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Biomedical subjects

A Koller

Publications and source records attributed to A Koller.

At least 109 records · Page 6Linked to original sources
PubMed1997

Endothelin and prostaglandin H2 enhance arteriolar myogenic tone in hypertension.

We hypothesized that endothelin in addition to prostaglandin (PG)H2 may also contribute to the enhanced myogenic tone of skeletal muscle arterioles of spontaneously hypertensive (SH) rats. Changes in the diameter of isolated, cannulated arterioles (approximately 60 microm) from cremaster muscles of 30-week-old normotensive Wistar Kyoto (WKY) and SH rats were measured as a function of perfusion pressure (20 to 140 mm Hg). Pressure-induced constrictions were significantly enhanced between 60 to 140 mm Hg in arterioles of SH rats compared with those of WKY rats; at 80 and 140 mm Hg the normalized diameter of arterioles (expressed as a percentage of corresponding passive diameter) of SH rats was 11.0% and 15.4% less (P<.05) than that of WKY rats. After inhibition of thromboxane A2-PGH2 receptors by SQ 29,548 (10[-6] mol/L), the still enhanced myogenic response of SH arterioles was eliminated by the removal of endothelium or the administration of BQ-123 (10[-7] mol/L), an endothelin A (ET-A) receptor blocker, which also inhibited constrictions to exogenous ET-1 (10[-11] to 5x10[-10] mol/L). ET-1 elicited comparable responses in arterioles of SH and WKY rats. Thus, in SH rats the enhanced arteriolar constriction to increases in intravascular pressure seems to be due to the production of endothelium-derived constrictor factors PGH2 and endothelin.

Animals↗
PubMed1997

Myogenic responses of isolated lymphatics: modulation by endothelium.

OBJECTIVE: To characterize the effect of increases of intraluminal pressure on the spontaneous diameter oscillations of isolated lymphatics and on the maximum and minimum diameter, in the presence and absence of endothelium. METHODS: Afferent lymphatics were isolated from rat iliac lymph nodes. After cannulation of both ends, lymphatics were equilibrated for 60 minutes at a pressure of 6 cm H2O, and then changes in diameter oscillations to increases in perfusion pressure (from 2-10 cm H2O, were measured. The endothelium was removed by intraluminal infusion of air. Changes in diameter were expressed as a percentage of the corresponding passive diameter obtained in Ca(2+)-free solution. RESULTS: Isolated lymphatics showed phasic spontaneous constriction and dilation (approximately 50 to approximately 150 microns). Removal of extracellular Ca2+ abolished spontaneous diameter oscillations, and the passive diameter increased from 183.0 +/- 5.3 to 205.1 +/- 8.8 microns as pressure increased from 2 to 10 cm H2O. In response to increases in pressure, the normalized minimum diameter (Dmin) increased (from 30.1% +/- 1.1% to 54.8% +/- 1.9% while the normalized maximum diameter (Dmax) of lymphatics did not change. With increasing pressure the amplitude of vasomotion (Dmax-Dmin) decreased, whereas the oscillation frequency increased. Removal of endothelium significantly reduced Dmax; hence, the oscillation amplitude decreased while the frequency increased. Also, endothelium removal elicited a significant change in the slope of the pressure-Dmax curve (from 0.01 +/- 0.4 to -1.43 +/- 0.34). CONCLUSIONS: Increases in intraluminal pressure greatly affect the spontaneous vasomotion of lymphatics and activate the myogenic mechanism intrinsic to the smooth muscle. In addition, endothelial factors are important to maintain adequate lymphatic vasomotion. These findings suggest that intraluminal pressure and endothelial factors can be important contributors to the tone and pumping activity of lymphatics in vivo.

Animals↗
PubMed1996

[Arthroscopic replacement of the anterior cruciate ligament with a double semitendinosus tendon].

