Significant Change In Tension Research Articles

A study of tension and deformation of flexible net under the action of current

ABSTRACT With the decrease of fishery resources, offshore fish farm aquaculture has become the current development trend of the marine aquaculture industry. Flexible net are subject to collision by fish and erosion by seawater, which can lead to breakage of the net. In this paper, the validity of the net mesh concentration method is verified by the model tests of others. The effects of current direction, current velocity, and ten different forms of net breakage on net tension and deformation were further analyzed. The results show that under different forms of net breakage, the tension of the net only decreases significantly in the direction of breakage of the net when the net breaks, while there is no significant change in tension in other directions; for the motion of the nodes, which increases only around the break, while the motion of all other nodes does not change significantly.

Neuroendocrine and inflammatory responses to DHEA administration in young healthy women

DHEA is reported to have beneficial effects for the elderly and for several pathologies because of its behavioral and anti-inflammatory properties. However, these properties have never been investigated in a young healthy population. The purpose of this double-blind, randomized study was therefore to investigate the effects of short-term DHEA administration (100 mg/day/4 weeks) on neuroendocrine (i.e., beta-endorphin and prolactin) and inflammatory (i.e., interleukin-6 and TNF-alpha) parameters in 10 young healthy female volunteers with regular sports practice. In parallel, the stress state was assessed with the Profile of Mood States (POMS) questionnaire. DHEA administration did not alter prolactin, interleukin-6 or TNF-alpha, and no significant change in tension, depression, anger, vigor, fatigue or confusion was noted. However, beta-endorphin levels increased significantly (p < 0.05) with the DHEA treatment. The results of this investigation indicate that short-term DHEA administration improves neuroendocrine modulation but does not affect the inflammatory status or psychological state in recreationally trained female athletes. Further studies are needed to determine the exact mechanisms and the responses of these parameters to DHEA administration at higher dosages and/or for longer durations, especially in response to physical/psychological stress.

Angiotensin-(1-7) Augments Endothelium-dependent Relaxations of Porcine Coronary Arteries to Bradykinin by Inhibiting Angiotensin-Converting Enzyme 1

Angiotensin-converting enzyme 2 (ACE2) converts angiotensin II to angiotensin-(1-7) that activates Mas receptors, inhibits ACE1, and modulates bradykinin receptor sensitivity. This in vitro study compared the direct and indirect effects of angiotensin-(1-7), the ACE1 inhibitor captopril, and diminazene aceturate (DIZE) an alleged ACE2 activator in rings of porcine coronary arteries, by measuring changes of isometric tension. Angiotensin-(1-7), captopril, and DIZE did not cause significant changes in tension before or after desensitization of bradykinin receptors in preparations contracted with U46619. Bradykinin caused concentration-dependent and endothelium-dependent relaxations that were not affected by DIZE but were potentiated to a similar extent by angiotensin-(1-7) and captopril, given alone or in combination. Bradykinin responses potentiated by angiotensin-(1-7) and captopril were not affected by the BK1 antagonist SSR240612 and remained augmented in the presence of either N-nitro-L-arginine methyl ester hydrochloride plus indomethacin or TRAM-34 plus UCL-1684. ACE2 was identified in the coronary endothelium by immunofluorescence, but its basal activity was not influenced by DIZE. These results suggest that in coronary arteries, angiotensin-(1-7) and captopril both improves NO bioavailability and enhances endothelium-dependent hyperpolarization to bradykinin solely by ACE1 inhibition. Endothelial ACE2 activity cannot be increased by DIZE to produce local adequate amounts of angiotensin-(1-7) to influence vascular tone.

Angiotensin‐(1–7) augments endothelium‐dependent relaxations of porcine coronary arteries to bradykinin by inhibiting ACE1

Angiotensin converting enzyme 2 (ACE2) converts angiotensin II to angiotensin‐(1–7) that activates Mas receptors, inhibits ACE, modulates bradykinin (BK) receptor sensitivity. The present study compared the direct and indirect (on the response to BK) effect(s) of the ACE2 activator diminazene aceturate (DIZE) and angiotensin‐(1–7) in rings of isolated porcine coronary arteries, with or without endothelium, suspended in conventional organ chambers for isometric tension recording. In preparations contracted with U46619 (10−7 M), increasing concentrations of DIZE, angiotensin‐(1–7) or of the ACE inhibitor captopril, did not cause significant changes in tension before or after desensitization of BK receptors. B K caused concentration‐dependent and endothelium‐dependent relaxations which were inhibited partially by L‐NAME or TRAM‐34 plus UCL‐1684, but not by indomethacin. The response to BK was not affected by DIZE, but significantly potentiated, to a similar extent, by angiotensin‐(1–7) and captopril. The two compounds augmented the response in the presence of either L‐NAME or TRAM‐34 plus UCL‐1684, indicating potentiation of NO bioavailability and endothelium‐dependent hyperpolarizations, respectively. These results indicate that in coronary arteries angiotensin‐(1–7) enhances both endothelium‐dependent relaxations and hyperpolarization to bradykinin solely by ACE inhibition.Research support: World Class University program (R31–20029), Ministry of Education, Science and Technology, South Korea.

