PubMed · 6110165
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H D Renovanz, H Rensch. 1980. [Broncholytics--a review].. https://pubmed.ncbi.nlm.nih.gov/6110165/
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The aim of the present study was to elucidate the influence of the hepatic sympathetic and parasympathetic (vagal) nerves on the hepatic blood flow (HBF), both tonically and when stimulated, using urethane-anesthetized rats as an in vivo experimental model. HBF was measured at the surface of the lateral left lobe of the liver using laser Doppler flowmetry and the hydrogen gas clearance method. Denervation of the hepatic sympathetic nerves had no influence on the HBF, while electrical stimulation of the hepatic sympathetic nerves caused the HBF to decrease in a frequency-dependent manner. This decrease was shown to occur via alpha-adrenergic receptors. In contrast, neither denervation nor electrical stimulation of the hepatic vagal nerves elicited significant changes in the HBF. These results demonstrate that the sympathetic and vagal hepatic nerves have little or no tonic influence on the HBF of rats under urethane anesthesia, whereas the HBF decreases in response to activation of the hepatic sympathetic nerves.
The action of orexin A on one-way passive avoidance learning was studied in rats. Orexin A administered into the lateral brain ventricle in conscious rats facilitated learning, the consolidation of learning and also retrieval processes in a dose-dependent manner in a passive avoidance paradigm. The involvement of transmitters was studied by pretreating the animals with receptor antagonists, which had proved to be effective with other neuropeptides in attenuating or blocking the action of orexin A. The following receptor blockers were used: haloperidol, phenoxybenzamine, propranolol, atropine, bicuculline, naloxone and nitro-L-arginine, which can block nitric oxide synthase. In the doses used all of the receptor blockers attenuated, but none of them fully blocked the action of orexin A on the consolidation of passive avoidance learning. The results demonstrate that orexin A is able to facilitate learning, consolidation of learning and also retrieval processes in a passive avoidance paradigm. A number of transmitters could be involved in the action of consolidation, but none of them is absolutely essential.
BACKGROUND: Although carvedilol attenuates left ventricular (LV) remodeling in coronary occlusion-reperfusion, it is not known whether it attenuates ischemic LV remodeling because of coronary stenosis (CS) or permanent coronary occlusion (CO). METHODS AND RESULTS: We administered a vehicle, carvedilol, propranolol (2, 10, and 30 mg/kg per day, each), metoprolol (6, 30, and 90 mg/kg per day), or bunazosin (0.2 and 1 mg/kg per day), orally for 12 weeks to a total of 608 rats with CS or CO. In these groups and the sham (n=40), we assessed LV function by echocardiography, CS severity, myocardial blood flow and coronary flow reserve, serum ascorbyl free radical, and vitamin C. Both CS and CO increased LV end-diastolic and end-systolic diameters and decreased ejection fraction. The 4 agents failed to attenuate LV remodeling caused by CO. In contrast, the 3 beta-blockers attenuated (P<0.01) or tended to attenuate the increase in LV end-diastolic diameters caused by CS. With similar blood pressure and heart rate lowering by 3 beta-blockers, carvedilol additionally attenuated the increase in end-systolic diameters and improved ejection fraction. The CS reduced myocardial blood flow and coronary flow reserve, which was reversed by carvedilol without modifying the CS severity. Among the 4 agents, only carvedilol decreased ascorbyl free radical and increased vitamin C. CONCLUSIONS: The effects of beta blockade on ischemic cardiac dysfunction seem to depend on the different properties of the beta-blockers and the doses used. Among the beta-blockers tested, carvedilol provided potent cardioprotection for compromised ischemic but viable myocardium rather than for infarcted myocardium.