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Query: UNIPROT:P06889 (Mol)
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The distribution of fluorescent adrenergic nerve fibers in the proximal portion (horizontal segment, Hs) and the three distal portions (major branches) of the middle cerebral arteries (MCA) was examined in stroke-prone spontaneously hypertensive rats (SHRSP) aged 10, 30, 60, 90, and 180 days, by the glyoxylic acid method. The results were compared with those in age-matched normotensive Wistar Kyoto (WKY) rats. While the distribution pattern of fluorescent nerve fibers in the proximal portion of WKY rats changed from a straight linear arrangement at 10 and 30 days of age to a network-like arrangement after 60 days, those from SHRSP showed a constant meshwork pattern throughout the entire examination period. In the distal portions of the MCA of both SHRSP and WKY rats at all ages examined, fluorescent nerve fibers formed a coarse network. The distribution densities of adrenergic nerve fibers in the proximal and distal portions of the MCA of SHRSP were significantly higher (P less than 0.01 and 0.05) than those of WKY rats at all ages examined, except in the proximal portion at 90 and 180 days of age. The difference in nerve fiber density between SHRSP and WKY rats reached a peak at 30 days of age in both proximal and distal portions, and then gradually decreased with age. The present study suggests that sympathetic hyperinnervation is an important factor in the development of hypertension, and is involved in its maintenance in SHRSP.
Virchows Arch B Cell Pathol Incl Mol Pathol 1991
PMID:Increased density of fluorescent adrenergic fibers around the middle cerebral arteries of stroke-prone spontaneously hypertensive rats. 168 19

Cerebral ischemia and reperfusion results in an active series of metabolic events, eventually leading to cell death. The expression of specific genes during cerebral ischemia and reperfusion may play an important, determinant role in the mechanisms controlling cellular processes. Ten minutes of bilateral carotid occlusion in the Mongolian gerbil was found to increase the messenger RNA for both the c-fos and c-jun protooncogenes. The changes in gene expression were detected in the regions of ischemia, specifically the cortex and striatum, and no increases were seen in either the brain stem or the cerebellum, which possess a separate circulation. Induction of protooncogene mRNA is correlated to the duration of ischemia, i.e., the longer the time of ischemia, the greater the increase in c-fos expression. Pretreatment of animals with pentobarbital reduced the effect of the ischemic insult and prevented the increase in c-fos mRNA. Analysis of the c-fos and c-jun proteins after ischemia demonstrated an increase in the formation of a functional transcriptional complex and association with the AP-1 binding region. These findings suggest that ischemic cell death and recovery in neurodegenerative disorders such as stroke may involve the regulated expression of these protooncogenes early in the pathway of ischemia.
J Mol Neurosci 1991
PMID:Ischemic induction of protooncogene expression in gerbil brain. 190 65

Plasminogen activator inhibitor activity was determined in patients (26 men, 6 women) with acute ischemic stroke (n = 28) and transient ischemic attack (TIA) (n = 4). Age-matched patients (22 men, 10 women) with various nonvascular neurologic diseases served as controls. Plasma levels of plasminogen activator inhibitor activity were significantly higher in the stroke group (p less than 0.003). Serum triglycerides and plasminogen activator inhibitor activity correlated positively in the stroke group (p less than 0.03) and in controls (p less than 0.0001). Our data suggest a possible involvement of plasminogen activator inhibitor activity in the pathophysiology of stroke.
Mol Chem Neuropathol 1991 Apr
PMID:Plasminogen activator inhibitor in acute stroke. 191 Mar 59

The ultrastructure of the vascular smooth muscle cells of the middle cerebral artery in 6-month-old male stroke-prone spontaneously hypertensive rats (SHRSP) was studied by scanning (SEM) and transmission electron microscopy (TEM) and compared with that of age-matched normotensive Wistar Kyoto rats (WKY). Although the smooth muscle cells of WKY rats by SEM had a typical spindle shape and smooth surface texture, those of SHRSP were structurally modified by numerous surface invaginations and projections, bearing some structural resemblance to the myotendinous junction of skeletal muscle. Structural modifications affected more than half the surface of medial smooth muscle cells in SHRSP, but less than 0.6% of the surface of these cells in WKY rats. About 10% of medial smooth muscle cells were necrotic in SHRSP, but no necrotic cells were identified in WKY rats. By TEM, smooth muscle cells in SHRSP were shown to be irregular in profile with deep indentations of the plasma membrane and were surrounded by many layers of basal lamina-like material. The present study suggests that most smooth muscle cells in the middle cerebral artery of SHRSP may be modified to adapt to chronic hypertension by increasing the junctional area between muscle cells and connective tissue and that some cells may undergo necrosis.
Virchows Arch B Cell Pathol Incl Mol Pathol 1990
PMID:Morphological changes in cerebral vascular smooth muscle cells in stroke-prone spontaneously hypertensive rats (SHRSP). A scanning and transmission electron microscopic study. 197 Nov 33