P38-MAPK Induced Dephosphorylation of α-Tropomyosin Is Associated With Depression of Myocardial Sarcomeric Tension and ATPase Activity

Our objective in work presented here was to understand the mechanisms by which activated p38alpha MAPK depresses myocardial contractility. To test the hypothesis that activation of p38 MAPK directly influences sarcomeric function, we used transgenic mouse models with hearts in which p38 MAPK was constitutively turned on by an upstream activator (MKK6bE). These hearts demonstrated a significant depression in ejection fraction after induction of the transgene. We also studied hearts of mice expressing a dominant negative p38alpha MAPK. Simultaneous determination of tension and ATPase activity of detergent-skinned fiber bundles from left ventricular papillary muscle demonstrated a significant inhibition of both maximum tension and ATPase activity in the transgenic-MKK6bE hearts. Fibers from hearts expressing dominant negative p38alpha MAPK demonstrated no significant change in tension or ATPase activity. There were no significant changes in phosphorylation level of troponin-T3 and troponin-T4, or myosin light chain 2. However, compared with controls, there was a significant depression in levels of phosphorylation of alpha-tropomyosin and troponin I in fiber bundles from transgenic-MKK6bE hearts, but not from dominant negative p38alpha MAPK hearts. Our experiments also showed that p38alpha MAPK colocalizes with alpha-actinin at the Z-disc and complexes with protein phosphatases (PP2alpha, PP2beta). These data are the first to indicate that chronic activation of p38alpha MAPK directly depresses sarcomeric function in association with decreased phosphorylation of alpha-tropomyosin.

Guanylyl cyclase mediates ANP-induced vasoconstriction of murine splenic vessels.

We have previously shown that ANP causes differential constriction of the splenic vasculature of the rat (veins greater than arteries), which may be inhibited by blocking the production of cGMP with A7195. In this paper, we report experiments done on vessels derived from guanylyl cyclase (GC)-A knockout mice. Small splenic arteries ( approximately 150-microm diameter) and veins ( approximately 250-microm diameter) were dissected from male GC-A-deficient 129sv mice or age-matched wild-type controls and mounted in a wire myograph. In the wild-type mice, ANP exhibited higher potency in the veins than in the arteries (EC(50) values wild-type mice: artery, 8 +/- 3 x 10(-9) M, n = 5 vs. vein, 6 +/- 4 x 10(-10) M, n = 5; P < 0.05). The concentration-response curve for ANP-induced vasoconstriction was also shifted leftward in denuded compared with intact arteries (EC(50) values: denuded artery: 5 +/- 3 x 10(-10) M, n = 5 vs. intact artery, 8 +/- 3 x 10(-9) M, n = 5; P < 0.05), i.e., the denuded vessels were more reactive. By contrast, ANP caused no significant change in tension from baseline in intact splenic arteries, intact splenic veins, or denuded splenic arteries derived from the GC-A-deficient mice, although these vessels did show normal concentration-dependent increases in tension to phenylephrine. We conclude that ANP causes vasoconstriction in the splenic vasculature by an endothelium-independent mechanism, mediated via guanylyl cyclase.

Effects of dietary L-arginine on the reactivity of canine coronary arteries.

Experiments were designed to determine the effects of supplemental dietary L-arginine on the endothelial and smooth muscle function of canine coronary arteries. One group of dogs was fed the standard laboratory chow while another group was supplemented with 250 mg/kg per day L-arginine. All dogs had undergone bilateral reversed interposition saphenous vein grafting and received 325 mg/day oral aspirin. After 5 weeks of arginine feeding, left circumflex coronary arteries were removed, cut into rings, and suspended for the measurement of isometric force in organ chambers. Concentration-response curves were obtained to L-arginine, UK-14,304 (alpha2-adrenergic agonist) and A23187 (calcium ionophore) in the absence and presence of N(G)-monomethyl-L-arginine (L-NMMA) and tetraethylammonium (TEA) alone or in combination. Serum concentrations of L-arginine increased by about 20% following 2 weeks of arginine feeding and remained elevated throughout the study. In rings with and without endothelium contracted with prostaglandin F2alpha, L-arginine caused concentration-dependent contractions in rings from control animals but no significant change in tension in rings from arginine-fed animals. Contractions to L-arginine in control animals were reduced by either L-NMMA or TEA. Endothelium-dependent relaxations to the alpha2-adrenergic agonist were decreased with arginine feeding while relaxations to the calcium ionophore and the endothelium-derived factor nitric oxide were similar among groups. Relaxations to UK-14,304 were reduced by L-NMMA in both groups but by TEA only in rings from control animals. These results suggest that dietary supplementation with L-arginine modifies reactivity of endothelium and smooth muscle by at least two mechanisms: one associated with activation of potassium channels and the other with receptor-coupled release of nitric oxide.

