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Biomedical subjects

S Q Liu

Publications and source records attributed to S Q Liu.

At least 37 records · Page 2Linked to original sources
PubMed2000

[Derivative-ratio derivative spectrum method for determining nitrate and nitrite radicals (NO3- and NO2-) in environmental water].

A derivative-ratio derivative spectrum method was devised for resolving the interference of two components in a two-component mixture measured in derivative spectrum method. The ratio derivative spectrum was obtained from the derivative absorption spectrum of the mixture divided by a derivative absorption spectrum of one of the components. The derivative of ratio derivative spectrum against wavelength resulted in the derivative-ratio derivative spectrum that was determined by the concentration of one component of the mixture. The results suggest that this method is better than ratio derivative spectrum method and it can be applied for determining nitrate and nitrite (NO3- and NO2-) in environment water samples. Being simple and stable, it can eliminate the influence of the interfering materials, giving a recovery rate of more than 96.7%.

Nitrates↗
PubMed2000

Kinetics of the arginine metabolism of malolactic wine lactic acid bacteria Lactobacillus buchneri CUC-3 and Oenococcus oeni Lo111.

The excretion of citrulline, a precursor of carcinogenic ethyl carbamate, formed from arginine degradation by malolactic bacteria in wine is of toxicological concern. The arginine metabolism of resting cells of Lactobacillus buchneri CUC-3 and Oenococcus oeni Lo1l1 was examined. The citrulline excretion rate was found to be linearly correlated to the arginine degradation rate. It was possible to calculate an arginine to citrulline conversion ratio which could be used to predict the amount of citrulline expected after the degradation of a known quantity of arginine. The conversion ratios determined in this study were similar to data calculated from other authors for fermentations in wine and ranged between 4.0% and 7.7%. Ribose, fructose and glucose inhibited the degradation of arginine in Lact. buchneri CUC-3, and inhibition of arginine degradation by glucose correlated with higher arginine to citrulline conversion ratios. The work presents new results of arginine metabolism in malolactic bacteria and gives starting points for investigations in wine.

Arginine↗
PubMed2000

Prevention of mechanical stretch-induced endothelial and smooth muscle cell injury in experimental vein grafts.

Vein grafts are subject to increased tensile stress due to exposure to arterial blood pressure, which has been hypothesized to induce endothelial cell (EC) and smooth muscle cell (SMC) injury. This study was designed to verify this hypothesis and to develop a tissue engineering approach that can be used to prevent these pathological events. Two experimental models were created in rats to achieve these goals: (1) a nonengineered vein graft with increased tensile stress, which was created by grafting a jugular vein into the abdominal aorta using a conventional end-to-end anastomotic technique; and (2) an engineered vein graft with reduced tensile stress, which was created by restricting a vein graft into a cylindrical sheath constructed using a polytetrafluoroethylene membrane. The integrity of ECs in these models was examined by using a silver nitrate staining method, and the integrity of SMCs was assessed by using a fluorescein phalloidin-labeling technique. It was found that nonengineered vein grafts were associated with early EC denudation with a change in EC coverage from 100 percent in normal jugular veins to 36 +/- 10, 28 +/- 12, 18 +/- 9, 44 +/- 15, 80 +/- 13, and 97 +/- 6 percent at 1 and 6 hours and 1, 5, 10, and 30 days, respectively. Similarly, rapid SMC actin filament degradation was found during the early period with a change in SMC coverage from approximately 94 percent in normal jugular veins to 80 +/- 10, 41 +/- 17, 25 +/- 9, 51 +/- 15, 79 +/- 15, 98 +/- 2 percent at 1 and 6 hours and 1, 5, 10, and 30 days, respectively, in nonengineered vein grafts. In engineered vein grafts with reduced tensile stress, EC denudation and SMC actin filament degradation were prevented significantly. These results suggested that mechanical stretch due to increased tensile stress contributed to EC and SMC injury in experimental vein grafts, and these pathological events could be partially prevented when tensile stress was reduced by using a biomechanical engineering approach.

Anastomosis, Surgical↗
PubMed2000

Involvement of aldose reductase in vascular smooth muscle cell growth and lesion formation after arterial injury.

