PubMed · 4956360
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A S Hall, A L Knezevic. 1965-11-15. Bone marrow sampling in monkeys.. https://pubmed.ncbi.nlm.nih.gov/4956360/
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This study examined the effect of intrathecal (i.t.) injection of the endocannabinoid anandamide in urethane-anesthetized rats. The tip of the i.t. cannula was positioned at the T(12)-L(1) level of the spinal cord. Either anandamide or its metabolically stable analogue methanandamide (25 to 100 nmol) produced dose-dependent decreases in the blood pressure that persisted at least for up to 30 min. The hypotensive responses to 100 nmol anandamide and to 100 nmol methanandamide were -17.7+/-1.6 mmHg ( n=5) and -17.9+/-2.0 mmHg ( n=4), respectively. Hypotensive effects were also obtained with the CB(1) cannabinoid receptor agonist WIN 55212-2 (20 nmol; i.t.) as well as with the vanilloid VR(1) receptor agonist capsaicin (3 nmol; i.t.). Nicotinic ganglionic blockade with hexamethonium bromide [10 mg/kg; intravenous(i.v.)] abolished the responses to both anandamide and capsaicin. The i.t. administration of the CB(1) receptor antagonist, 20 nmol SR 141716A, as well as the VR(1) receptor antagonist, 20 nmol capsazepine, prevented almost completely the hypotensive responses to both anandamide and methanandamide. SR 141716A prevented the hypotension caused by WIN 55212-2 but did not modify the response to the vanilloid receptor agonist capsaicin. On the contrary, capsazepine antagonized the hypotension caused by capsaicin but failed to affect the decrease in blood pressure caused by the CB1 cannabinoid receptor agonist WIN 55212-2. These results suggest that anandamide could modulate the blood pressure through the activation of cannabinoid CB(1) receptors and vanilloid VR(1) receptors localized at the spinal cord.
Fast oscillations in the beta (15-40 Hz in awake rats) and gamma (50-100 Hz) frequency ranges are prominent in field potentials induced by odorants in the mammalian olfactory bulb (OB) and piriform cortex (PC). Whereas the gamma oscillation has been studied for >50 yr, the beta oscillation has attracted attention only recently, and its origin, mechanism, and relationship to gamma are unknown. To address these questions, we have examined responses induced by odorants in the urethane-anesthetized rat-a preparation well-suited for the analysis of mechanisms. We found that both oscillations could be induced by odorants in a concentration-dependent manner. Analysis with a concentration series and spectral methods revealed that the beta and gamma oscillations were distinct and not harmonically related, indicating generation by independent mechanisms. The beta oscillation was synchronous at sites < or =4 mm apart in the OB, the greatest distance tested. In contrast, the gamma oscillation was synchronous in some experiments and asynchronous in others (frequency differed slightly at different sites, resulting in progressive phase shifts). Current source-density analysis indicated that, for both oscillations, the field potentials in the OB were generated by synaptic currents in granule cells. The two oscillations were differently affected by surgical interruption of the lateral olfactory tract. This lesion abolished the beta oscillation, whereas the gamma oscillation was still induced in the OB. Our results confirm previous reports that the gamma oscillation is generated within the OB but indicate that the beta oscillation requires the participation of PC.
OBJECTIVE: To compare the effects of infusions of adrenaline, noradrenaline and dopamine on cerebral autoregulation under steady-state propofol anaesthesia with the awake state. DESIGN: Prospective, randomised, interventional animal study. SETTING: University laboratory. SUBJECTS: Six studies in two cohorts of adult ewes: awake and steady-state propofol anaesthesia (15 mg/min). INTERVENTIONS: In random order, each animal received ramped infusions of adrenaline, noradrenaline (0-40 microg/min) and dopamine (0-40 microg/kg per min). MEASUREMENTS AND RESULTS: Cerebral blood flow (CBF) was measured continuously from changes in Doppler velocities in the sagittal sinus and normalised to a PaCO(2) 35 mmHg. Propofol decreased CBF by 55% relative to pre-anaesthesia values (p=0.0001). All three catecholamines significantly and equivalently increased mean arterial pressure (MAP) from baseline in a dose-dependent manner in both awake and propofol cohorts. Adrenaline significantly increased CBF from baseline in both awake sheep (p<0.01) and during propofol anaesthesia (p<0.001); noradrenaline and dopamine did not statistically increase CBF. When comparing the effects of individual catecholamines with each other within each cohort, no statistically significant difference between the catecholamines was demonstrated. (p>0.05). Using linear regression analysis, normalised CBF was correlated against associated changes in MAP. No significant differences were demonstrated between the slopes of regression lines for adrenaline, noradrenaline and dopamine in either cohort (ANCOVA). There was a statistically significant difference between the intercepts of the awake and propofol cohorts (p<0.0001), but no difference between the slopes (p=0.69). CONCLUSIONS: Over a specific dose range, catecholamine-induced hypertension caused increased CBF during steady-state propofol anaesthesia. This effect was offset by an associated reduction in CBF caused by propofol. The concomitant administration of propofol and catecholamines was not associated with altered autoregulatory function compared to the awake state.