Stress Relieving Heat Treatment of 316L Stainless Steel Made by Additive Manufacturing Process.

Residual stress occurs in the materials after different methods of processing due to the application of pressure and/or thermal gradient. The occurrence of residual stresses can be observed in both subtractive and additive-manufactured (AM) materials and objects. However, pressure residual stresses are considered, in some cases, to have a positive effect; there are applications where the neutral stress state is required. As there is a lack of standards describing the heat treatment of AM materials, there is a need for experimental research in this field. The objective of this article is to determine the heat treatment thermal regime to achieve close to zero stress state in the subsurface layer of additively manufactured AM316L stainless steel. The presented objective leads to the long-term goal of neutral etalons for eddy current residual stress testing preparation. A semi-product intended for the experiment was prepared using the Selective Laser Melting (SLM) process and subsequently cut, using Abrasive Water Jet (AWJ) technology, into experimental specimens, which were consequently heat-treated in combination with four temperatures and three holding times. Residual stresses were measured using X-ray diffraction (XRD), and microstructure variations were observed and examined. A combination of higher temperature and longer duration of heat treatment caused more significant stress relaxation, and the original stress state of the material influenced a degree of this relaxation. The microstructure formed of cellular grains changed slightly in the form of grain growth with randomly occurring unmolten powder particles, porosity, and inclusion precipitation.

Effect of Crosshead Speed and Volume Ratio on Compressive Mechanical Properties of Mono- and Double-Gyroid Structures Made of Inconel 718.

The current development of additive technologies brings not only new possibilities but also new challenges. One of them is the use of regular cellular materials in various components and constructions so that they fully utilize the potential of porous structures and their advantages related to weight reduction and material-saving while maintaining the required safety and operational reliability of devices containing such components. It is therefore very important to know the properties of such materials and their behavior under different types of loads. The article deals with the investigation of the mechanical properties of porous structures made by the Direct Metal Laser Sintering (DMLS) of Inconel 718. Two types of basic cell topology, mono-structure Gyroid (G) and double-structure Gyroid + Gyroid (GG), with material volume ratios of 10, 15 and 20 %, were studied within our research to compare their properties under quasi-static compressive loading. The testing procedure was performed at ambient temperature with a servo-hydraulic testing machine at three different crosshead testing speeds. The recorded data were processed, while the stress-strain curves were plotted, and Young's modulus, the yield strength Re0.2, and the stress at the first peak of the local maximum σLocMax were identified. The results showed the best behavior under compression load among the studied structures displayed by mono-structure Gyroid at 10 %. At the same time, it can be concluded that the wall thickness of the structure plays an important role in the compressive properties but on the other hand, crosshead speed doesn´t influence results significantly.

The Role of Perivascular Adipose Tissue in Early Changes in Arterial Function during High-Fat Diet and Its Combination with High-Fructose Intake in Rats.

The aim of the current study was to evaluate the influence of a high-fat diet and its combination with high-fructose intake on young normotensive rats, with focus on the modulatory effect of perivascular adipose tissue (PVAT) on the reactivity of isolated arteries. Six-week-old Wistar-Kyoto rats were treated for 8 weeks with a control diet (10% fat), a high-fat diet (HFD; 45% fat), or a combination of the HFD with a 10% solution of fructose. Contractile and relaxant responses of isolated rat arteries, with preserved and removed PVAT for selected vasoactive stimuli, were recorded isometrically by a force displacement transducer. The results demonstrated that, in young rats, eight weeks of the HFD might lead to body fat accumulation and early excitation of the cardiovascular sympathetic nervous system, as shown by increased heart rate and enhanced arterial contractile responses induced by endogenous noradrenaline released from perivascular sympathetic nerves. The addition of high-fructose intake deteriorated this state by impairment of arterial relaxation and resulted in mild elevation of systolic blood pressure; however, the increase in arterial neurogenic contractions was not detected. The diet-induced alterations in isolated arteries were observed only in the presence of PVAT, indicating that this structure is important in initiation of early vascular changes during the development of metabolic syndrome.

Expression of Melatonin Receptor 1 in Rat Mesenteric Artery and Perivascular Adipose Tissue and Vasoactive Action of Melatonin.

