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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the effects of acute myocardial infarction on the extent and distribution of systolic and diastolic wall stress on the surviving myocardium, coronary artery occlusion was produced in rats, and the animals were killed 1 wk later. After hemodynamic measurements in vivo, the characteristics of cardiac anatomy at end diastole and peak systole were mimicked in vitro by fixing hearts under diastolic conditions or barium-induced contracture. In the presence of infarcts inducing a 48% loss of myocytes, left ventricular failure was documented by increases in left ventricular minimal and end-diastolic pressures and decreases in peak systolic pressure and positive and negative rates of pressure change with time. End-diastolic and end-systolic volumes increased, whereas stroke volume and cardiac output diminished. Ventricular remodeling in diastole consisted of an increase in the longitudinal axis while both longitudinal and transverse mid-chamber diameters were augmented after systolic contraction. Left ventricular chamber volume enlarged by 44% through a 20% augmentation in the longitudinal diameter and increases in the transverse luminal diameter of 13, 21, 32, and 37% in four consecutive sites from the equatorial region to the apex. As a consequence of infarction, systolic thickening of the spared myocardium of the free wall was reduced progressively from the base to the apex. In the interventricular septum of the infarcted heart, systole thickening occurred mostly in the equatorial region and was reduced at the basal and apical portions. The interaction of hemodynamic impairment with the architectural rearrangements of the wall and chamber provoked a 1.9-fold increase in overall stress on the spared myocardium. However, diastolic stress was augmented by 6.8-fold, markedly exceeding the 1.1-fold increase in systolic stress. Thus large infarcts of the rat left ventricle due to left main coronary occlusion lead to a change in shape of the heart from ellipsoidal to cylindrical. The elevation in overall stress may condition the unfavorable long-term outcome of the infarcted heart.
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PMID:Heterogeneity of ventricular remodeling after acute myocardial infarction in rats. 153 7

Oropharyngeal functional impairment increases with age so that radiologists frequently are asked to determine the cause of aspiration in elderly patients. Neuromuscular and cognitive impairment often make it difficult to perform and interpret videofluoroscopic deglutition examinations in these patients. We retrospectively reviewed the barium swallow examinations in 50 elderly patients (mean age, 87 years) who were known to aspirate. We looked for specific patterns of oropharyngeal dysfunction that resulted in bolus misdirection. Analysis revealed that aspiration was due to abnormalities of the oral stage in 23, pharyngeal stage in 10, and both stages in 17. Dysfunction in the oral stage was due to ingestion of large volumes or rapid acquisition rates in nine, failure of containment during processing (bolus manipulation) in 18, and dissociation of lingual delivery and swallowing initiation in the transitional phase in 13. Dysfunction in the pharyngeal stage was due to incomplete transport (bolus retention) in 21 and defective closure of the laryngeal vestibule in 11. No significant relationship between conditions known to cause oropharyngeal dysfunction (dementia, stroke, Parkinson disease, disuse deconditioning) and the specific pattern of dysfunction was identified. These results indicate that an accurate and valid assessment of oropharyngeal dysfunction in elderly patients with aspiration is possible if specific patterns of dysfunction are sought. Our study indicates the importance of evaluating the oral and pharyngeal stages of deglutition in elderly patients who aspirate.
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PMID:Videofluoroscopy in elderly patients with aspiration: importance of evaluating both oral and pharyngeal stages of deglutition. 187 55

In hypertension, membrane potassium permeability and vascular reactivity are increased. This study characterizes a potassium-selective channel and contractions to barium, a potassium channel inhibitor, in vascular smooth muscle (tail artery) from spontaneously hypertensive stroke-prone rats (SHRSP) and normotensive Wistar-Kyoto (WKY) rats. Smooth muscle cells were isolated by enzymatic digestion, and potassium channel activity was characterized by using patch-clamp technique (inside-out configuration). Isometric contractile activity was evaluated in helically cut arterial strips by using standard muscle bath methodology. In membrane patches, a voltage-gated, calcium-insensitive, potassium-selective channel of large conductance (200 picosiemens) was observed. The channel did not conduct sodium or rubidium. Barium (10(-6) to 10(-4) M) produced a dose-dependent blockade of channel activity. These channel characteristics did not differ in SHRSP and WKY rat cells. After treatment with 35 mM KCl, barium (10(-5) to 10(-3) M) caused greater contractions in SHRSP arteries compared with arteries in WKY rats. The contractions to barium were markedly attenuated in calcium-free solution, and nifedipine and verapamil abolished contractions induced by barium in depolarizing solution. We conclude that increased vascular reactivity to barium in SHRSP arteries is not due to an alteration in the biophysical properties of the potassium channel studied.
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PMID:Potassium channels and vascular reactivity in genetically hypertensive rats. 235 24

