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Biomedical subjects

A Koller

Publications and source records attributed to A Koller.

At least 91 records · Page 5Linked to original sources
PubMed1998

Adaptation of flow-induced dilation of arterioles to daily exercise.

We aimed to test the hypothesis that daily exercise elicits an adaptation of blood flow/shear stress-induced dilation of arterioles. To this end we investigated the responses of isolated, pressurized arterioles of mesentery (MES) and plantaris (PL) skeletal muscle of sedentary (SED) and exercised (EX) rats to increases in perfusate flow (PF, range 0-30 microl/min). Rats were run on a treadmill, once daily for 3 to 4 weeks (with gradually increasing intensity up to 40 min at 28 m/min; a total of 15-19 sessions on the treadmill). The passive diameters of arterioles (obtained in Ca2+-free solution) were similar ( approximately 140 microm) but the pressure-induced active diameter (at 80 mmHg) of skeletal muscle arterioles was significantly smaller than that of mesenteric arterioles. The basal diameter of MES arterioles of SED and EX rats was: 83.5 +/- 3.6 and 83.9 +/- 2.9 microm, respectively; increases in PF increased the diameter of SED and EX arterioles to a similar degree by 33.2 +/- 4. 7 and 31.9 +/- 6.1 microm, respectively). The diameters of PL muscle arterioles of SED and EX rats were 62.1 +/- 6.2 and 68.0 +/- 5.5 microm. In contrast to arterioles of MES, the highest PF increased the diameters of arterioles of PL muscle from EX rats to a significantly greater extent than those from SED rats (52.4 +/- 7.8 vs 30.3 +/- 3.9 microm). Thus, there is a functional adaptation to exercise activity in arterioles of skeletal muscle but not in those of arterioles of mesentery. We speculate that the intermittent increase in blood flow/shear stress in arterioles of skeletal muscle during the periods of exercise activity may be the underlying mechanism responsible for this adaptation.

Adaptation, Physiological↗
PubMed1998

[Heterogeneity of seminal vesicle amyloid. Immunohistochemical detection of lactoferrin and amyloid of the prealbumin-transthyretin type].

Localized depositions of amyloid in the seminal vesicles may occur in elderly men. Earlier immunohistochemical studies have failed to identify immunoreactivity of known amyloid material. In this autopsy study, all seminal vesicles of males older than 50 years were histologically examined to determine incidence and phenotype of seminal vesicle amyloidosis. Seven out of 50 patients (14%) showed depositions of amyloid in the seminal vesicles. These amyloid depositions as well as one additional case were characterized histochemically, immunohistochemically and electronmicroscopically. All but two of these patients (75%) showed simultaneously amyloid depositions in the heart. Lactoferrin immunoreactivity was found in 6 patients (75%). Lactoferrin is an iron-binding, bacteriostatic glycoprotein, which is produced in the seminal vesicles. Four patients with lactoferrin positive amyloid in seminal vesicle showed different amyloid depositions in the heart (immunoglobulin light chain amyloid AL-lambda). Two cases (25%) showed the same amyloid type in heart and seminal vesicles (prealbumin-transthyretin type amyloid). Our study shows that most amyloidoses of the seminal vesicles are organ-limited depositions of lactoferrin. These forms of localized amyloidosis have to be separated from senile systemic amyloidosis with seminal vesicle involvement.

Aged↗
PubMed1998

The therapeutic potential of oral creatine supplementation in muscle disease.

The decrease in intracellular creatine concentration observed in a number of muscle diseases may deplete energy homeostasis and may, therefore, be one of the factors determining and/or aggravating muscle weakness and degeneration. Two hypotheses are put forward in the present communication to explain: (i) the mechanisms leading to the disturbances in creatine metabolism found in various muscle diseases; and (ii) the potential of oral creatine supplementation in alleviating the clinical symptoms.

Animals↗
PubMed1998

Early assessment of exercise induced skeletal muscle injury using plasma fatty acid binding protein.

OBJECTIVE: To test whether fatty acid binding protein (FABP) is a useful plasma marker for the early detection of exercise induced skeletal muscle injury in healthy subjects. METHODS: Plasma concentrations of FABP and myoglobin (Mb) were measured in six healthy physical education teacher trainees after 20 minutes of downhill running (16% incline; mean lactate 4 mmol/l; 70% (VO2MAX). Creatine kinase (CK) was measured for comparison. RESULTS: Significant increases were found in plasma FABP (mean peak level 50 micrograms/l), Mb (823 micrograms/l), and CK (491 U/l). Mb and FABP concentrations were already significantly elevated (p < 0.05) at 30 minutes, but CK not until two hours after exercise. Whereas Mb and FABP decreased to normal levels within 24 hours, CK activity remained elevated until 48 hours. The Mb to FABP ratio in plasma after exercise induced muscle injury was 15.0 (1.3) (mean (SEM)) (range 7.4-31.1), which is within the range of ratios calculated for skeletal muscle tissue contents of Mb and FABP, but different from the reported plasma ratio after myocardial injury (4-6). CONCLUSIONS: After eccentric exercise induced muscle injury, plasma FABP and Mb increase and decrease more rapidly than CK, indicating that both FABP and Mb are more useful than CK for the early detection of such injuries and the monitoring of injury during repeated exercise bouts. In addition, the Mb to FABP ratio in the plasma identifies the type of muscle injured.