Abnormal proliferation of vascular smooth muscle cells (VSMCs) is an important feature of atherosclerosis, restenosis, and hypertension. Although multiple mediators of VSMC growth have been identified, few effective pharmacological tools have been developed to limit such growth. Recent evidence indicating an important role for oxidative stress in cell growth led us to investigate the potential role of aldose reductase (AR) in the proliferation of VSMCs. Because AR catalyzes the reduction of mitogenic aldehydes derived from lipid peroxidation, we hypothesized that it might be a potential regulator of redox changes that accompany VSMC growth. Herein we report several lines of evidence suggesting that AR facilitates/mediates VSMC growth. Stimulation of human aortic SMCs in culture with mitogenic concentrations of serum, thrombin, basic fibroblast growth factor, and the lipid peroxidation product 4-hydroxy-trans-2-nonenal (HNE) led to a 2- to 4-fold increase in the steady-state levels of AR mRNA, a 4- to 7-fold increase in AR protein, and a 2- to 3-fold increase in its catalytic activity. Inhibition of the enzyme by sorbinil or tolrestat diminished mitogen-induced DNA synthesis and cell proliferation. In parallel experiments, the extent of reduction of the glutathione conjugate of HNE to glutathionyl-1,4-dihydroxynonene in HNE-exposed VSMCs was decreased by serum starvation or sorbinil. Immunohistochemical staining of cross sections from balloon-injured rat carotid arteries showed increased expression of AR protein associated with the neointima. The media of injured or uninjured arteries demonstrated no significant staining. Compared with untreated animals, rats fed sorbinil (40 mg. kg(-1). d(-1)) displayed a 51% and a 58% reduction in the ratio of neointima to the media at 10 and 21 days, respectively, after balloon injury. Taken together, these findings suggest that AR is upregulated during growth and that this upregulation facilitates growth by enhancing the metabolism of secondary products of reactive oxygen species.

Aldehyde Reductase↗
PubMed2000

[Determination of flavonoids in Ginkgo biloba L. leaves from different producing areas].

OBJECTIVE: To compare the contents of flavonoids in the leaves of Ginkgo biloba gathered from 35 producing areas. METHODS: Separating and determining 3 flavonoid aglycones, quercetin, kaempferol and isorhamnetin, by high performance liquid chromatography, and there by calculating the total contents of flavonoids. RESULTS: The contents of flavonoids in the leaves of G. biloba gathered from different producing areas are different, but in those gathered from Pizhou, Zheng'an Xing'an, Anlu, etc. appear higher.

Flavonoids↗
PubMed1999

T-cell stimulation through the T-cell receptor/CD3 complex regulates CD2 lateral mobility by a calcium/calmodulin-dependent mechanism.

T lymphocyte activation through the T cell receptor (TCR)/CD3 complex alters the avidity of the cell surface adhesion receptor CD2 for its ligand CD58. Based on the observations that activation-associated increases in intracellular [Ca2+] ([Ca2+]i) strengthen interactions between T cells and antigen-presenting cells, and that the lateral mobility of cell surface adhesion receptors is an important regulator of cellular adhesion strength, we postulated that [Ca2+]i controls CD2 lateral mobility at the T cell surface. Human Jurkat T leukemia cells were stimulated by antibody-mediated cross-linking of the TCR/CD3 complex. CD2 was labeled with a fluorescently conjugated monoclonal antibody. Quantitative fluorescence microscopy techniques were used to measure [Ca2+]i and CD2 lateral mobility. Cross-linking of the TCR/CD3 complex caused an immediate increase in [Ca2+]i and, 10-20 min later, a decrease in the fractional mobility of CD2 from the control value of 68 +/- 1% to 45 +/- 2% (mean +/- SEM). One to two hours after cell stimulation the fractional mobility spontaneously returned to the control level. Under these and other treatment conditions, the fraction of cells with significantly elevated [Ca2+]i was highly correlated with the fraction of cells manifesting significantly reduced CD2 mobility. Pretreatment of cells with a calmodulin inhibitor or a calmodulin-dependent kinase inhibitor prevented Ca2+-mediated CD2 immobilization, and pretreatment of cells with a calcineurin phosphatase inhibitor prevented the spontaneous reversal of CD2 immobilization. These data suggest that T cell activation through the TCR/CD3 complex controls CD2 lateral mobility by a Ca2+/calmodulin-dependent mechanism, and that this mechanism may involve regulated phosphorylation and dephosphorylation of CD2 or a closely associated protein.

Biophysical Phenomena↗
PubMed1999

Partial prevention of monocyte and granulocyte activation in experimental vein grafts by using a biomechanical engineering approach.

