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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to examine whether small biopsy specimens are representative of the whole human skeletal muscle or whether the different fibre types are unevenly distributed at different depths of the muscle. Ten micrometre thick cross-sections of whole human tibialis anterior were prepared using LKB PMV Cryo-Microtomes with a stroke length of 160 to 480 mm and the sections were stained for myofibrillar ATPase according to a modified procedure. The total and relative number of different fibres (Types 1 and 2) was determined in every 9th mm2 of the section. The data obtained were analysed by means of a computer program, which allowed assessment of bivariate data in the form of contour plots. The total number of fibres varied greatly between individuals (from 96 000 to 162 000; five individuals). The relative number of different fibres varied systematically in all individuals as a function of depth in the muscle. There was a gradual, often dramatic, relative increase in Type 2 fibre occurrence from the surface of the muscle (about 10--25%) towards the deeper regions (30--50%), the maximum being approximately along a line slightly posterior to the middle of the muscle. Additionally, superficial peaks were seen in places. In conclusion, the fibre type distribution in the tibialis anterior is not random. These results point to the importance of defining biopsy depth.
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PMID:Distribution of different fibre types in human skeletal muscles. I. Method for the preparation and analysis of cross-sections of whole tibialis anterior. 634 6

Pulmonary emboli may impair myocardial performance, causing declines in cardiac index (CI) and right and left ventricular stroke work (LVSW) because of mechanical events. We postulate that embolism also leads to the generation of a humoral factor(s) that may reduce cardiac contractility. Eleven mongrel dogs were infused with 0.5 gm/kg clot. Decreases in CI and LVSW were observed 1 hour after embolization. The stable metabolites of prostacyclin and thromboxane (Tx) A2--6-keto-PGF1 alpha and TxB2, respectively--increased within 30 minutes (P less than 0.005, P les than 0.001) and then decreased. These changes did not correlate with the declines in CI or LVSW. Plasma from embolized animals used to bathe an isolated rat papillary muscle reduced developed tension (Tpd) (P less than 0.001) and decreased calcium ATPase (Ca++-ATPase) activity of a myofibril preparation (P less than 0.001) obtained from rat cardiac muscle. The correlation between the reduction of TPd and myofibril Ca++-ATPase activity was 0.72 (P less than 0.001). The decline in Ca++-ATPase was also related to the decreases in CI (r = 0.59, P less than 0.001) and LVSW (r = 0.57, P less than 0.001). Five animals pretreated with indomethacin prior to embolization had no decrease in LVSW as compared with controls (P less than 0.001). Postembolism plasma did not depress papillary muscle Tpd and did not lower Ca++-ATPase activity of myofibrils. Anesthesia itself did not alter cardiopulmonary function. These results suggest that pulmonary emboli cause the release of a negative inotropic agent(s) into plasma that affects energy availability in the heart and reduces contractility. The production of this agent(s) is inhibited by indomethacin pretreatment.
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PMID:Circulating negative inotropic agent(s) following pulmonary embolism. 646 Oct 81

We performed a chronologic investigation of left (LV) and right (RV) ventricular myosin ATPase activity and hemodynamics in newborn lambs. We found an elevation in myosin ATPase activity for the LV, which was achieved by 6 to 8 weeks of age and which correlated directly with increasing ventricular stroke work. Myosin ATPase activity did not increase with age for the RV, a finding which was associated with a postnatal decrease in ventricular stroke work. These findings may represent an important postnatal adaptation of newborn myocardium to the demands of extrauterine life.
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PMID:Maturational changes in cardiac muscle myosin adenosine triphosphatase activity relative to hemodynamic alterations in newborn lambs. 646 50

Hearts of rats made hypertensive (BP greater than 150 mmHg) by left renal artery clipping and sham operated controls were studied in two series of experiments. In series I, cardiac function was studied in an isolated working heart apparatus at weeks 4, 9 to 10 and 16 to 17 post-surgery. In series II, coronary flow was studied during normoxic and anoxic retrograde perfusions at days 6 to 9 and at weeks 4 and 10 post-surgery. In series I, when compared with controls, hypertensives had lower body weights at weeks 4 and 9 to 10, and higher left ventricular weights at each period. Heart function was depressed for hypertensives when compared with controls as measured by lower stroke volume, peak left ventricular systolic pressure, stroke work, ejection fraction, positive dP/dt, peak aortic flow, and maximal flow acceleration. Relaxation rate as measured by negative dP/dt was also depressed. Hearts from hypertensives had significantly lower coronary flows and MVO2, and increased percent oxygen extraction and effluent lactate/pyruvate ratios. LVEDP was significantly elevated for hypertensives, when LVEDV (ml) was similar for hypertensives and controls. Myocardial actomyosin ATPase activity was depressed for hypertensives at weeks 9 to 10 and 16 to 17 post-surgery. In series II, when hearts were perfused retrogradely, coronary flow was lower for hypertensives than for controls during normoxia at days 6 to 9 and at week 4, and during anoxia at all time periods. The findings demonstrate that impaired coronary vascular reserve develops within days of the development of hypertension in rats, and this can be associated with impaired ventricular function.
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PMID:Impaired coronary flow and ventricular function in hearts of hypertensive rats. 662 76