Endothelium-dependent vasodilation in response to Pseudomonas aeruginosa lipopolysaccharide: an in vitro study on canine arteries.

Early systemic arterial hypotension is a common clinical feature of Pseudomonas septicemia. To determine if Pseudomonas aeruginosa endotoxin induces the release of endothelium-derived nitric oxide (EDNO), an endogenous nitrovasodilator, segments of canine femoral, renal, hepatic, superior mesenteric, and left circumflex coronary arteries were suspended in organ chambers (physiological salt solution, 95% O2/5% CO2, pH 7.4, 37 degrees C) to measure isometric force. In arterial segments contracted with 2 microM prostaglandin F2 alpha, Pseudomonas endotoxin (lipopolysaccharide (LPS) serotype 10(Habs) from Pseudomonas aeruginosa (0.05 to 0.50 mg/ml) induced concentration-dependent relaxation of segments with endothelium (P < 0.05) but no significant change in tension of arteries without endothelium. Endothelium-dependent relaxation in response to Pseudomonas LPS occurred in the presence of 1 microM indomethacin, but could be blocked in the coronary artery with 10 microM NG-monomethyl-L-arginine (L-NMMA), a competitive inhibitor of nitric oxide synthesis from L-arginine. The inhibitory effect of L-NMMA on LPS-mediated vasorelaxation of the coronary artery could be reversed by exogenous 100 microM L-arginine but not by 100 microM D-arginine. These experiments indicate that Pseudomonas endotoxin induces synthesis of nitric oxide from L-arginine by the vascular endothelium. LPS-mediated production of EDNO by the endothelium, possibly through the action of constitutive nitric oxide synthase (NOSc), may decrease systemic vascular resistance and may be the mechanism of early hypotension characteristic of Pseudomonas septicemia.

Changes in Mechanical Tension in the Median Nerve: Possible implications for the upper limb tension test

Summary Movements which increase neural tension have been considered useful in determining whether pathology of neural tissue is associated with clinical symptoms. In order to investigate changes in neural tension a buckle force transducer was attached to the median nerve at a site approximately 2 cm distal to the axilla in five unembalmed cadavers. A series of ipsilateral and contralateral upper and lower limb manoeuvres was performed and changes in tension were recorded. The results showed a significant increase in the tension in the median nerve when the ipsilateral movements of elbow extension and wrist extension were applied. The movements of contralateral cervical side flexion and ipsilateral straight leg raise were also found to increase tension significantly. No significant change in tension was recorded during ipsilateral shoulder depression, glenohumeral abduction and glenohumeral external rotation. Further, there was no significant change in tension when the contralateral arm movement or the contralateral straight leg raise was applied. These findings indicate that certain manoeuvres increase tension in the median nerve. Further research is required to determine the relevance of neural tension tests in the assessment and treatment of patients suffering from neuromusculoskeletal pathology.

Mechanical and metabolic determination of VO2 and fatigue during repetitive isometric contractions in situ.

Repetitive isometric tetanic contractions (1/s) of the canine gastrocnemius-plantaris muscle were studied either at optimal length (Lo) or short length (Ls; approximately 0.9 . Lo), to determine the effects of initial length on mechanical and metabolic performance in situ. Respective averages of mechanical and metabolic variables were (Lo vs. Ls, all P < 0.05) passive tension (preload) = 55 vs. 6 g/g, maximal active tetanic tension (Po) = 544 vs. 174 (0.38 . Po) g/g, maximal blood flow (Q) = 2.0 vs. 1.4 ml . min-1 . g-1, and maximal oxygen uptake (VO2) = 12 vs. 9 micromol . min-1 . g-1. Tension at Lo decreased to 0.64 . Po over 20 min of repetitive contractions, demonstrating fatigue; there were no significant changes in tension at Ls. In separate muscles contracting at Lo, Q was set to that measured at Ls (1.1 ml . min-1 . g-1), resulting in decreased VO2 (7 micromol . min-1 . g-1), and rapid fatigue, to 0.44 . Po. These data demonstrate that 1) muscles at Lo have higher Q and VO2 values than those at Ls; 2) fatigue occurs at Lo with high VO2, adjusting metabolic demand (tension output) to match supply; and 3) the lack of fatigue at Ls with lower tension, Q, and VO2 suggests adequate matching of metabolic demand, set low by short muscle length, with supply optimized by low preload. These differences in tension and VO2 between Lo and Ls groups indicate that muscles contracting isometrically at initial lengths shorter than Lo are working under submaximal conditions.