Adult↗
PubMed1998

Flow-induced responses in skeletal muscle venules: modulation by nitric oxide and prostaglandins.

Skeletal muscle arterioles dilate in response to increases in flow velocity/wall shear stress (WSS). The effect of flow/WSS on the diameter of skeletal muscle venules and the possible endothelial mediation of the response, however, have not yet been characterized. Thus changes in diameter of pressurized (10 mmHg) and norepinephrine-preconstricted venules (179 +/- 8 micron in diameter) to increases in perfusate flow before and after endothelium removal or application of inhibitors of NO and prostaglandin (PG) synthesis, Nomega-nitro-L-arginine (L-NNA, 10(4) M) and indomethacin (Indo, 2.8 x 10(5) M), respectively, were measured. Increases in perfusate flow [elicited by increases in the pressure difference (Pdiff) between proximal and distal cannulas] evoked with a delay of 17 +/- 2 s dilations, up to 36 +/- 9 micron at the highest flow, a response that was completely eliminated by removal/disruption of the venular endothelium. Calculation of WSS indicated that in endothelium-intact venules, the midpoint of the shear stress-diameter curve was at approximately 8 dyn/cm2, whereas in endothelium-denuded vessels, shear stress increased in a linear fashion with increases in flow, up to 40 dyn/cm2. L-NNA significantly reduced flow-induced dilations (from 38 +/- 11 to 17 +/- 9 micron at 14 mmHg Pdiff), whereas in the additional presence of Indo, flow elicited constriction of venules decreasing basal diameter (by 21 +/- 8 micron at Pdiff 12 mmHg). Thus in skeletal muscle venules an increase in shear stress due to increases in perfusate flow stimulates the release of endothelium-derived NO and PGs eliciting dilation, which in turn, regulates WSS, albeit at a lower value than what is observed in arterioles. In the absence of NO and PGs, flow-induced constriction is revealed, the cause of which remains obscure. From these data, we propose that shear stress-related responses of venules are involved in the regulation of venular resistance, especially during high flow conditions, such as reactive and exercise hyperemia.

Animals↗
PubMed1998

Regulation of the vasomotor activity of lymph microvessels by nitric oxide and prostaglandins.

It was shown previously that the presence of endothelium modulates spontaneous vasomotion of small lymphatic vessels. In the present study, we aimed to elucidate the nature of endothelium-derived factors, produced in basal conditions and in response to agonists, that affect the smooth muscle tone of lymph microvessels in vitro. Afferent lymph microvessels were isolated from rat iliac lymph nodes, cannulated with glass micropipettes, and pressurized (6 cmH2O), and changes in their diameter were investigated with video microscopy. In resting conditions, isolated lymph vessels exhibited spontaneous constrictions and dilations. The maximum and minimum diameters (Dmax and Dmin) were 149.8 +/- 2.9 and 85.8 +/- 3.6 microns, respectively. Acetylcholine (ACh, 10(-7) to 10(-5) M) and sodium nitroprusside (SNP, 10(-8) to 10(-6) M) temporarily abolished diameter oscillations, increasing the diameter of lymphatics dose dependently. For example, 10(-5) M ACh and 10(-6) M SNP increased the diameter (Dmax) by 15.2 +/- 2.2 and 25.0 +/- 2.7 microns, respectively. Treatment of vessels with NG-nitro-L-arginine (10(-4) M) significantly reduced the amplitude of diameter oscillations and nearly completely eliminated ACh-induced dilation of lymph microvessels, whereas SNP (10(-6) M) elicited a significantly greater dilation (55.6 +/- 7.5 microns). Arachidonic acid (AA, 10(-8) to 10(-6) M) constricted (up to 50 microns), whereas prostaglandin E2 (PGE2, 10(-9) to 10(-7) M) dilated (up to 40 microns), lymphatic vessels. Indomethacin (10(-5) M) increased both Dmax and Dmin and completely inhibited AA-induced constrictions, but did not affect PGE2-induced dilations of lymph microvessels. AA-induced constrictions of lymphatics were converted into dilations after treatment with SQ-29,548, a selective PGH2-thromboxane A2 (PGH2-TxA2, 10(-6) M) receptor antagonist, whereas PGE2-induced dilations were not affected. We conclude that endothelial nitric oxide and prostaglandins are important modulators of lymphatic vasomotion, hence pumping activity of lymph microvessels in vivo.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1998

Gender difference in flow-induced dilation and regulation of shear stress: role of estrogen and nitric oxide.