After myocardial infarction, the renin-angiotensin system is found to be activated. While this response may be beneficial in acute failure, it could be detrimental in chronic stages. Therefore effects of captopril therapy were investigated during early and later phases after myocardial infarction in conscious rats, chronically instrumented for hemodynamic measurements. Hemodynamics were measured at baseline and after stimulating the heart by a volume load (cardiac function curve). Myocardial infarction decreased baseline cardiac output and impaired cardiac function, without effects on baseline mean arterial pressure, central venous pressure and heart rate. Captopril given 3 to 5 weeks after infarction improved cardiac function in a dose-dependent manner by increasing stroke volume, whereas stroke work was not affected. In contrast, captopril given from 1 to 21 days after infarction did not lead to improved cardiac function; instead, tachycardia together with a decreased stroke volume suggested deterioration, rather than improvement, of cardiac function. These data indicate that captopril therapy in chronically infarcted conscious rats improved cardiac function when treatment was started after completion of the healing process, but that early treatment not only failed to improve ventricular function, but may have a deleterious effect of the heart.
J Mol Cell Cardiol 1991 Feb
PMID:Delayed but not immediate captopril therapy improves cardiac function in conscious rats, following myocardial infarction. 206 27

Hearts from three species of fish with varying myoglobin content were perfused with stepwise changes in input perfusate PO2 from approximately 160 to 10 mmHg. Flow through the heart, rate of contraction, and afterload were kept constant. This standardized stroke volume and bulk flow of perfusate to the myocytes since these hearts are nourished by the fluid in the ventricular lumen. In some cases NaNO2 was added to the perfusion medium to decrease existing levels of functional myoglobin. Myoglobin-rich hearts were able to extract a constant amount of oxygen until perfusate PO2 had fallen below 80 mmHg. At this point oxygen uptake began to decline. These hearts consumed oxygen until input PO2 was 10 mmHg or less. When normoxic conditions were restored the myoglobin-rich hearts showed complete recovery. Performance was maintained at a constant level over the entire range of input PO2. Myoglobin-poor hearts and nitrite-treated hearts were unable to sustain constant levels of oxygen consumption in the face of a declining perfusate PO2. These hearts were unable to extract oxygen from the medium and failed at perfusate PO2's of 40 mmHg for naturally myoglobin-poor hearts and 30 mmHg for nitrite-treated hearts. Half-maximal oxygen consumptions were attained by myoglobin-rich hearts at lower input PO2's than either myoglobin-poor or nitrite-treated hearts. The impact of myoglobin in intact heart is apparent at relatively high extracellular PO2's (40-80 mmHg) in this model system.
J Mol Cell Cardiol 1990 Oct
PMID:Oxygen uptake by isolated perfused fish hearts with differing myoglobin concentrations under hypoxic conditions. 209 36

In order to study the mechanochemical coupling in actomyosin energy transduction, the sliding distance of an actin filament induced by one ATP hydrolysis cycle was obtained by using an in vitro movement assay that permitted quantitative and simultaneous measurements of (1) the movements of single fluorescently labeled actin filaments on myosin bound to coverslip surfaces and (2) the ATPase rates. The sliding distance was determined as (the working stroke time in one ATPase cycle, tws) x (the filament velocity, v). tws was obtained from the ATPase turnover rate of myosin during the sliding (kt), the ATP hydrolysis time (delta t) and the ON-rate at which myosin heads enter into the working stroke state when they encounter actin (kON); tws approximately 1/kt-delta t-1/kON. kt was estimated from the ATPase rates of the myosin-coated surface during the sliding of actin filaments. delta t has been determined as less than 1/100 per second, kON was estimated by analyzing the movements of very short (40 nm) filaments. The resulting sliding distance during one ATP hydrolysis cycle near zero load was greater than 100 nm, which is about ten times longer than that expected for a single attachment-detachment cycle between an actin and a myosin head. This leads to the conclusion that the coupling between the ATPase and attachment-detachment cycles is not determined rigidly in a one-to-one fashion.
J Mol Biol 1990 Nov 05
PMID:Mechanochemical coupling in actomyosin energy transduction studied by in vitro movement assay. 214 98