At the university hospital of emergency surgery in Innsburck and at the emergency services department of the hospital in Schwaz, anterior cruciate ligament reconstruction was performed in 467 patients between January 1992 and September 1993. In 117 cases, a double semitendinous tendon was used as an autograft. A total of 60 of these patients were followed up at an average of 20 months (13-33) after reconstruction. The results were rated according to the OAK and the Tegner scores. Objective measurements of instability were carried out by a KT 1000 arthrometer. In addition, 21 patients underwent computer-interfaced dynamometer testing using a Cybex 6000. Standardized loading of the thigh muscles was performed at angular velocities of 60 degrees/s (3 repetitions) and 240 degrees/s (30 repetitions): peak torques and total work were analyzed. The mean age was 23.5 years (17-55): 48 were male, 21 female. The main reasons for the ACL ruptures were sports injuries (51 cases). The patients were classified into three groups according to the data of the repair (group 1 reconstruction up to 1 week after trauma-28 patients: group 2: reconstruction between the 2nd and 6th week after trauma-15 patients: group 3: reconstruction 6 and more weeks after trauma-26 patients). In group 1. additional ruptures of the menisci. lesions of the MCL. and chondromalacia were seen in 71.4%. in group 2 in 73.3% and in group 3 in 80.8%. The average rating in the OAK score was 90.16 points: 38 patients (55.70%) had excellent results. 18(26.09%) were good. 9(13.04%) were fair and 4(5.80%) were poor. The Tegner activity score showed a reduction of 0.36 points on average. The largest amount of anterior translation was performed with the KT 1000 manual drawer test (2.29 mm on average compared with the contralateral side). Dynamometer testing showed a statistically significant difference in flexor and extensor mechanism (compared with the non-involved side) in both peak torques and total work. A repeat arthroscopy became necessary in five cases: arthrofibrosis in three and incipient joint infection in two cases.

Adolescent↗
PubMed1996

Successful twin pregnancy in homozygous beta-thalassemia after ovulation induction with growth hormone and gonadotropins.

OBJECTIVE: To describe infertility treatment and pregnancy outcome in a patient with transfusion-dependent beta-thalassemia major and hypopituitarism. DESIGN: Case report. SETTING: University-affiliated infertility clinic. PATIENT: Twenty-four-year-old infertile patient with homozygous beta-thalassemia. INTERVENTION: Co-treatment with GH and gonadotropins. RESULTS: Ovulation induction with clomiphene citrate or gonadotropins alone was unsuccessful. Combined treatment with hMG, hCG, and recombinant human GH followed by intrauterine insemination resulted in a viable twin pregnancy. CONCLUSION: Human GH as an adjunct to hMG and hCG seems to be a sensible approach in the treatment of infertile homozygous beta-thalassemic patients among which very few pregnancies are reported.

Adult↗
PubMed1996

Regional bivalent-univalent pairing versus trivalent pairing of a trisomic chromosome in Saccharomyces cerevisiae.

In meiosis I, homologous chromosomes pair, recombine and segregate to opposite poles. These events and subsequent meiosis II ensure that each of the four meiotic products has one complete set of chromosomes. In this study, the meiotic pairing and segregation of a trisomic chromosome in a diploid (2n + 1) yeast strain was examined. We find that trivalent pairing and segregation is the favored arrangement. However, insertions near the centromere in one of the trisomic chromosomes leads to preferential pairing and segregation of the "like" centromeres of the remaining two chromosomes, suggesting that bivalent-univalent pairing and segregation is favored for this region.

Chromosomes, Fungal↗
PubMed1996

Both nitric oxide and prostaglandin-mediated responses are impaired in skeletal muscle arterioles of hypertensive rats.

