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The cardiac hypertrophy observed in hypertension is thought to be responsible for the accompanying deficiency in the baroreflex control of heart rate. In this study, we assessed the baroreflex relationship between heart rate and arterial pressure on a group of seven rabbits during a normotensive period, during the early phase of angiotensin II (Ang II)-induced hypertension II week) (50 ng/kg per minute i.v. via osmotic minipumps), after 7 weeks of continuous hypertension, then 2 days after Ang II was stopped, and finally 7 days after Ang II. Left ventricles were weighed for measurement of left ventricular weight-body weight ratio. One week of intravenous Ang II infusion produced hypertension (mean arterial pressure from 80 +/- 2 up to 115 +/- 8 mm Hg), with significantly increased heart rate and hematocrit. The heart rate-arterial pressure baroreflex curve was shifted to the right, with a significant 45% reduction in the gain of the reflex (-6.4 +/- 1.5 to -3.5 +/- 0.2 beats per minute/mm Hg). After 7 weeks of Ang II, arterial pressure was still elevated (112 +/- 4 mm Hg) and the gain of the baroreflex curve still somewhat attenuated, although it was no longer markedly different from normotensive levels (gain, -5.09 +/- 0.95, 20% reduction from normotensive level). Two days after the Ang II infusion was stopped, arterial pressure had returned to normotensive levels, although hematocrit and heart rate remained elevated. At this time, the baroreflex curve was similar to prehypertensive control levels, with no further changes when measured again 7 days after Ang II. Cardiac hypertrophy was present when measured at 7 days after angiotensin (left ventricular weight-body weight ratio: 1.78 +/- 0.05 versus 1.35 +/- 0.04 g/kg, hypertensive versus normotensive, P < .05). Thus, although Ang II infusion produced an initial deficit in the baroreflex control of heart rate, this effect became less as the hypertension continued. Furthermore, although cardiac hypertrophy developed, its presence did not appear to be sufficient to produce a decrease in barosensitivity independent of raised arterial pressure. 相似文献
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MJ Tebbe WA Spitzer F Victor SC Miller CC Lee TR Sattelberg E McKinney JC Tang 《Canadian Metallurgical Quarterly》1997,40(24):3937-3946
In an effort to find an orally bioavailable antiviral for the treatment of rhino/enteroviral infections, a series of vinylacetylene benzimidazoles (11a-o, 12, and 18a) was made. Initial studies of this class of antivirals showed that fluorine substitution on the left-hand phenyl ring in combination with the vinylacetylene moiety gave the requisite mix of physical properties to achieve good in vitro antiviral activity as well as respectable oral bioavailability in rhesus monkeys. To ascertain the generality of this finding and to broaden the scope of the structure-activity relationship (SAR), the present study concentrated on fluoro substitution of this class of molecules. The initial antiviral activity for each analogue was measured using human rhinovirus 14 (HRV-14). This served as an indicator of general antiviral activity for SAR purposes. Subsequently, the spectrum of antirhino/enteroviral activity of the more interesting analogues was evaluated through testing against a panel of seven additional rhino/enteroviruses. Broad-spectrum activity was present and consistent for all analogues tested, and it tracked closely with the antiviral activity observed against HRV-14. A simple screening protocol for oral bioavailability was established whereby compounds were administered orally to mice and plasma levels were measured. This procedure facilitated the evaluation of numerous analogues in a rapid manner. The Cmax was used as a measure of oral bioavailability to allow relative ranking of compounds. In general, fluorine substitution directly on the left-hand aromatic ring does give good oral blood levels. However, fluorine incorporation at other positions in the molecule was not as effective at maintaining either the activity or the oral plasma levels. The constructive combination of activity and oral plasma levels was maximized in three derivatives: 11a,e,g. 相似文献
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The susceptibility of 46 pneumococcal isolates collected during October 1989 to May 1995 from National Taiwan University Hospital and Taipei Municipal Yang Ming Hospital was studied. Among these isolates, the resistant rate of penicillin G was 21.7%; the penicillin G-resistant strains were more frequently resistant than the penicillin-sensitive strains to other beta-lactam antimicrobial drugs. The minimum bactericidal concentrations (MBCs) of penicillin G for all isolates were equal to, or one dilution higher than, minimum inhibitory concentrations (MICs). Three strains were false positive for penicillin resistance among isolates of Streptococcus pneumoniae screened with oxacillin. On the other hand, resistance to penicillin G was often independent of resistance to erythromycin. Vancomycin was the most active agent tested. 相似文献
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M Ferrer KL Godbout BJ Sullivan DA Austen CT Sanderson KC Kelley MS Osburne SC Harrison MR van Schravendijk 《Canadian Metallurgical Quarterly》1997,210(2):215-225
Drug-selected intrachromosomal gene amplification by breakage-fusion-bridge (BFB) cycles is well documented in mammalian cells, but factors governing this mechanism are not clear. Here, we show that only some clastogenic drugs induce drug resistance through intrachromosomal amplification. We strictly correlate triggering of BFB cycles to induction of fragile site expression. We demonstrate a dual role for fragile sites in intrachromosomal amplification: a site telomeric to the selected gene is involved in initiation, while a centromeric site defines the size and organization of early amplified units. The positions of fragile sites relative to boundaries of amplicons found in human cancers support the hypothesis that fragile sites play a key role in the amplification of at least some oncogenes during tumor progression. 相似文献
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