Tail arteries isolated from the stroke-prone substrain of the spontaneously hypertensive rat (SHR-SP) exhibit oscillatory contractile responses to norepinephrine. Simultaneous recording of force generation and membrane potential (Em) has previously demonstrated that the contractile phase of these oscillations is associated with bursts of calcium-dependent action potentials. The smooth muscle cells are electrically quiescent during the relaxation phase of the oscillations. The present studies were designed to test the hypothesis that this quiescent period results from the stimulation of a calcium-activated potassium conductance (gKCa) in the cells responsible for triggering the bursting activity. Isolated tail artery strips from SHR-SP and Wistar-Kyoto rats (WKY) were prepared for measurement of isometric force generation or for simultaneous recording of force and Em. The channel-specific toxins apamin (4 x 10(-7) mol/l) and charybdotoxin (4.7 x 10(-8) did not alter the oscillatory pattern of contraction in response to norepinephrine. Oscillations were converted to sustained contraction by barium (10(-4) mmol), quinidine (5.8 x 10(-5) mmol) and elevation of extracellular potassium (20 mmol/l). Em recordings show that both potassium and barium convert bursting activity into tonic firing. Only 20 mmol/k+ caused significant depolarization in addition to that produced by norepinephrine. In contrast, quinidine appears to alter oscillatory behavior by interfering with calcium-spike generation. Norepinephrine-induced electrical activity is diminished in the presence of quinidine. These results suggest that potassium conductance plays an important role in controlling Em, electrical spiking and therefore oscillatory contractile activity in response to norepinephrine in the tail arteries of SHR-SP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Potassium conductance and oscillatory contractions in tail arteries from genetically hypertensive rats. 277 13

The term "penetrating aortic ulcer" refers to an ulceration of an atheromatous plaque that extends deeply through the intima and into the aortic media. It may precipitate an intramedial dissection (usually localized) or may rupture into the adventitia to form a pseudoaneurysm. The typical patient with penetrating atheromatous aortic ulcer is elderly and has hypertension, atherosclerosis, and back or chest pain, but pulse deficit, stroke, aortic insufficiency, and compromise of a visceral vessel are not present. Classic aortic dissection and symptomatic thoracic aortic aneurysms are among possibilities in the differential diagnosis. Aortography demonstrates the presence of an aortic ulcer similar in appearance to gastric ulcers seen on barium examination; in addition, an intramural aortic hematoma may be present. Our experience with penetrating aortic ulcers in symptomatic patients indicates that conservative medical therapy leads to recurrence of symptoms and a need for surgical intervention. We present a case that illustrates the salient features of this distinct clinical entity.
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PMID:The penetrating aortic ulcer: pathologic manifestations, diagnosis, and management. 338 11

This study characterizes a cellular mechanism for oscillatory contractions induced by norepinephrine in vascular smooth muscle from spontaneously hypertensive stroke prone rats (SHRSP). Helically cut strips of tail arteries from SHRSP and normotensive Wistar-Kyoto rats (WKY) were mounted in a muscle bath for measurement of isometric force generation. Norepinephrine-induced responses of arteries from SHRSP were characterized by fluctuations in contractile activity, whereas those in arteries from WKY remained constant with time. The magnitude of the oscillatory contractile activity (frequency X mean amplitude) varied directly with norepinephrine concentration (5.9 X 10(-9) to 1.8 X 10(-7) M). The oscillatory contractile activity varied inversely with the potassium concentration (3-20 mM) of the buffer solution and directly with the calcium concentration (0.1-5.0 mM) of the buffer solution. The oscillatory activity was converted to maintained contraction by barium (10(-4) M), quinidine (3 X 10(-6) M), sparteine (10(-3) M), D-600 (10(-7) M), and nifedipine (10(-8) M). Tetraethylammonium and 3,4-diaminopyridine, inhibitors of voltage-dependent potassium channels, did not alter the oscillatory contractile activity induced by norepinephrine. These observations suggest that oscillatory contractile activity in tail arteries from SHRSP is caused by an abnormal variation in potassium efflux during stimulation with norepinephrine. The altered potassium efflux appears to be related to calcium entry, which is sensitive to inhibition by channel blockers. This altered membrane property may contribute to changes in vascular sensitivity in hypertension.
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PMID:Oscillatory contractions in tail arteries from genetically hypertensive rats. 399 33

