cerebrocortical blood flow (CoBF).
Mean ± SEM percentual changes are shown after NO synthase inhibition by 100 mg/kg of L-NAME, compared to the steady state pre-injection values presented on Table 1 (n = 10, 6 and 7 in the case of MAP and HR, and n = 20, 12 and 14 in the case of CoBF in Groups IIa., IIb. and IIc., respectively).
Figure 2.
Weak activation of thromboxane receptors aggravates while inhibition of TXA2 synthesis attenuates CoBF oscillations developed in the absence of NO.
A–C: Original recordings of the cerebrocortical laser-Doppler flux in vivo before (left panels) and after (right panels) administration of the TP-receptor agonist U-46619 (A), the thromboxane synthase inhibitor ozagrel (C) or their vehicle (saline) (B) in rats pretreated by the NO synthase inhibitor L-NAME. D: Quantitative analysis of slow wave oscillations with discrete Fourier transformation. The peak magnitudes of the power spectra are compared before and after treatments in the three experimental groups. Values are mean ± SEM (n = 20, 12 and 14 in Group IIa, IIb, and IIc, respectively) *p<0.05 vs. “Before Treatment”.
Figure 3.
Activation of thromboxane or endothelin receptors induce Rho-kinase dependent vasomotion in NO synthase blocked MCAs.
Quantitative analysis of slow wave oscillations with discrete Fourier transformation in L-NAME treated vessels before and after the administration of the TP-receptor agonist U-46619 (Panel A) or endothelin-1 (Panel B) followed by the Rho-kinase inhibitor Y-27632. Values are mean ± SEM fold changes of the peak magnitudes of the power spectra compared to the baseline. *p<0.05, ***p<0.001 vs. L-NAME, ##<0.01 vs. ET-1 and ###<0.001 vs. U-46619 (n = 10–20).