Leukocytes interact with endothelial cells and contribute to the development of vascular diseases such as thrombosis and atherosclerosis. These processes are possibly influenced by mechanical factors. This study focused on the role of mechanical stretch in the activation of monocytes and granulocytes in experimental vein grafts. Two models were created by using rats: a nonengineered vein graft with increased tensile stress, which was created by grafting a jugular vein into the abdominal aorta, and an engineered vein graft with reduced tensile stress, which was created by restricting the vein graft into a cylindrical sheath constructed by using fixative-treated intestinal tissue. The density of activated monocytes and granulocytes, which attached to the endothelium, and the distribution of the intercellular adhesion molecule (ICAM)-1 in endothelial cells were examined using immunohistological assays. It was found that, in nonengineered vein grafts, the density of activated monocytes and granulocytes increased significantly compared to that in normal jugular veins at day 1, 5, 10 and 20. At each observation time, the cell density in the proximal region of the nonengineered vein grafts was significantly higher than that in the middle and distal regions, and the cell density in the distal region was significantly higher than that in the middle region. These changes were associated with ICAM-1 clustering at day 1 and 5 and focal ICAM-1 un-regulation at day 10 and 20. In engineered vein grafts, the density of activated monocytes and granulocytes decreased significantly compared to that in nonengineered vein grafts at all observation times, although it was significantly higher than that in normal jugular veins. At each observation time, the cell density in the proximal and distal regions was significantly higher than that in the middle region, but no significant difference was found between the proximal and distal regions. ICAM-1 clustering along endothelial cell borders was found at day 1 and 5, but no apparent focal ICAM-1 up-regulation was found at day 10 and 20. These results suggested that mechanical stretch due to exposure to increased tensile stress contributed to the activation of monocytes and granulocytes in experimental vein grafts, and this event could be partially prevented by reducing tensile stress using a biomechanical engineering approach.

Analysis of Variance↗
PubMed1999

Reduction of end-stage malignant glioma by injection with autologous cytotoxic T lymphocytes.

Autologous cytotoxic T lymphocytes (CTL) against primary-cultured malignant gliomas were generated from peripheral blood mononuclear cells in vitro in 4 patients. Activities of the CTL were highly specific to the corresponding autologous glioma and were inhibited, in one patient, with antibodies against CD3, CD8 and MHC-class I molecules. When the CTL were injected 3 times into the primary-tumor-resected cavity via an Ommaya tube, reduction of the recurrent tumors with magnetic resonance imaging (MRI)-measured volumes exceeding 45 cm3 was observed in 3 patients. In a patient with glioblastoma multiforme (GBM), the tumor volume (estimated, 130 cm3) was rapidly reduced to 1/3, although re-recurrence of the tumor followed 40 days later. A slight but distinct rapid reduction of the tumor volume was observed in another GBM patient and in an anaplastic astrocytoma patient; essentially no change was observed in a further GBM patient. These results suggest that adoptive immunotherapy with autologous CTL will be clinically effective against end-stage malignant gliomas.

Adult↗
PubMed1999

Focal expression of angiotensin II type 1 receptor and smooth muscle cell proliferation in the neointima of experimental vein grafts: relation to eddy blood flow.

Eddy flow has been shown to promote focal smooth muscle cell (SMC) proliferation and neointimal formation in experimental vein grafts. This study focuses on whether the angiotensin II type 1 (AT(1)) receptor mediates these events. Experimental vein grafts with and without eddy flow were created in the rat. Losartan was used to assess the influence of the AT(1) receptor on SMC proliferation. In vein grafts with eddy flow, apparent focal expression of AT(1) mRNA and protein was found in the leading region of the proximal focal neointima, where eddy flow occurred, but not in the trailing region, where eddy flow diminished, at days 5, 10, 20, and 30. The rate of SMC proliferation in the leading region (10.9+/-1.4%, 19.5+/-2.2%, 12.2+/-2.0%, and 6.9+/-1.3% at these times, respectively) was significantly higher than that in the trailing region (9.5+/-1.8%, 15.3+/-2.0%, 8.2+/-1.9%, and 3.2+/-0.7%) in these vein grafts. When eddy flow was prevented in engineered vein grafts, no apparent location difference was found in the distribution of AT(1) receptor mRNA and protein in the neointima, and the rate of SMC proliferation (5.3+/-1.0%, 5.8+/-0.9%, 3.4+/-1.0%, and 3.7+/-0.9% at days 5, 10, 20, and 30, respectively) was reduced significantly. In vein grafts with losartan, the rate of SMC proliferation in the leading region of the neointima (9.4+/-1.8%, 10.1+/-1.3%, 8.3+/-0.9%, and 4.2+/-0. 5% at days 5, 10, 20, and 30, respectively) was significantly lower than that in vein grafts without losartan. These results suggested that eddy flow upregulated the AT(1) receptor, which in turn mediated focal SMC proliferation in the neointima of experimental vein grafts.