This study examines the relation between Na+-K+ transport and metabolism in the canine brain. Cerebral oxygen and glucose consumption was measured by the sagittal sinus outflow technique. Synaptic transmission and related metabolism was blocked by pentobarbital 40 mg/kg (EEG flat). Lidocaine blocked an additional 15-20%, presumable by restricting Na+-K+ leak fluxes and reducing the demand for Na+-K+ transport. Ouabain blocked an additional 20-25% of metabolism. Ouabain also inhibited the Na+-K+ sensitive ATPase associated transport and caused a net efflux of K+ from the cellular compartment as evidenced by an increasing extracellular K+ concentration in the cortex. Accordingly, a total of 40% of metabolism in te EEG-arrested barbiturate inhibited brain could be related to Na+-K+ leak fluxes and associated transport. The remaining 60% are related to processes unidentified by this study. It is concluded that cerebral metabolism may be reduced below the hitherto described barbiturate minimum.
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PMID:Oxygen and glucose consumption related to Na+-K+ transport in canine brain. 730 61

We have investigated the cardiovascular actions of vanadate, a naturally occurring Na+-K+-ATPase inhibitor, in six series of pentobarbitalized dogs. In three of the series, isomotic sodium vanadate was infused intravenously at progressively faster rates while arterial pressure and other parameters were measured. In two other series, the solution was infused directly into the coronary artery with coronary flow held constant during measurement of perfusion pressure, left ventricular contractile force (LVCF), and dP/dt. In one series, the agent was infused into the brachial artery with brachial artery flow held constant, and small and large vessel resistances in skin and muscle were calculated. Intravenous infusion increased arterial pressure and reduced cardiac output, the latter resulting from both decreased heart rate and stroke volume. LVCF fell. Total peripheral, pulmonary, coronary, and renal resistances rose. Coronary and renal flows fell, and the latter was associated with reduced urine flow. Intracoronary infusion raised coronary resistance, but had little effect on heart rate, LVCF, and dP/dt. Intrabrachial infusion raisedthe resistance to flow through all components of the forelimb vascular bed. Thus, in the dog, vanadate activates vascular smooth muscle, but has little effect on cardiac muscle. In the latter respect, its action differs from that of ouabain.
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PMID:Cardiovascular effects of vanadate in the dog. 739 17

We have tested the hypothesis that altered vascular reactivity, specifically the appearance of spontaneous and BayK 8644 (L-type voltage gated calcium channel agonist)-induced oscillations in the carotid artery and the sarcoplasmic reticulum Ca(2+)-ATPase inhibitor cyclopiazonic acid (CPA)-induced oscillations in the aorta from stroke-prone spontaneously hypertensive rats (SHRS), are dependent upon angiotensin II production early in life. SHRSP and normotensive Wistar-Kyoto (WKY) rats were treated from 6-10 weeks of age with vehicle, hydralazine/hydrochlorothiazide (used as a control for lowered blood pressure) or the angiotensin converting enzyme inhibitor ramipril (3 mg/kg/day). Systolic blood pressures were measured weekly in rats from 6 to 17 weeks of age. In SHRSP (at 17 weeks of age), ramipril-treatment but not hydralazine/hydrochlorothiazide attenuated the long term expression of elevated systolic blood pressure in adult SHRSP while blood pressures of all adult WKY rats were unaffected by any treatment. At 17 weeks, rats were killed and arteries removed for in vitro measurement of isometric contractile activity. Only the incidence of spontaneous oscillations (carotid artery) was affected by ramipril treatment; ramipril did not change the frequency of BayK 8644-induced oscillations in the artery or the frequency of CPA-induced oscillations in aorta from either SHRSP or WKY. These data indicate that while spontaneous oscillations in the carotid artery may be dependent on an angiotensin II-sensitive mechanism during development, agonist-induced oscillations (CPA and BayK 8644) appear not to be angiotensin II-dependent. Thus, not all of the contractile oscillations which appear in vascular smooth muscle from SHRSP are angiotensin II-dependent, suggesting that some of these vascular abnormalities may develop at a time separate from that in which increased blood pressure is firmly established and may not be associated with the for maintenance of elevated blood pressure.
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PMID:Effects of ramipril on contractile oscillations in arteries from genetically hypertensive rats. 753 66

