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251.
The purpose of the present study was to elucidate if rats with myocardial infarction manifest altered responsiveness to central cardiovascular effects of low doses of angiotensin II (ANG II), and if ANG II and vasopressin (VP) cooperate in the central regulation of cardiovascular functions at rest and during stress. Conscious Sprague-Dawley rats with myocardial infarction induced by left coronary artery ligation, or sham-ligated (SL) controls were infused intracerebroventricularly with artificial cerebrospinal fluid (aCSF), ANG II, ANG II + VP or ANG II + V1a receptor antagonist (V1ANT) 4 weeks after cardiac surgery. In the infarcted but not in the SL rats, the resting mean arterial blood pressure (MABP) was significantly elevated by infusions of ANG II and ANG II + VP, while infusion of ANG II + V1ANT was not effective. During administration of aCSF, the pressor, and tachycardic responses to an air-jet stressor were significantly greater in the infarcted than in the SL rats. In the SL rats, the pressor responses to the stressor were significantly greater during infusions of ANG II, ANG II + VP and ANG II + V1ANT than during infusion of aCSF. The tachycardic response in the SL rats was enhanced only by the combined infusion of ANG II + VP. In the infarcted rats, the pressor and the tachycardic responses to the stressor were similar in all groups. It is concluded that: (1) under resting conditions the infarcted rats manifest sensitisation to the central pressor effect of ANG II and that this effect depends on concomitant stimulation of V1a VP receptors, (2) central ANG II may enhance the pressor response to an alarming stressor in the SL rats through an action which does not depend on the concomitant stimulation of V1a receptors, (3) the cooperative action of ANG II and VP is required for intensification of the tachycardic response to the alarming stressor in the SL rats and (4) exaggeration of the cardiovascular responses to the alarming stressor in the infarcted rats cannot be further augmented by an additional stimulation of central ANG II receptors or combined stimulation of ANG II and VP receptors.  相似文献   
252.
The paper analyzes the philosophical consequences of the recent discovery of direct violations of the time–reversal symmetry of weak interactions. It shows that although we have here an important case of the time asymmetry of one of the fundamental physical forces which could have had a great impact on the form of our world with an excess of matter over antimatter, this asymmetry cannot be treated as the asymmetry of time itself but rather as an asymmetry of some specific physical process in time. The paper also analyzes the consequences of the new discovery for the general problem of the possible connections between direction (arrow) of time and time-asymmetric laws of nature. These problems are analyzed in the context of Horwich’s Asymmetries in time: problems in the philosophy of science (1987) argumentation, trying to show that existence of a time–asymmetric law of nature is a sufficient condition for time to be anisotropic. Instead of Horwich’s sufficient condition for anisotropy of time, it is stressed that for a theory of asymmetry of time to be acceptable it should explain all fundamental time asymmetries: the asymmetry of traces, the asymmetry of causation (which holds although the electrodynamic, strong and gravitational interactions are invariant under time reversal), and the asymmetry between the fixed past and open future. It is so because the problem of the direction of time has originated from our attempts to understand these asymmetries and every plausible theory of the direction of time should explain them.  相似文献   
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