OBJECTIVE: To investigate the role played by endothelium-derived dilator factors in the regulation of peripheral vascular resistance by determining whether the dysfunction of the endothelium contributes to the reduced dilator responsiveness of skeletal muscle arterioles in hypertension. METHODS: The endothelial function of isolated, cannulated, pressurized (at 80 mmHg) gracilis muscle arterioles (45-50 microns diameter) of normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) was compared by utilizing vasoactive agents of known action. RESULTS: Acetylcholine (ACh, 10(-9), 10(-8) and 5 x 10(-8) mol/l) and sodium nitroprusside (SNP, 10(-8), 10(-7) and 10(-6) mol/l) elicited similar dilations in arterioles of WKY rats and SHR. Substance P (10(-9), 10(-8) and 5 x 10(-8) mol/l) caused significantly less dilation (by approximately 70%) of SHR arterioles compared with WKY rat arterioles. The calcium ionophore A23187 (5 x 10(-8), 5 x 10(-7) and 10(-6) mol/l) elicited dilations in WKY rat arterioles (9.1 +/- 1.1, 24.0 +/- 1.5, and 39.0 +/- 3.4%, respectively), whereas it evoked constrictions (6.5 +/- 1.1, 14.9 +/- 1.5, and 25.5 +/- 1.6%, respectively) in SHR arterioles. Removal of endothelium, inhibition of prostaglandin synthesis (indomethacin) or blockade of prostaglandin H2 (PGH2) receptors (by SQ 29548) eliminated A23187-induced constrictions of SHR arterioles. The nitric oxide synthase blocker, NG-nitro-L-arginine elicited a significantly greater inhibition of substance P-induced dilations and a greater reduction in basal diameter of WKY rat arterioles than it did in those from SHR. CONCLUSIONS: These data suggest that, in SHR arterioles, the synthesis and/or action of nitric oxide is, or are, impaired and the metabolism of arachidonic acid is altered, resulting in an enhanced production of PGH2. The simultaneous dysfunction of these two dilator pathways of arteriolar endothelium could contribute significantly to the enhanced peripheral resistance observed in hypertension.

Acetylcholine↗
PubMed1996

Myogenic responses of isolated rat skeletal muscle venules: modulation by norepinephrine and endothelium.

The pressure-induced myogenic response of large venules of skeletal muscle and its possible interactions with adrenergic receptor activation and endothelial factors have not yet been elucidated. Therefore, first-order venules of rat gracilis muscle were isolated, cannulated, and placed in an organ chamber. Changes in internal diameter of the vessels as a function of perfusion pressure (PP) were obtained. In response to increases in PP (0.5-17.5 mmHg), the diameter of venules increased from 197.1 +/- 23.96 to 369 +/- 14.1 microns. In passive conditions (in Ca(2+)-free solution), the pressure-diameter curve of venules shifted significantly upward. In the presence of norepinephrine (NE; 10(-6) M) in the bath solution, the pressure-diameter curve of active venules shifted significantly downward, and in the pressure-normalized diameter curve, a negative slope developed (-6.1 +/- 4.6). In both the absence and presence of NE, removal of endothelium significantly reduced venular diameters in the pressure ranges of 3-5 and 2-5 mmHg, respectively, but did not change significantly the characteristics of the pressure-diameter curves. These findings indicate that the smooth muscle of venules actively responds to changes in intraluminal pressure. This response is greatly facilitated by NE and modulated by the endothelium. The myogenic response of skeletal muscle venules, especially in the presence of NE, could have a role in the regulation of the resistance and capacitance of venules and, consequently, blood flow and tissue exchange in skeletal muscle.

Animals↗
PubMed1995

Preferential TCR V beta 1 gene usage by autoreactive T cells in spontaneous autoimmune thyroiditis of the obese strain of chickens.

We studied T cell receptor variable beta (TCR V beta) gene usage by autoreactive T cells in spontaneous autoimmune thyroiditis (SAT) of obese strain (OS) chickens. Chicken alpha beta T cells may express either V beta 1 or V beta 2 genes, the products of which can be recognized by TCR2 and TCR3 monoclonal antibodies, respectively. Selective depletion of V beta 1+ or V beta 2+ T cells in OS chickens was accomplished by repeated injections of TCR2 or TCR3 antibodies into embryonic and 1-3-week-old chickens. The birds were killed at 20 days of age and their spleens and thyroid glands evaluated by immunohistochemistry. We found that V beta 1+ T cells preferentially infiltrated OS chicken thyroid glands. Antibody treatments resulted in a 41% reduction in frequency of V beta 1+, and a 87% reduction of the frequency of V beta 2+ cells in the circulation, and in a profound decrease of the respective T cells in spleens and thyroid glands. Selective suppression of V beta 1+ T cells partially inhibited SAT development in that thyroid-infiltrating cells and destruction of thyroid follicles were reduced by more than 50%. Thyroglobulin autoantibody serum levels were also reduced in V beta 1+ T cell-depleted OS chickens, whereas selective depletion of V beta 2+ T cells did not inhibit SAT development. These findings indicate preferential TCR V beta 1 gene usage by autoreactive T cells in SAT of OS chickens.