Melatonin is released by the pineal gland and can modulate cardiovascular system function via the G protein-coupled melatonin receptors MT1 and MT2. Most vessels are surrounded by perivascular adipose tissue (PVAT), which affects their contractility. The aim of our study was to evaluate mRNA and protein expression of MT1 and MT2 in the mesenteric artery (MA) and associated PVAT of male rats by RT-PCR and Western blot. Receptor localization was further studied by immunofluorescence microscopy. Effects of melatonin on neurogenic contractions were explored in isolated superior MA ex vivo by measurement of isometric contractile tension. MT1, but not MT2, was present in MA, and MT1 was localized mainly in vascular smooth muscle. Moreover, we proved the presence of MT1, but not MT2 receptors, in MA-associated PVAT. In isolated superior MA with intact PVAT, neuro-adrenergic contractile responses were significantly smaller when compared to arteries with removed PVAT. Pre-treatment with melatonin of PVAT-stripped arterial rings enhanced neurogenic contractions, while the potentiating effect of melatonin was not detected in preparations with preserved PVAT. We hypothesize that melatonin can stimulate the release of PVAT-derived relaxing factor(s) via MT1, which can override the direct pro-contractile effect of melatonin on vascular smooth muscle. Our results suggest that melatonin is involved in the control of vascular tone in a complex way, which is vessel specific and can reflect a sum of action on different layers of the vessel wall and surrounding PVAT.

Quercetin Exerts Age-Dependent Beneficial Effects on Blood Pressure and Vascular Function, But Is Inefficient in Preventing Myocardial Ischemia-Reperfusion Injury in Zucker Diabetic Fatty Rats.

Background: Quercetin (QCT) was shown to exert beneficial cardiovascular effects in young healthy animals. The aim of the present study was to determine cardiovascular benefits of QCT in older, 6-month and 1-year-old Zucker diabetic fatty (ZDF) rats (model of type 2 diabetes). Methods: Lean (fa/+) and obese (fa/fa) ZDF rats of both ages were treated with QCT for 6 weeks (20 mg/kg/day). Isolated hearts were exposed to ischemia-reperfusion (I/R) injury (30 min/2 h). Endothelium-dependent vascular relaxation was measured in isolated aortas. Expression of selected proteins in heart tissue was detected by Western blotting. Results: QCT reduced systolic blood pressure in both lean and obese 6-month-old rats but had no effect in 1-year-old rats. Diabetes worsened vascular relaxation in both ages. QCT improved vascular relaxation in 6-month-old but worsened in 1-year-old obese rats and had no impact in lean controls of both ages. QCT did not exert cardioprotective effects against I/R injury and even worsened post-ischemic recovery in 1-year-old hearts. QCT up-regulated expression of eNOS in younger and PKCε expression in older rats but did not activate whole PI3K/Akt pathway. Conclusions: QCT might be beneficial for vascular function in diabetes type 2; however, increasing age and/or progression of diabetes may confound its vasculoprotective effects. QCT seems to be inefficient in preventing myocardial I/R injury in type 2 diabetes and/or higher age. Impaired activation of PI3K/Akt kinase pathway might be, at least in part, responsible for failing cardioprotection in these subjects.

Influence of Age on Anticontractile Effect of Perivascular Adipose Tissue in Normotensive and Hypertensive Rats.

Perivascular adipose tissue (PVAT) and its vasomodulatory effects play an important role in the physiology and pathophysiology of blood vessels. Alterations in PVAT associated with reduction in its anticontractile influence are proven to contribute to vascular dysfunction in hypertension. The aim of this study was to examine whether the changes in PVAT properties could participate in progression of vascular abnormalities in developing spontaneously hypertensive rats (SHR). Normotensive Wistar-Kyoto (WKY) rats and SHR, both in 5th and in 12th week of age, were used. Systolic blood pressure was similar between WKY rats and SHR in 5th week of age; however, in 12th week, it was significantly increased in SHR comparing to WKY rats. The amount of retroperitoneal fat was higher in WKY rats in both age groups, whereas body weight was higher in WKY rats only in 12th week, when compared to age-matched SHR. From isolated superior mesenteric arteries, two ring preparations were prepared for isometric tension recording, one with PVAT intact and other with PVAT removed. In WKY rats as well as in SHR, arterial contractile responses to noradrenaline, applied cumulatively on rings, were significantly inhibited in the presence of intact PVAT. In both age groups, anticontractile effect of PVAT was higher in WKY rats than in SHR. Neurogenic contractions, induced by electrical stimulation of perivascular sympathoadrenergic nerves, were significantly attenuated in the presence of PVAT in WKY mesenteric arteries from both age groups; however, in arteries from SHR, intact PVAT had no influence on this type of contractile responses. The results suggest that in SHR impairment of anticontractile effect of PVAT precedes hypertension and might contribute to its development.