This study examines the effects of a sour bolus (50% lemon juice, 50% barium liquid) on pharyngeal swallow measures in two groups of patients with neurogenic dysphagia. Group 1 consisted of 19 patients who had suffered at least one stroke. Group 2 consisted of 8 patients with dysphagia related to other neurogenic etiologies. All patients were selected because they exhibited delays in the onset of the oral swallow and delays in triggering the pharyngeal swallow on boluses of 1 ml and 3 ml liquid barium during videofluoroscopy. Results showed significant improvement in oral onset of the swallow in both groups of patients and a significant reduction in pharyngeal swallow delay in Group 1 patients and in frequency of aspiration in Group 2 patients with the sour as compared to the non-sour boluses. Other selected swallow measures in both subject groups also improved with the sour bolus. Volume effects were present but not as consistently as in prior studies. Implications for swallow therapy are discussed.
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PMID:Effects of a sour bolus on oropharyngeal swallowing measures in patients with neurogenic dysphagia. 767 47

This retrospective study was undertaken to review aspiration documented by videofluoroscopic modified barium swallow (VMBS) examination in a group of patients admitted to a stroke rehabilitation unit. Forty-two of 54 patients tested demonstrated evidence of aspiration of thin liquids on VMBS performed an average of over 5 weeks following the onset of stroke. However, only patients in whom there was clinical concern of aspiration (54 of 255 stroke patients admitted to the rehab unit) were tested with VMBS evaluation. With this limitation in mind, aspiration was demonstrated in at least 9.9% of all unilateral right hemispheric patients, 12.1% of unilateral left hemispheric, 24% of bilateral hemispheric, and 39.5% of brainstem stroke patients. Of the 42 patients in whom aspiration of thin liquids was demonstrated, 31 underwent repeat VMBS studies an average of 6 weeks after the initial VMBS. 7 of these 31 (22.6%) no longer showed aspiration on VMBS. Eighteen of the 42 patients (43%) clinically stopped aspirating over this 6-week period.
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PMID:Prevalence and recovery of aspiration poststroke: a retrospective analysis. 813 23

In order to assess the risk of pneumonia, dehydration, and death associated with videofluoroscopic evidence of aspiration following stroke, the clinical records of 26 patients with aspiration and 33 randomly selected, case-matched, dysphagic controls without videofluoroscopic evidence of aspiration were reviewed. The videofluoroscopic modified barium swallow technique included 5 ml-thin and thick liquid barium, 5 ml barium pudding, and 1/4 cookie coated with barium, plus additional 20 and 30 ml of thin liquid barium. Patients were assessed a mean of 2 +/- 1 SD months poststroke and were followed for a mean of 16 +/- 8 SD months poststroke. The odds ratio for developing pneumonia was 7.6 times greater for those who aspirated any amount of barium irrespective of its consistency (p = 0.05). The odds ratio for developing pneumonia was 5.6 times greater for those who aspirated thickened liquids or more solid consistencies compared with those who did not aspirate, or who aspirated thin liquids only (p = 0.06). Dehydration was unrelated to the presence or absence of aspiration. The odds ratio for death was 9.2 times greater for those aspirating thickened liquids or more solid consistencies compared with those who did not aspirate or who aspirated thin liquids only (p = 0.01). Aspiration documented by modified videofluoroscopic barium swallow technique is associated with a significant increase in risk of pneumonia and death but not dehydration following stroke.
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PMID:Videofluoroscopic evidence of aspiration predicts pneumonia and death but not dehydration following stroke. 813 29

The goal of this study was to characterize differences in contractile responsiveness to several potassium channel antagonists in vascular smooth muscle from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto normotensive rats (WKY). Helically-cut strips of carotid arteries (endothelium removed) from SHRSP and WKY were mounted in muscle baths for measurement of isometric force generation. Contractile responses to tetraethylammonium (10(-4) to 3 x 10(-2) mol/L) and barium (3 x 10(-5) mol/L), blockers of the voltage-dependent and large conductance, calcium activated potassium channels, were greater in carotid arteries from SHRSP than in those from WKY. In contrast, contractile responses to the voltage-dependent potassium channel blockers 3,4-diamino-pyridine (10(-6) to 3 x 10(-3) mol/L) and sparteine (10(-6) to 3 x 10(-2) mol/L) in arteries from SHRSP did not differ from WKY values. Carotid arteries from SHRSP and WKY did not contract to apamin (10(-9) to 10(-6) mol/L), an antagonist of the small conductance, calcium activated potassium channel. Furthermore, relaxation responses to diazoxide (3 x 10(-4) mol/L), an activator of the ATP-sensitive potassium channel, and subsequent contractions to the ATP-sensitive potassium channel blocker glyburide (10(-8) to 3 x 10(-6) mol/L) in arteries from SHRSP did not differ from WKY values. Carotid artery segments from SHRSP were more sensitive to the contractile effects of elevated potassium than those from WKY. We conclude that altered activity of the large conductance, calcium activated potassium channel may play a role in the increased responsiveness observed in arteries from SHRSP.
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PMID:Potassium channel antagonists and vascular reactivity in stroke-prone spontaneously hypertensive rats. 834 37


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