Animals↗
PubMed1995

Light concentric exercise and heavy eccentric muscle loading: effects on CK, MRI and markers of inflammation.

The consequences of a single bout of heavy eccentric exercise with and without repeated concentric exercises on MRI images, serum CK levels and markers of inflammation were studied. Two groups (ECC and ECCON), each consisting of 18 male volunteers, performed 70 eccentic contractions of the quadriceps femoris muscle. The study group (ECCON) performed additional concentric contractions on a dynamometer (Cybex II+) one day before and two hours, 1, 2, 3, 6 and 9 days after eccentric loading. Serum levels of creatine kinase (CK) were examined as a function of time, and correlated with measurements of magnetic resonance imaging (MRI) of the involved muscle groups. T2-weighted images of the thigh muscles were studied. Serum C-reactive protein, complement factors C3c and C4, haptoglobin and transferrin were measured as markers of inflammation. Additional concentric contractions (ECCON group) significantly increased CK, compared to the ECC group. However, it has no apparent effect on MRI signal intensity changes, which were of equal magnitude in the loaded vastus intermedius and deep parts of the vastus lateralis in both groups. Likewise, the serum markers of inflammation of the exercised muscles appeared to be absent. Based on MRI-images, additional concentric contractions had no statistically significant effect on muscle damage and breakdown of connective tissue. The five-fold increase in CK in the ECCON group could be a reflection of "massaging out" of the CK from the muscles into the circulation by additional concentric exercises. However, it could also be an indication for a superior sensitivity of assessing muscle fiber damage in comparison to the MRI.

Adult↗
PubMed1995

Rapid adaptation to eccentric exercise-induced muscle damage.

This study examined eccentric exercise-induced muscle damage and rapid adaptation. Twenty-two male subjects performed 70 eccentric actions with the knee extensors. Group A (n = 11) and group B (n = 11) repeated the same exercise 4 and 13 days after the initial bout, respectively. Criterion measures included muscle soreness, muscle force generation (vertical jump height on a Kistler platform), and plasma levels of creatine kinase (CK), slow-twitch skeletal (cardiac beta-type) myosin heavy chains (MHC), and cardiac troponin I. Subjects were tested pre-exercise and up to day 4 following each bout. The initial exercise resulted in an increase in CK and MHC, a decrement in muscle force, and delayed onset muscle soreness in all participants. CK and MHC release correlated closely (rho = 0.73, p = 0.0001), both did not correlate with the decrement in muscle force generation after exercise. Because cardiac troponin I could not be detected in all samples, which excluded a protein release from the heart (cardiac beta-type MHC), this finding provides evidence for a injury of slow-twitch skeletal muscle fibers in response to eccentric contractions. Repetition of the initial eccentric exercise bout after 13 days (group B) did not cause muscle soreness, a decrement in muscle reaction force with vertical jump or significant changes in plasma MHC and CK concentrations, whereas in case of repetition after 4 days (group A) only the significant increases in CK and MHC were abolished. The decrement in reaction force with vertical jump did not differ significantly from that after the initial exercise session, but perceived muscle soreness was less pronounced.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1995

Effects of Hoe-140 and ramiprilat on arteriolar tone and dilation to bradykinin in skeletal muscle of rats.

