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Biomedical subjects

J Smeda

Publications and source records attributed to J Smeda.

5 recordsLinked to original sources
PubMed1999

Effect of poststroke captopril treatment on mortality associated with hemorrhagic stroke in stroke-prone rats.

We tested the ability of captopril treatment (50 mg/kg/day p.o.), initiated 2 weeks before stroke or up to 5 days after stroke, to alter the onset of stroke and death after stroke in Kyoto Wistar stroke-prone spontaneously hypertensive rats (SHRsp). The benefits of blood pressure and aldosterone suppression during captopril treatment were assessed. SHRsp developed a 100% mortality rate with intracerebral hemorrhage by 16 weeks of age. Captopril treatment, started 2 weeks before or at the initiation of stroke, suppressed plasma aldosterone and equally prevented mortality to a mean age of >27 weeks. Treatment started 5 days after stroke extended the mean lifespan to >23 weeks. The re-elevation of plasma aldosterone (via osmotic pumps to levels in untreated SHRsp) during captopril treatment, before stroke, allowed stroke to develop. The initiation of the latter manipulation in pre- or poststroke captopril-treated SHRsp at a latter age (23 weeks) didn't alter the lifespan of SHRsp (death occurred at about 28 weeks). The antistroke effects of captopril treatment occurred without an antihypertensive effect, weren't altered by enhancing hypertension during treatment (with dexamethasone), and couldn't be duplicated by antihypertensive treatment with hydralazine. Spironolactone treatment didn't duplicate the effects of captopril. The suppression of plasma aldosterone may retard the onset of stroke in SHRsp during captopril treatment but likely other factors prolong life in pre- and poststroke SHRsp receiving long-term captopril treatment. The observation that spironolactone treatment couldn't duplicate the effects of captopril suggests that aldosterone may facilitate stroke through nongenomic receptor mechanisms.

Aldosterone↗
PubMed1986

Effect of reduced oxygen availability upon myogenic depolarization and contraction of cat middle cerebral artery.

The goal of this study was to determine whether electrophysiological mechanisms contribute to the relaxation of cat middle cerebral artery in response to decreased ambient Po2 and whether decreased Po2 alters the myogenic depolarization and contraction of this vessel in response to elevations in transmural pressure. In one series of experiments, arterial segments (200-500 micron outer diameter) were isolated and mounted in an in vitro tension transducer to allow continuous measurement of active tension as bath Po2 was reduced. In these experiments, vessel relaxation occurred primarily between 150 mm Hg Po2 and 40 mm Hg Po2, suggesting that cerebral arteries are sensitive to alterations of Po2 in the physiological range. Relaxation did not result from the activation of dilator nerves in the vessel wall, since it was unaffected by tetrodotoxin. Arterial segments were also cannulated with micropipettes and subjected to elevations in transmural pressure during 300 mm Hg Po2 and 50 mm Hg Po2 superfusion. During 300 mm Hg Po2 superfusion, cannulated vessels exhibited myogenic depolarization and maintained their diameter as transmural pressure was increased; 50 mm Hg Po2 superfusion inhibited spontaneous spike activity, decreased the slope of the myogenic depolarization, and partially inhibited vessel contraction in response to elevated transmural pressure. These effects are independent of the parenchymal cell environment and appear to be mediated, at least in part, by electrophysiological mechanisms.

Animals↗
PubMed1985

Enhanced myogenic depolarization in hypertensive cerebral arterial muscle.

We have previously demonstrated pressure-dependent membrane depolarization and action potential generation in cat cerebral arteries. It was the purpose of this study to examine and compare the membrane electrical responses to increasing transmural pressure in spontaneously hypertensive rats with those of their normotensive Wistar-Kyoto controls. It was found that at transmural pressures from 40-160 mm Hg, spontaneously hypertensive rat cerebral arterial muscle depolarized more than normotensive counterparts. Pressure-induced action potentials could be recorded from arterial segments from both animal strains; however, the amplitude and upstroke velocity was significantly greater in spontaneously hypertensive rat cerebral arterial muscle. These data suggest that there are altered ionic permeabilities in spontaneously hypertensive rat cerebral arterial muscle which result in enhanced response to increasing transmural pressure. The implications of these findings are discussed.

Action Potentials↗
PubMed1984

Early structural changes in precapillary vessels in hypertension and their relationship to functional changes.

This presentation has reviewed evidence from our laboratory that both structural and functional changes participate in the initiation and maintenance of hypertension in spontaneously hypertensive rats (SHR). Structural changes are present in the muscular arteries of the mesenteric and renal vasculature at 3- to 5-week-old SHR as compared with WKY. The major structural change in SHR arteries was increased cross-section area with increased thickness of the media owing to hyperplasia of smooth muscle; lumen sizes were interchanged. Later, at 10-12, 21, and 28 weeks of age, there was further increase in medial thickness owing to hyperplasia, and some hypertrophy and changes in elastic arteries also became evident. Increases in medial thickness of elastic arteries included hypertrophy as well as hyperplasia. Changes in lumen diameter were never observed in arteries fixed in a relaxed state at physiological flow rates. In addition, a deficit in Ca handling (decreased ATP-dependent Ca2+ accumulation) was observed in plasma-membrane vesicles from mesenteric arteries of SHR prior to and after the development of hypertension. It persisted when hypertension was reversed by hydralazine in SHR. It was present in various forms of experimental hypertension. It was present whenever hypertension was present and disappeared with normalization of blood pressure by withdrawal of the stimulus. The Ca-handling deficit was found in several nonarterial tissues and may be a generalized genetic defect in SHR. It was always accompanied by increased alkaline phosphatase activity of plasma membranes, and this was suggested to reflect the smooth-muscle hyperplasia occurring simultaneously. A model of the initiation and maintenance of hypertension based on medial thickening and deficient Ca handling as primary, interacting causes of genetic hypertension is proposed.

Animals↗