Animals↗
PubMed1999

Biomechanical basis of vascular tissue engineering.

Blood vessels develop under the influence of mechanical stresses and strains and remodel in response to alterations in these factors. It has long been hypothesized that mechanical stresses and strains contribute to the development of vascular diseases such as atherosclerosis and hypertrophy. A large number of studies have been conducted to verify this hypothesis and have demonstrated that increased tensile stress and strain due to hypertension may induce and/or facilitate vascular hypertrophy, and oscillatory low fluid shear stress and/or altered shear gradients due to eddy blood flow may initiate and/or promote focal atherosclerosis and intimal hyperplasia. A variety of cellular components, including growth-related factors, cell membrane proteins and lipids, intracellular signaling molecules and transcriptional factors, and immediate early genes and mitogenic genes, have been shown to mediate these mechanical stress-related pathological processes. These discoveries suggest that a modulation of tensile and fluid shear stresses and strains, if possible, may prevent mechanical stress-induced pathological changes in blood vessels and thus constitute a foundation for the development of vascular engineering approaches. Recent studies have demonstrated by using an experimental vein graft model that biomechanical engineering approaches can be used to reduce tensile stress and strain due to exposure to arterial blood pressure and to prevent eddy blood flow in vein grafts. Such engineering modulations significantly reduced the rate of focal intimal hyperplasia and medial and adventitial hypertrophy in vein grafts. These preliminary studies have provided convincing evidence for further development of vascular biomechanical engineering approaches. In this article, the background, principles, clinical potentials, as well as the limitations of vascular biomechanical engineering are discussed.

Arteriosclerosis↗
PubMed1999

Autologous high-killing cytotoxic T lymphocytes against human lung cancer are induced using interleukin (IL)-1beta, IL-2, IL-4, and IL-6: possible involvement of dendritic cells.

Although CTLs bear main immune responses in human tumors, stable CTL clones against human lung cancer have rarely been generated. Our previous study demonstrated efficient autologous CTL induction in human gastric cancer and glioblastoma by cytokine combination of interleukin (IL)-1beta (167 IU/ml), IL-2 (67 IU/ml), IL-4 (67 IU/ml), and IL-6 (134 IU/ml). In this study, we demonstrated successful induction of autologous stable CTLs in five of six patients with lung adenocarcinoma from mixed-lymphocyte tumor culture using this cytokine combination. All CTLs revealed potent and specific killing activity against autologous target cells (over 75% in CD8+ CTLs and over 50% in CD4+ CTLs at an E:T ratio of 10 for 24 h). Using a series of antibodies, CD8+ CTLs showed to recognize tumor-specific antigens of lung cancer cells through HLA class I. In the separate experiments, failure of CTL induction from monocyte-depleted peripheral blood mononuclear cells and appearance of cells with characteristics of dendritic cells from adherent peripheral blood mononuclear cells in the culture of the same concentration of IL-1beta, IL-4, and IL-6 indicated that CTLs can be efficiently generated by this cytokine combination via possible dendritic cell induction. This is the first study of an efficient and reproducible in vitro CTL induction against human lung cancer.

Adenocarcinoma↗
PubMed1998

Depolarization selectively increases the expression of the Kv3.1 potassium channel in developing inferior colliculus neurons.

The Kv3.1 channel subunit, when expressed heterologously, gives rise to a high-threshold noninactivating potassium current. Experiments with auditory neurons have suggested that the presence of this channel subunit enables them to fire action potentials at high frequencies. We have found that the expression levels of Kv3.1 transcripts increase in inferior colliculus neurons before the onset of hearing and then remain relatively constant. Because spontaneous neuronal activity plays an important role in modulating neuronal excitability during development, we examined the effects of depolarization with an elevated concentration of external potassium ions on the expression of Kv3.1 channel subunits in immature inferior colliculus neurons. Elevated potassium produced a marked increase in Kv3.1 mRNA levels and in the amplitude of a high-threshold, noninactivating current before the onset of hearing. This increase was prevented by the presence of a calcium channel blocker, indicating that calcium influx mediated the depolarization-induced increase in this current. In contrast, treatment with an elevated external potassium concentration caused only a moderate increase in the peak amplitude of a lower-threshold inactivating current. The repolarization of action potentials in the high-potassium-treated cells was more rapid and complete than in the control cells. Computer simulations confirmed that this change could be explained by a change in Kv3.1-like current of the same magnitude as recorded in voltage-clamp experiments. Thus, depolarization and calcium influx may alter the excitability of immature inferior colliculus neurons by selectively increasing the levels of a Kv3. 1-like potassium current.