Heart disease, stroke, and kidney failure are leading causes of death. Essential hypertension is the major predisposing risk factor of cardiovascular disease. Yet, after several decades of intensive investigation, the initiating causative mechanism of essential hypertension is still unknown. However, investigators in the field generally agree that an increased total peripheral resistance (TPR) is the fundamental hemodynamic disorder in essential hypertension. This review addresses the hypothesis that the increased TPR of essential hypertension is due to a defective mechanism in the contractility of arterial smooth muscle. Force-velocity and length-tension studies have shown that both caudal arterial muscle and mesenteric resistance arterial muscle from spontaneously hypertensive rats (SHR) can shorten more and faster than muscle from normotensive control Wistar-Kyoto rats (WKY). In addition, the SHR muscle relaxation rate is slower compared with the WKY muscle. These alterations in mechanical behavior of SHR arterial muscle appear to be primary to the high blood pressure since MK-421 (enalapril maleate)-treated SHR arterial muscle shows the same increased velocity of shortening, increased shortening ability, and decreased relaxation rate as the untreated SHR muscle. MK-421 is an angiotensin-converting enzyme blocker. SHR maintained on MK-421 treatment have normal blood pressures in spite of being of the genetically hypertensive strain. While these findings are encouraging, several other important issues supporting the hypothesis require resolution and warrant review. Firstly, structural alterations of blood vessel walls in hypertension cause the walls to thicken and encroach on the vessel lumens contributing to the increased TPR. Whether such wall thickening is the cause or consequence of high blood pressure has been controversial in the literature. In this report, data are presented from a study in which MK-421-treated SHR were utilized as a model of prehypertensive SHR. Light micrograph observations and morphometric analyses were made of cross-sections of mesenteric resistance arteries from SHR, MK-421-treated SHR, and WKY. Results show that the MK-421-treated SHR resistance arteries had media thicknesses and a number of smooth muscle cell layers that were significantly less than in the untreated SHR and not different from the WKY. Secondly, velocity of shortening is dependent on actomyosin ATPase activity, and, since maximum velocity of shortening has been shown to be increased in SHR arterial muscle, it became necessary to know whether or not an increased actomyosin ATPase activity might be responsible. Therefore, data from a study of SHR and WKY caudal arterial myofibrillar ATPase activities are compared.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes in arterial smooth muscle contractility, contractile proteins, and arterial wall structure in spontaneous hypertension. 793 46

Movement of single myosin filaments, synthesized by copolymerization of intact myosin and fluorescently labeled light meromyosin, were observed along a single actin filament suspended in solution by a dual laser trap in a fluorescence microscope. The sliding velocity of the myosin filaments was 11.0 +/- 0.2 micron/s at 27 degrees C. This is similar to that of actin moving toward the center from the tip (the physiological direction) of myosin filaments bound to a glass surface but several times larger than that in the opposite direction (Ishijima and Yanagida, 1991; Yanagida, 1993). This indicates that the movement of myosin filaments is dominated by the myosin heads on one side of the myosin filament, which are correctly oriented relative to the actin filament. The incorrectly oriented myosin heads on the other side do not interfere with the fast movement. The step size (displacement produced during one ATPase cycle) of correctly oriented myosin was estimated from the minimum number of myosin heads necessary to produce the maximum velocity. This was determined by measuring the velocities of various lengths of myosin filaments. The minimum length of the myosin filaments moving near the maximum velocity was 0.30-0.40 microns, which contains 20 +/- 5 correctly oriented myosin heads. This number leads to a myosin step size of 71 +/- 22 nm. This value probably represents the lower limit, because all of the myosin heads on the filament would not always interact with the actin filament. Thus, the myosin step size is considerably larger than the length of a power stroke expected from the physical size of a myosin head, 10-20 nm (Huxley, 1957, 1969).
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PMID:Movement of single myosin filaments and myosin step size on an actin filament suspended in solution by a laser trap. 801 9

The force developed by a muscle during steady shortening is due to cyclic interactions between the cross-bridges extending from the thick myosin filament to the thin actin filament. Each interaction consists of a power stroke of the myosin molecule that accounts for a limited amount of sliding between the two sets of filaments (about 12 nm according to quick release experiments), and is widely believed to be coupled to the hydrolysis of one ATP molecule. On the other hand both energetics studies in muscle and in vitro motility assays, indicating that shortening per ATP split is much larger than 12 nm, postulate that during shortening cross-bridges interact at a rate much faster than the ATP splitting rate. In the experiments reported here, made on intact fibres from frog skeletal muscle, the rate of regeneration of the power stroke was determined. Tension transients were elicited by imposing test step releases at different times (2-20 ms) after a conditioning release of about 5 nm. When the test step was imposed at 2 ms after the conditioning step, the tension attained at the end of the quick phase of recovery (T2, due to the force generating stroke of the attached cross-bridges) was depressed and the T2 curve (the plot of T2 tension versus size of the test step) intercepted the length axis to the right, with respect to the intercept of the control T2 curve, by an amount similar to the size of the conditioning step. By increasing the interval between conditioning and test step the T2 tension increased progressively and the T2 curve intercept approached the intercept of the control curve with a time constant of 6-7 ms. These results indicate that the force generating stroke elicited by a shortening step is followed by a relatively rapid process of detachment and reattachment by most of the cross-bridges, allowing for the generation of another power stroke. The rate of this process, 150/s, is one order of magnitude higher than that expected from the ATPase rate, suggesting that several actomyosin interactions occur in shortening muscle by the time one ATP is split. The results are stimulated with a mechanical kinetic model of contraction, in which, for a critical amount of shortening, cross-bridges can detach, rapidly reattach and generate force before the completion of the "normal" isometric cycle.
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PMID:Kinetics of regeneration of cross-bridge power stroke in shortening muscle. 810 79


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