Effects of vasoactive intestinal polypeptide and substance P on human intramyometrial arteries and stem villous arteries in term pregnancy

The effects of vasoactive intestinal polypeptide (VIP) and substance P on isolated human intramyometrial arteries and fetal stem villous arteries obtained from term pregnant women were compared. Ring preparations of small intramyometrial arteries and fetal stem villous arteries obtained at caesarean section were mounted in organ baths, and isometric tension was recorded. None of the peptides affected resting tension. In intramyometrial arteries precontracted by vasopressin (2.8 x 10(-9) M) both substance P (10(-12) to 10(-8) M) and VIP (10(-8) to 10(-6) M) caused relaxation. In fetal stem villous arteries precontracted by prostaglandin F2 alpha (10(-5) M) cumulative addition of substance P (10(-11) to 10(-6) M) did not produce significant changes in tension as compared with controls, while addition of single doses produced moderate relaxation. VIP (10(-8) to 10(-6) M) induced relaxation with similar effects for the addition of cumulative and single doses. The responses to VIP and substance P remained unaffected after pretreatment by atropine (10(-6) M), propranolol (10(-6) M), and indomethacin (10(-6) M). The results support a role for VIP and substance P in the regulation of uteroplacental blood flow in term pregnancy.

Neuromuscular physiology of Hymenolepis diminuta and H. microstoma (Cestoda).

The physiology of the neuromuscular systems in Hymenolepis diminuta and H. microstoma was studied in vitro using intact, adult worm and strips of worm body wall. Intact worms were insensitive to ionic changes in the in vitro buffering system. However, strips of body wall containing longitudinal muscles were extremely sensitive to ionic manipulation. In intact worms tension generated in the strobila had two components; small brief tension peaks up to 500 mg amplitude are superimposed on larger, longer peaks of up to 1200 mg amplitude. Removal of the scolex and neck region either failed to show significant changes in tension, or showed a reduction in amplitude but not of frequency. Muscle contraction of both H. diminuta and H. microstoma were qualitatively similar. In split-worm preparations the concentration of Ca2+ in the bathing solution significantly affected both spontaneous and evoked contractions in H. diminuta and H. microstoma; the addition of CaCl2 greatly reduced the amplitude and frequency of the contractions. The chloride salts of cobalt, barium, cadmium and manganese elicited prolonged contractions of the longitudinal musculature of both H. diminuta and H. microstoma. While CoCl2 was the most effective in stimulating muscle contraction, the magnitude of the response varied with the concentration of Ca2+ in the bath. The results indicate that peripheral inhibition is extremely important in cestode motor control and that extracellular calcium ions may regulate the peripheral inhibitory mechanisms.

Interaction of hyperoxia and blood flow during fatigue of canine skeletal muscle in situ.

Right and left gastrocnemius-plantaris muscle preparations in 20 dogs anesthetized with pentobarbital sodium were used to investigate the effect of hyperoxia on tension maintenance. Muscles were stimulated via the sciatic nerve for 20 min at 60 200-ms tetanic contractions/min (10 impulses/contraction). Direct muscle stimulation after the experimental period resulted in no significant change in tension. In control experiments the tension developed by the right or left muscles over the 20 min was not different. The tension developed by muscles perfused with hyperoxic blood decreased 14% after 20 min, whereas tension in the normoxic muscles decreased 35%. Blood flow in the hyperoxic muscles was significantly higher at 20 min (P less than 0.05). Pump perfusion of one of a pair of normoxic muscles resulted in a tension decrease of 13% in the pump-perfused muscles, whereas tension in the control muscles decreased 34%. Tension maintenance was flow dependent. The effect of hyperoxia could be mediated through the involvement of oxygen in the long-term control of muscle blood flow.