Aging↗
PubMed1998

Prevention of focal intimal hyperplasia in rat vein grafts by using a tissue engineering approach.

The present study focused on the role of blood flow in the formation of focal intimal hyperplasia in vein grafts, as well as the development of an engineering approach that can be used to eliminate disturbed blood flow and prevent blood flow-related focal intimal hyperplasia. A rat vein graft model was constructed by interposing a jugular vein into the abdominal aorta with end-to-end anastomoses. Locally disturbed flow was identified by analyzing particle streak-lines in methyl salicylate-cleared and perfused vein grafts in vitro with a physiological Reynolds number. At day 10, 20, and 30 after surgery, focal intimal hyperplasia of the vein grafts was examined using a histological approach and the density of alpha-actin positive cells was determined using immunohistological and fluorescent approaches. Results showed that apparent eddy blood flow formed at the proximal, but not at the distal, end of the vein grafts due to graft-host diameter mismatch and local geometric distortions, and was associated with apparent focal intimal hyperplasia. The thickness of the alpha-actin positive layers of the proximal vein grafts was significantly higher than that of the distal grafts (192 +/- 27 vs. 94 +/- 18 microm, 278 +/- 55 vs. 124 +/- 20 microm, and 288 +/- 24 vs. 131 +/- 23 microm for day 10, 20. and 30, respectively). The density of the alpha-actin positive cells, however, was similar between the proximal and the distal regions (3569 +/- 361 vs. 3285 +/- 343 cells/mm2, 5540 +/- 650 vs. 5376 + 887 cells/mm2, and 5465 +/- 791 vs. 5278 +/- 524 cells/mm2 for day 10, 20, and 30, respectively). When eddy blood flow was eliminated by matching the graft-host diameters using a tissue engineering approach, the average thickness of the alpha-actin positive layers of the proximal (71 +/- 15, 86 +/- 16, and 85 +/- 14 microm for day 10, 20, and 30, respectively) and the distal vein grafts (68 +/- 13, 80 +/- 14, and 79 +/- 13 microm for day 10, 20, and 30, respectively) was reduced significantly. The density of the alpha-actin positive cells was also reduced significantly in the proximal (2946 +/- 359, 3261 +/- 295, 3472 +/- 599 cells/mm2 for day 10, 20, and 30, respectively) and in the distal regions (3151 +/- 511, 3466 +/- 687, 3593 +/- 688 cells/mm2 for day 10, 20, and 30, respectively). The thickness of the alpha-actin positive layers and the density of the alpha-actin positive cells were not significantly different between the proximal and distal regions of the engineered vein grafts at each observation time. These results suggest that eddy flow may develop in vein grafts and may facilitate the formation of focal intimal hyperplasia, and the vascular tissue engineering approach developed in this study may be used to prevent blood flow-related focal intimal hyperplasia in vein grafts.

Actins↗
PubMed1998

High rate of induction of human autologous cytotoxic T lymphocytes against renal carcinoma cells cultured with an interleukin cocktail.

A high rate of induction (9 of 10 cases) of human autologous cytotoxic T lymphocytes (CTL) was achieved in vitro from peripheral blood mononuclear cells of renal carcinoma patients by applying an interleukin (IL)-cocktail consisting of IL-1, -2, -4, and -6. The CTL specifically lysed their own target carcinoma cells within 24 h but did not kill neighboring autologous normal kidney cells or allogeneic renal cancer cell lines. In the case of TUHR4TKB, for which autologous CTL were not induced, no expression of MHC class-I molecules was observed on the surface of these carcinoma cells, although they were sensitive to autologous natural killer cells. The results imply that adoptive immunotherapy for metastasized renal carcinoma will be feasible with autologous CTL in combination with natural killer cells.

Cell Survival↗
PubMed1998

Influence of tensile strain on smooth muscle cell orientation in rat blood vessels.