Agmatine Modulation of Noradrenergic Neurotransmission in Isolated Rat Blood Vessels.

Agmatine, a vasoactive metabolite of L-arginine, is widely distributed in mammalian tissues including blood vessels. Agmatine binding to imidazoline and α2-adrenoceptors induces a variety of physiological and pharmacological effects. We investigated the effect of agmatine on contractile responses of the rat pulmonary artery and portal vein induced by electrical stimulation of perivascular nerves and by exogenous adrenergic substances. Experiments were performed on isolated segments of rat main pulmonary artery and its extralobular branches, and portal vein suspended in organ bath containing modified Krebs bicarbonate solution and connected to a force-displacement transducer for isometric tension recording. Electrical field stimulation (EFS) produced tetrodotoxin-sensitive contractile responses of pulmonary artery and portal vein. Besides the well known vasorelaxant actions, we found that agmatine also produced a concentration-dependent inhibition of neurogenic contractions induced by EFS in pulmonary arteries; however, the agmatine treatment did not influence the responses to exogenous noradrenaline. The inhibitory effect on EFS-induced contractions was not abolished by the α2-adrenoceptor antagonist rauwolscine. In portal vein, in contrast, agmatine increased spontaneous mechanical contractions and enhanced the contractions induced by EFS. The results suggest that agmatine can significantly influence vascular function of pulmonary arteries and portal veins by modulating sympathetically mediated vascular contractions by pre- and postsynaptic mechanisms.

Comparison Of Cardiovascular Characteristics In Normotensive And Hypertensive Rat Strains.

BACKGROUND: Hypertensive rats serve as valuable tools for studies of dysregulations in cardiovascular functions before and during pathological elevation of blood pressure. They exhibit many defects in structure and function of heart and vessels which are often related to severity of hypertension. OBJECTIVE: The relationship of blood pressure level and manifestation of aberrations in selected cardiovascular and metabolic parameters were determined in 20-week-old normotensive Wistar-Kyoto (WKY) rats, spontaneously hypertensive rats (SHR) and in their F1 offspring borderline hypertensive rats (BHR), and also in normotensive Wistar rats which are genetically less compatible with the other mentioned rat strains. METHODS: Systolic blood pressure and heart rate were measured in conscious rats by the non-invasive tail-cuff method. At the end of the treatment, rats were sacrificed, relative weight of their left heart ventricle and liver were determined and plasma concentration of glucose and triglycerides were measured. Thoracic aorta and superior mesenteric artery were isolated and prepared for isometric tension recording. Neurogenic contractions were elicited by electrical stimulation of perivascular adrenergic nerves. RESULTS: The level of systolic blood pressure in WKY rats (106.0 ± 0.4 mmHg), BHR (149.5 ± 2.5 mmHg) and SHR (186.4 ± 3.9 mmHg) corresponded with the impairment of acetylcholine-induced relaxation of isolated thoracic aorta and with the increase in sensitivity of contractile responses to exogenous noradrenaline and to electrical stimulation of perivascular adrenergic nerves in mesenteric artery. However, rats of the normotensive strain Wistar (118.1 ± 2.0 mmHg) exhibited arterial contractions similar to those obtained in hypertensive rats. Wistar rats had also the highest relative liver weight and plasma triglyceride concentration. CONCLUSION: These observations indicate that when comparing non-related rat strains the higher magnitude of arterial contractions and abnormal lipid parameters may not correlate with hypertensive state.

Cardiovascular effects of high-fructose intake in rats with nitric oxide deficiency.