Myocardial infarctions were induced in rats by ligation of the left anterior descending (LAD) coronary artery. After 4 weeks, parameters of left (LV) and right ventricular (RV) function and of peripheral circulation were measured in the intact, anesthetized animals. The morphology of the heart chambers was examined at the macroscopic and cell size level. In animals with slight reduction in LV function, LVEDP was elevated from 3.4 +/- 0.8 to 8.8 +/- 1.5 mmHg, LV stroke work was reduced by 14%, and dP/dtmax of both ventricles was depressed by 10% compared with sham-operated controls. Myocytes isolated from the LV and RV were elongated to some extent and had a greater cell volume, but there was no change in heart weight. These rats had infarctions that were small or medium in size. In rats with severe depression in left heart function, cardiac output, LVSP, LV stroke work, mean arterial pressure, and the LV weight/body weight ratio were markedly lower than in sham-operated controls. LVEDP was elevated up to 32 +/- 2 mmHg. These rats had large infarctions. RVSP, RV weight/body weight ratio, and the volume of myocytes isolated from the RV were doubled. RV stroke work was increased by 58%. Myocytes from the LV, RV and from the septum were elongated to about the same extent. The septum had developed a 23% hypertrophy. Histological examination of the lungs revealed marked thickening of the tunica medica of small pulmonary arteries with narrowing of the lumen. These changes are considered to represent the morphological basis for the increased pulmonary vascular resistance that was associated with RV pressure overload and hypertrophy.
J Mol Cell Cardiol 1990 Nov
PMID:Changes in heart function and cardiac cell size in rats with chronic myocardial infarction. 214 93

The low-angle X-ray diffraction pattern from Lethocerus flight muscle fibres was recorded in rigor or under two conditions that modify crossbridge structure and behaviour, aqueous adenylylimidodiphosphate (AMPPNP) and AMPPNP + calcium in an ethylene glycol-water mixture. The effects on the 38.7 nm layer-line peaks (hk.6) of the diffraction patterns were studied in detail. In aqueous AMPPNP at room temperature, a condition in which rigor tension drops to half without loss of stiffness, the peaks remained nearly as intense as in rigor except for the 10.6, which dropped to half. In 20% (v/v) ethylene glycol-AMPPNP + 100 microM-Ca2+ at 23 degrees C (gly + pnp + Ca), a condition which removed muscle tension but left stiffness close to the rigor value, the 10.6 and 11.6 peaks greatly decreased but the 31.6 remained relatively high. The 14.5 nm meridional peak (00.16) became stronger on addition of AMPPNP and again on adding glycol + calcium. Considered in terms of constructively interfering filaments and crossbridges, the X-ray data indicated a transfer of diffracting crossbridge mass towards the thick filament as relaxation proceeds. We compared the X-ray diffraction patterns and crossbridge structure seen with electron microscopy (EM) under the same chemical conditions. EM and X-ray observations were mutually quite consistent overall. However, X-ray data indicated that more crossbridge mass was stereospecifically related to actin before fixation in the partially relaxed state (gly + pnp + Ca) than was suggested by the disordered crossbridge profiles seen by EM. We conclude that myosin heads at the start of the power stroke may both be closely related to their thick filament origins and form actin-determined attachments to the thin filament.
J Mol Biol 1990 Jul 05
PMID:X-ray diffraction and electron microscopy from Lethocerus flight muscle partially relaxed by adenylylimidodiphosphate and ethylene glycol. 237 Jun 60

In order to understand the role of monoamines in cerebral ischemia, 3-methoxy-4-hydroxyphenylglycol(MHPG), 5-hydroxyindoleacetic acid (5-HIAA), and homovanillic acid(HVA), the three major unconjugated monoamine metabolites in cerebrospinal fluid (CSF), of 33 patients and 18 controls were measured with high performance liquid chromatography. Results showed all three metabolites were raised in patients with severe ischemia, but only MHPG and 5-HIAA were elevated significantly, MHPG changes more quickly and regularly as a consequence of cerebral ischemia than the two others. A positive correlation between any pair of metabolites was found in controls and in patients in the first week after stroke, but not at the end of the second week. Computer assisted multivariate analysis indicated 5-HIAA and MHPG correlated more closely with the state of illness in the acute stage, whereas HVA correlated the least. Possible explanations for the changes of CSF levels of amine metabolites are discussed.
Mol Chem Neuropathol 1989 Apr
PMID:Monoamine metabolites in cerebrospinal fluid during and after acute cerebral ischemia. 247


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