Blood vessels are subject to tensile stress and associated strain which may influence the structure and organization of smooth muscle cells (SMCs) during physiological development and pathological remodeling. This study focused on the influence of the major tensile strain on the SMC orientation in the blood vessel wall. Several blood vessels, including the aorta, the mesenteric artery and vein, and the jugular vein of the rat were used to observe the normal distribution of tensile strains and SMC orientation; and a vein graft model was used to observe the influence of altered strain direction on the SMC orientation. The circumferential and longitudinal strains in these blood vessels were measured by using a biomechanical technique, and the SMC orientation was examined by fluorescent microscopy at times of 10, 20, and 30 days. Results showed that the SMCs were mainly oriented in the circumferential direction of straight blood vessels with an average angle of approximately 85 deg between the SMC axis and the vessel axis in all observed cases. The SMC orientation coincided with the principal direction of the circumferential strain, a major tensile strain, in the blood vessel wall. In vein grafts, the major tensile strain direction changed from the circumferential to the longitudinal direction at observation times of 10, 20, and 30 days after graft surgery. This change was associated with a decrease in the angle between the axis of newly proliferated SMCs and that of the vessel at all observation times (43 +/- 11 deg, 42 +/- 10 deg, and 41 +/- 10 deg for days 10, 20, and 30, respectively), indicating a shift of the SMC orientation from the circumferential toward the longitudinal direction. These results suggested that the major tensile strain might play a role in the regulation of SMC orientation during the development of normal blood vessels as well as during remodeling of vein grafts.

Actins↗
PubMed1997

Functional interactions between cytoplasmic domains of the skeletal muscle Ca2+ release channel.

The skeletal muscle Ca2+ release channel (RYR1), which plays a critical role in excitation-contraction coupling, is a homotetramer with a subunit molecular mass of 565 kDa. Oxidation of the channel increases its activity and produces intersubunit cross-links within the RYR1 tetramer (Aghdasi, B., Zhang, J., Wu, Y., Reid, M. B., and Hamilton, S. L. (1997) J. Biol. Chem. 272, 3739-3748). Alkylation of hyperreactive sulfhydryls on RYR1 with N-ethylmaleimide (NEM) inhibits channel function and blocks the intersubunit cross-linking. We used calpain and tryptic cleavage, two-dimensional SDS-polyacrylamide gel electrophoresis, N-terminal sequencing, sequence-specific antibody Western blotting, and [14C]NEM labeling to identify the domains involved in these effects. Our data are consistent with a model in which 1) diamide, an oxidizing agent, simultaneously produces an intermolecular cross-link between adjacent subunits within the RYR1 tetramer and an intramolecular cross-link within a single subunit; 2) all of the cysteines involved in both cross-links are in either the region between amino acids approximately 2100 and 2843 or the region between amino acids 2844 and 4685; 3) oxidation exposes a new calpain cleavage site in the central domain of the RYR1 (in the region around amino acid 2100); 4) sulfhydryls that react most rapidly with NEM are located in the N-terminal domain (between amino acids 426 and 1396); 5) alkylation of the N-terminal cysteines completely inhibits the formation of both inter- and intrasubunit cross-links. In summary, we present evidence for interactions between the N-terminal region and the putatively cytoplasmic central domains of RYR1 that appear to influence subunit-subunit interactions and channel activity.

Animals↗
PubMed1997

Regression of hypoxic hypertension-induced changes in the elastic laminae of rat pulmonary arteries.

The elastic laminae of the pulmonary arteries (PAs) undergo a progressive structural change in hypoxic hypertension. This study focused on the reversibility of altered PA elastic laminae of the rat due to hypoxic hypertension. The structure and cross-sectional area of the PA medial elastic laminae were examined by using electron-microscopic and image-analytic approaches during recovery from 12 h and 10 days of hypoxic hypertension. At 12 h of hypoxic hypertension, the elastic laminae, which appeared homogeneous in normal control animals, were reorganized into structures composed of randomly oriented filaments, with an increase in the cross-sectional area of 70%. At 10 days of hypoxic hypertension, the elastic laminae appeared homogeneous in structure and normal in cross-sectional area despite continuous exposure to hypoxia. During recovery from 12 h of hypoxic hypertension, the medial elastic laminae regained their homogeneous structure and normal cross-sectional area after day 2. During recovery from 10 days of hypoxic hypertension, the medial elastic laminae changed from homogeneous to filamentous structures, with a progressively altered cross-sectional area that increased by 89% from recovery day 0 to day 10 and returned to the normal level on day 30. These changes were associated with alterations in the PA wall tensile stress. These results indicated that structural changes in the PA elastic laminae were reversible and that the regression process depended on the duration of exposure to hypoxia, the state of the elastic laminae, and possibly the tensile stress level in the PA wall.

Animals↗