Temporal relation of epicardial electrographic, contractile and biochemical changes after acute coronary occlusion and reperfusion

The increasing use of changes in the S-T segment of local epicardial electrograms to quantitate myocardial infarct size has led to the need for a better understanding of this method. Accordingly, we studied the local electrographic, tension and biochemical changes that occurred after coronary occlusion and subsequent reperfusion in 44 dogs using epicardial electrograms from 10 to 12 sites, Walton-Brodie strain gauge arches and myocardial ratios of potassium ion to sodium ion ( K + Na + ). After coronary occlusion for 1 hour, total S-T segment elevation increased from 10.2 ± 2.4 to 78.3 ± 13.7 mv ( P < 0.001) and tension development decreased to 63.6 ± 7.0 percent of control value ( P < 0.001); occlusion for 3 hours resulted in a total S-T segment elevation increase from 5.8 ± 3.4 to 56.7 ± 8.7 mv ( P < 0.001) and a tension decrease to 61.4 ± 5.3 percent ( P < 0.001) of control value. After reperfusion two types of response were observed. In nine experiments new local pathologic Q waves appeared in an average of 5.3 of 8.2 ischemic electrode sites within 5 to 10 minutes of reperfusion concomitant with a marked further decrease in total tension from 67.3 ± 05.5 percent to 42.4 ± 6.0 percent of control value ( P < 0.001). Simultaneously, total S-T elevation decreased from 66.1 ± 8.2 to 25.3 ± 3.4 mv ( P < 0.001). In seven experiments no Q waves appeared after reperfusion and there was no significant change in tension. Total S-T elevation again decreased from 58.3 ± 12.7 to 27.1 ± 5.7 mv ( P < 0.025). When normal saline solution was perfused distal to the coronary arterial occlusion total S-T elevation decreased from 68.0 ± 3.6 to 36.3 ± 5.2 mv ( P < 0.001). After 3 hours of coronary occlusion, myocardial K + decreased and Na + increased in the ischemic zone, resulting in a significant decrease in the K + Na + ratio ( P < 0.005). Reperfusion for 2 hours resulted in a further depletion of K + and an increase in Na + with a resultant complete reversal of the K + Na + ratio ( P < 0.001). In summary, after reperfusion the S-T segment abnormalities rapidly decreased in all experiments despite the appearance of new Q waves in more than half of these studies concomitant with either a decrease or no change in contractile ability and continuing myocardial K + loss and Na + accumulation. S-T segment mapping therefore appears to be of limited value in assessing the effect of reperfusion on infarct size. The decrease in S-T segments that occurred with perfusion of either blood or saline solution suggests a “washout” phenomenon.

Nitroglycerin in experimental myocardial infarction effects on regional left ventricular length and tension

Controversy has existed concerning the value of nitroglycerin therapy in acute myocardial infarction. With use of Walton-Brodie strain gauge arches and mercury-in-Silastic segment length gauges, the effects of nitroglycerin (30 μg/kg intravenously) were studied on local tension and length characteristics of the ischemic, border and nonischemic zones of the left ventricle in 10 open chest dogs. In the nonischemic zone total tension increased to 144.8 ± 13.6 (mean ± standard error of the mean) percent ( P <0.005) of control levels, and segment length decreased to 79.4 ± 4.4 percent ( P <0.01) with infusion of nitroglycerin 15 to 30 minutes after coronary ligation. Changes were similar in the groups given nitroglycerin 45 to 60 minutes and 2 to 3 hours after ligation. The border zone exhibited an increase in total tension to 132.3 ± 8.4 percent ( P <0.005) of control level and a decrease in segment length to 79.0 ± 2.4 percent ( P <0.001) in the 15 to 30 minute group. In the 45 to 60 minute group, tension increased to 117.9 ± 4.8 percent ( P <0.005), whereas length decreased to 86.8 ± 1.4 percent ( P <0.001); and in the 2 to 3 hour group tension increased to 124.9 ± 6.0 percent ( P <0.005), and length decreased to 91.9 ± 3.5 percent ( P <0.001). The decrease in magnitude of responsiveness in the 45 to 60 minute and 2 to 3 hour postligation groups compared with the 15 to 30 minute postligation group was highly significant ( P <0.005). The central ischemic zone showed no significant change in tension or length in any group. Maximal response to nitroglycerin administration in both tension and length parameters was observed within 30 to 60 seconds and was concomitant with a decrease in systolic pressure to 73.3 ± 1.9 percent ( P <0.001) and an increase in heart rate to 107.2 ± 1.0 percent. Nitroglycerin improves the contractile performance of the nonischemic and border zones after coronary occlusion without affecting the central ischemic zone. However, the border zone exhibits a progressive decrease in contractile response as a function of time. These data suggest that nitroglycerin has the overall effect of functionally reducing the extent of the ischemic area and strongly supports its potential clinical usefulness in acute myocardial infarction.