The aim of this study was to evaluate the involvement of nitric oxide (NO) system damage in the deleterious effects of high-fructose intake in rats. Fructose was administered as 10% solution in drinking water to twelve-week-old male Wistar rats for the period of 8 weeks. Blood pressure was measured by tail-cuff plethysmography. After sacrificing the rats at the end of the treatment, relative weights of heart and liver and biochemical parameters in blood plasma were determined. Reactivity of isolated conduit arteries was measured using a force-displacement transducer for recording isometric tension. Fructose drinking rats had increased blood pressure and impaired acetylcholine-induced relaxation of the thoracic aorta in comparison with control rats drinking just tap water. Relative liver weight and plasma concentrations of glucose and triglycerides were also elevated after fructose administration. In a further group of Wistar rats, inhibition of NO production by administration of N(G)-nitro-L-arginine methyl ester (L-NAME; 40 mg/kg/day) was performed throughout fructose intake. L-NAME treatment itself induces increase in blood pressure and relative heart weight as well as impairment in arterial relaxation and contractility. However, in these rats, fructose administration did not cause further elevation of blood pressure and other abnormalities observed in rats receiving fructose without L-NAME. Our results showed that in the state of NO deficiency (induced by L-NAME administration) fructose does not induce cardiovascular and metabolic alterations which develop in rats with a functional NO system. This indicates that impairment of the NO system may participate in many of the adverse effects induced by high-fructose intake.

Diminished contractile responses of isolated conduit arteries in two rat models of hypertension.

Hypertension is accompanied by thickening of arteries, resulting in marked changes in their passive and active mechanical properties. The aim of this study was to demonstrate that the large conduit arteries from hypertensive individuals may not exhibit enhanced contractions in vitro, as is often claimed. Mechanical responses to vasoconstrictor stimuli were measured under isometric conditions using ring arterial segments isolated from spontaneously hypertensive rats, N(omega)-nitro-L-arginine methyl ester (L-NAME)-treated Wistar rats, and untreated Wistar rats serving as normotensive control. We found that thoracic aortas from both types of hypertensive rats had a greater sensitivity but diminished maximal developed tension in response to noradrenaline, when compared with that from normotensive rats. In superior mesenteric arteries, the sensitivity to noradrenaline was similar in all examined rat groups but in L-NAME-treated rats, these arteries exhibited decreased active force when stimulated with high noradrenaline concentrations, or with 100 mM KCl. These results indicate that hypertension leads to specific biomechanical alterations in diverse arterial types which are reflected in different modifications in their contractile properties.

Reactivity of the mesenteric bed arteries of normotensive rats exposed to chronic social stress.

The aim of this study was to investigate the effects of chronic social stress on endothelium-dependent relaxation in the superior mesenteric artery (SMA) and its first branches (1MA) as well as on neurogenic contractions of SMA in adult, male Wistar-Kyoto (WKY) rats. Mesenteric arteries were isolated from control (living space: 480 cm(2)/rat) or stressed rats exposed to 8-week-lasting crowding stress (living space: 200 cm(2)/rat). Blood pressure (BP) and heart rate, determined by tail-cuff plethysmography, were not affected by crowding. Stress increased neurogenic contractions of SMA elicited by electrical stimulation of perivascular nerves and significantly elevated vasoconstriction induced by exogenous noradrenaline in SMA, without modulation of its endothelial function. In 1MA, nitric oxide (NO)-dependent component of endothelium-dependent relaxation to acetylcholine was investigated. In 1MA, stress failed to affect noradrenaline- and phenylephrine-induced vasoconstriction, total acetylcholine-induced relaxation as well as its NO-dependent and NO-independent components. Moreover, endothelium-independent sodium nitroprusside-induced relaxations of 1MA from the stressed rats did not differ from those of controls. In conclusion, chronic stress produced by crowding failed to induce an increase of BP, presumably because endothelial function of SMA and vascular function of small mesenteric arteries, which are rather important in BP regulation, remained preserved.

Protein remodeling of the heart ventricles in hereditary hypertriglyceridemic rat: effect of ACE-inhibition.