In skeletal muscle of pentobarbital sodium-anesthetized rats, the mechanism of action and possible role of the potent vasodilator bradykinin (BK) in regulation of arteriolar tone were investigated. Changes in diameter of third-order arterioles of cremaster muscle in response to topical administration of BK and other vasoactive agents were measured with an image-shearing monitor and recorded with video microscopy. All agonists were administered topically on the exteriorized muscle. With use of Hoe-140, a B2-receptor antagonist, the presence of kinin receptors in arterioles was studied. In control preparations, 10(-5) M arachidonic acid (AA), 0.5 x 10(-6) M acetylcholine (ACh), and 10(-5) M adenosine (ADO) evoked dilation of arterioles of up to 70% of resting diameter. BK (10(-9), 10(-8), 10(-7), and 10(-6) M) elicited dose-dependent arteriolar dilations (1.3 +/- 1.3, 4.1 +/- 0.5, 10.3 +/- 1.6, and 13.3 +/- 1.3 microns, respectively). In the presence of 10(-7) M Hoe-140, dilations to AA, ACh, and ADO were not affected, but those to 10(-9)-10(-7) M BK were eliminated or significantly inhibited (10(-6) M BK: to 2.9 +/- 1.8 microns). Also, whereas Hoe-140 significantly reduced basal arteriolar diameters (from 16.7 +/- 0.9 to 13.8 +/- 1.1 microns, P < 0.05), it did not affect constrictions to norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Shear stress-induced dilation is attenuated in skeletal muscle arterioles of hypertensive rats.

Hypertension is thought to alter many of the functions of the vascular endothelium. The present study examines whether shear stress-induced endothelium-dependent skeletal muscle arteriolar dilation is compromised in genetically hypertensive rats. Changes in the diameter of isolated, perfused arterioles (approximately 60 microns) from gracilis muscles of 12-week-old normotensive Wistar rats (NWR) and spontaneously hypertensive rats (SHR) were investigated. At a constant perfusion pressure (80 mm Hg), the active diameter of NWR and SHR arterioles was 57.1 +/- 2.0 and 50.9 +/- 3.5 microns, respectively (mean +/- SEM), while the passive diameter (in Ca(2+)-free solution) was 113.2 +/- 3.1 and 100.6 +/- 2.9 microns, respectively. Increases in wall shear stress (from 0 to 100 dyne/cm2) elicited by increases in perfusate flow (from 0 to 25 microL/min) resulted in marked increases in the diameter of NWR arterioles, but such increases produced substantially smaller dilations in SHR arterioles (43.0 versus 18.9 microns). The prostaglandin synthesis inhibitor indomethacin (10(-5) mol/L) significantly attenuated the shear stress-induced dilations in both strains of rats. In contrast, the nitric oxide synthase inhibitor N omega-nitro-L-arginine (10(-4) mol/L) significantly shifted the shear stress-diameter curve to the right in vessels from NWR (by 50 dyne/cm2) but not in those from SHR. Thus, in gracilis muscle arterioles of SHR, the reduced dilation to increases in shear stress seems to be due to the lack of nitric oxide synthesis and/or release in response to shear stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Exercise training augments flow-dependent dilation in rat skeletal muscle arterioles. Role of endothelial nitric oxide and prostaglandins.

We aimed to test the hypothesis that as a consequence of short-term daily exercise, flow (shear stress)-dependent dilation and its mediation by the endothelium are altered in skeletal muscle arterioles. After initial familiarization with the protocol, rats ran on a treadmill once a day (with gradually increasing intensity up to 40 minutes and 28 m/min) for approximately 3 weeks (EX group); a control group remained sedentary (SED group). The active (internal) diameters of isolated gracilis muscle arterioles of SED and EX rats at 80 mm Hg were significantly different (55.2 +/- 2.1 and 49.3 +/- 2.0 microns, P < .05), and their passive diameters (in Ca(2+)-free solution) were 105.3 +/- 3.1 and 111.2 +/- 2.4 microns (not significantly different), respectively. Increases in flow of the perfusion solution from 0 to 12 microL/min elicited a significantly greater increase in diameter of EX arterioles (by 83.5% at maximum flow). This enhanced sensitivity maintained a lower shear stress in EX arterioles (15 to 20 dyne/cm2) compared with SED arterioles (25 to 35 dyne/cm2). In both SED and EX arterioles, flow-dependent dilation was eliminated after removal of the endothelium. Either N omega-nitro-L-arginine, a nitric oxide synthase inhibitor, or indomethacin, an inhibitor of prostaglandin synthesis, shifted the flow-diameter and calculated wall shear stress-diameter curves significantly to the right. Each of the inhibitors reduced flow-dependent dilation to a similar degree (approximately 40% to 45%); their combined administration nearly completely eliminated the dilation of arterioles of both SED and EX rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗
PubMed1995

Flow-dependent dilation and myogenic constriction interact to establish the resistance of skeletal muscle arterioles.

OBJECTIVE: To test the hypothesis that the diameter of skeletal muscle arterioles is determined by the interaction of responses elicited by intravascular pressure and flow. METHODS: Experiments were conducted on isolated, cannulated, first-order arterioles of cremaster muscle of male Wistar rats. The diameter of arterioles was followed by videomicroscopy. Perfusion pressures and flows were controlled. RESULTS: In the absence of perfusate flow, increases in perfusion pressure (from 0 to 120 mm Hg), after initial dilation, elicited endothelium independent constrictions of arterioles. At 60 mm Hg of perfusion pressure, the active diameter of vessels was 84.9 +/- 1.9 microns. The passive diameter of arterioles (Ca2(+)-free solution)was 150.6 +/- 2.4 microns. Increases in perfusate flow resulted in a significant upward shift in the pressure-diameter curves; in the presence of perfusate flows of 20, 40, and 60 microL/min, the constriction of the vessels at a pressure of 60 mm Hg was attenuated by 25.1 +/- 3.9%, 35.2 +/- 3.0%, and 46.8 +/- 4.4%, respectively. In contrast, the corresponding diameter of arterioles at perfusate flows of 10 to 60 microL/min was significantly reduced when perfusion pressure was increased from 60 to 80 and 100 mm Hg (at a flow of 60 microL/min) by 12.0 +/- 4.3% and 37.1 +/- 2.8%, respectively. Hence, both flow- and shear stress-diameter curves were significantly shifted downward when perfusion pressure increased from 60 to 100 mm Hg. CONCLUSION: These results demonstrate that an interplay between pressure and flow-sensitive mechanisms is an important determinant of the arteriolar resistance in skeletal muscle.

Animals↗
PubMed1994

Increases in oxygen tension evoke arteriolar constriction by inhibiting endothelial prostaglandin synthesis.

In vivo and in vitro studies concerned with the role of oxygen in the regulation of blood flow have primarily investigated the response of blood vessels to decreases in oxygen tension. In this study, we examined the response of isolated rat cremaster skeletal muscle arterioles to increases in oxygen tensions. First-order arterioles with an average diameter of 90 microns were cannulated and pressurized to 65 mm Hg and studied under constant pressure in a no-flow state. Arterioles were equilibrated in a Krebs bicarbonate-buffered solution (ph 7.4) gassed with 21% O2, 5% CO2, 74% N2. Changes in arteriolar diameters were continuously measured and recorded in response to increases in bath PO2 (20 to 660 mm Hg). Arterioles were studied before and after either the removal of the endothelium or the administration of indomethacin (IND, 10(-5) M), to inhibit prostaglandin synthesis. When the bath PO2 was increased from 20 to 150 mm Hg, arteriolar diameters decreased by 37%; they then decreased an additional 14% when bath PO2 was increased from 150 to 660 mm Hg. Removal of the endothelium or administration of IND completely eliminated the arteriolar constrictions in response to increases in PO2 from 20 to 150 mm Hg, and from 150 to 660 mm Hg. These observations suggest that rat cremaster arterioles constrict to increases in oxygen tension by reduction in the synthesis of endothelium-derived dilator prostaglandins.

Animals↗