The aim of this study was to determine whether protein remodeling of the heart ventricles and remodeling of the aorta were present in hereditary hypertriglyceridemic (hHTG) rats and whether treatment with the angiotensin-converting enzyme inhibitor, captopril could prevent these alterations. Three groups of rats were investigated in a four week experiment control Wistar /C/rats, hHTg rats, hHTg rats given captopril (100 mg/kg/day) (hHTg + CAP). In the hHTg group, the increased systolic blood pressure (SBP) was associated with hypertrophy of the LV and RV. Protein profile analysis revealed an enhancement of metabolic protein concentration in both ventricles. The concentration of total collagenous proteins was not changed in either ventricles. However, alterations in composition of cardiac collagen were detected, characterized by higher concentration of hydroxyproline in pepsin-insoluble fraction and lower concentration of hydroxyproline in pepsin soluble faction in the LV. Hypertrophy of aorta, associated with the reduction of nitric oxide dependent relaxation, was also present in hHTG rats. Captopril normalized SBP, reduced left ventricular hypertrophy (LVH), diminished metabolic protein concentration in both ventricles, and improved NO-dependent relaxation of the aorta. Furthermore, captopril partially reversed alterations in hydroxyproline concentration in soluble and insoluble collagenous fractions of the LV. We conclude that hypertrophy of both ventricles and the aorta are present in hHTG rats, along with protein remodeling of both ventricles. Captopril partially prevented left ventricular hypertrophy development and protein remodeling of the myocardium.

Rilmenidine prevents blood pressure increase in rats with compromised nitric oxide production.

AIM: To search tools of high blood pressure in the model of nitric oxide (NO)-defective hypertension, and the study focused on the effect of rilmenidine, agonist of imidazoline receptors, which was suggested to modulate central sympathetic outflow. METHODS: Three experimental groups, each consisting of 7 rats, were used: (I) rats with inhibition of NO synthase (NOS) by N(G)-nitro-L-arginine methyl ester (L-NAME) 40 mg.kg(-1).d(-1) for 4 weeks in drinking water, (II) rats with inhibited NOS as in group I , plus agonist of imidazoline receptors rilmenidine 3 mg.kg(-1).d(-1) for 4 weeks by gavage, and (III) control rats. Systolic blood pressure was measured weekly noninvasively. At the end of experiment aortic ring isometric tension was followed, NOS expression (aorta, left ventricle), and NOS activity (left ventricle and brain) were determined. RESULTS: In the group I systolic blood pressure increased significantly, aortic ring relaxation to acetylcholine was significantly attenuated. Rilmenidine administered simultaneously with L-NAME (group II) prevented the increase of blood pressure which did not differ significantly from control values; aortic ring relaxation to acetylcholine did not differ from control. No change in NOS expression (aorta and left ventricle) was found in groups I and II. Significant decline in NOS activity (left ventricle and brain) was found in groups I and II. CONCLUSION: Rilmenidine has a remarkable role in NO-defective hypertension, possibly by inhibiting central sympathetic outflow and by affecting receptors in vascular smooth muscle also. The prime cause of hypertension in this experimental model--the compromised production of NO due to inhibition of NOS--was not affected by rilmenidine.

Beneficial effect of pentaerythrityl tetranitrate on functional and morphological changes in the rat thoracic aorta evoked by long-term nitric oxide synthase inhibition.

The present study examined whether pentaerythrityl tetranitrate (PETN), a tolerance-devoid exogenous donor of nitric oxide (NO), could attenuate functional and morphological changes in the rat thoracic aorta evoked by 6-week NO synthase inhibition by NG-nitro-L-arginine methyl ester (L-NAME). Systolic blood pressure in L-NAME + PETN-treated rats (163 +/- 1 mm Hg) was significantly lower than in L-NAME-treated rats (172 +/- 2 mm Hg) but was still higher than in age-matched controls (126 +/- 2 mm Hg). Six weeks of treatment of rats with L-NAME significantly inhibited endothelium-dependent relaxation of the isolated thoracic aorta induced by acetylcholine. The inhibitory effect of L-NAME was entirely reversed by the simultaneous treatment with PETN. The enhancing effect of L-NAME on noradrenaline-induced contraction was antagonised by long-term treatment with PETN. Wall thickness, cross-sectional area and wall/diameter ratio of the thoracic aorta in L-NAME-treated rats were markedly increased. In the L-NAME + PETN-treated rats, the increment of these parameters was significantly lower. The results suggest that PETN administered to rats during development of NO-deficient hypertension prevented functional impairment and at the same time reduced structural changes in the thoracic aorta induced by long-term inhibition of NO synthase.