Previous studies show that agonist-induced, nitric oxide (NO)-mediated arteriolar dilations are greater in female than in male rats. Thus we hypothesized that flow-dependent arteriolar dilation, which is in part mediated by NO, is also greater in females than in males. Gracilis muscle arterioles from 12-wk-old female and male Wistar rats were isolated, cannulated, and pressurized. At 80 mmHg of perfusion pressure, the active diameter and passive diameter (PD) of arterioles of female and male rats were 58.3 +/- 3.4 and 53.2 +/- 2.6 micrometer as well as 103.6 +/- 4.0 and 115.3 +/- 4.8 micrometer, respectively. Dilations to step increases in perfusate flow from 0 to 25 microliter/min were significantly greater in arterioles of female rats and ovariectomized rats with estrogen replacement (OVE) than in male and ovariectomized female (OV) rats (98.6 +/- 0.6 and 97.4 +/- 1.1% vs. 72.6 +/- 3.3 and 72.5 +/- 3.6% of PD at 25 microliter/min). Calculation of wall shear stress (WSS) revealed that the maintained WSS was significantly lower in arterioles of female than in those of male rats (approximately 20 vs. approximately 35 dyn/cm2). After indomethacin pretreatment, Nomega-nitro-L-arginine methyl ester (L-NAME; 10(-4) M) eliminated flow-dependent dilation in arterioles of male and OV rats but only attenuated (by approximately 50%) the responses in arterioles of female and OVE rats. In vessels of these latter two groups of rats, the remaining flow-induced dilation was completely eliminated by administration of 10(-5) M Hb or 10(-3) M L-NAME. The greater flow/shear stress-induced dilation of arterioles of female rats indicates a gender difference in the regulation of WSS, which is likely to be due to the greater release of NO in female vessels requiring the chronic presence of estrogen. These findings suggest an important role for estrogen in the regulation of peripheral resistance in females.

Animals↗
PubMed1998

Estrogen preserves regulation of shear stress by nitric oxide in arterioles of female hypertensive rats.

Previously we found that flow-induced arteriolar dilation in male spontaneously hypertensive rats (SHR) is significantly impaired, due to the absence of the nitric oxide (NO)-mediated portion of the response, resulting in an elevation of maintained wall shear stress. Since estrogen has been shown to affect NO-mediated responses, we hypothesized that in female SHR (fSHR) the NO-mediated portion of flow-induced responses is preserved. Gracilis muscle arterioles (approximately 45 to 55 microm) from 12-week-old fSHR, ovariectomized fSHR (OV fSHR), or ovariectomized and supplemented with estrogen fSHR (OVE fSHR) were isolated, cannulated, and pressurized at 80 mm Hg of perfusion pressure. Arteriolar dilations elicited by step increases in perfusate flow from 0 to 25 microL/min were significantly less (by approximately 30%) in OV fSHR compared with fSHR and OVE fSHR (delta19.4+/-1.5 versus 26.0+/-0.9 and 26.8+/-2.0 microm, respectively at maximum flow rate). Inhibition of prostaglandin synthesis with indomethacin elicited a approximately 50% reduction in flow-dependent dilation in all three groups of rats. N(omega)-nitro-L-arginine (L-NNA) significantly inhibited flow-induced responses in arterioles of fSHR and OVE fSHR (by approximately 50%) but not in those of OV fSHR. Constrictions to norepinephrine (10(-7)-3 x 10(-7) mol/L) were significantly greater (up to approximately 40%) in arterioles of OV fSHR compared with those of fSHR and OVE fSHR; these differences, however, were abolished in the presence of L-NNA. In conclusion, estrogen seems to preserve the NO-mediated portion of flow/shear stress-induced dilation in female hypertensive rats resulting in a lower maintained wall shear stress in female than in male SHR. The lower wall shear stress may contribute to the mechanisms by which estrogen lowers systemic blood pressure and the incidence of cardiovascular diseases in women.

Animals↗
PubMed1998

Effects of prolonged strenuous endurance exercise on plasma myosin heavy chain fragments and other muscular proteins. Cycling vs running.

BACKGROUND: This study evaluates creatine kinase, myosin heavy chain, and cardiac troponin blood levels following three types of exercise: 1) short-distance uphill or downhill running; 2) alpine ultramarathon; and 3) alpine long-distance cycling. METHODS EXPERIMENTAL DESIGN: Comparative field study; follow-up up to 10 days. SETTING: Department of Sports Medicine. All biochemical markers were analysed at the Department of Medical Chemistry and Biochemistry. PATIENTS OR PARTICIPANTS: Subjects included healthy, trained males (N = 53). All subjects were nonsmokers and free from medication prior to and during the study. Each volunteer was an experienced runner or cyclist, who had at least once successfully finished the Swiss Alpine Marathon of Davos or the Otztal-Radmarathon before. INTERVENTIONS: Running or cycling. MEASURES: Plasma concentrations of creatine kinase, myosin heavy chain fragments and cardiac troponins were measured to diagnose skeletal and cardiac muscle damage, respectively. RESULTS: Skeletal muscle protein release is markedly different between uphill and downhill running, with very little evidence for muscle damage in the uphill runners. There is considerable muscle protein leakage in the ultramarathoners (67 km distance; 30 km downhill running). In contrast, only modest amounts of skeletal muscle damage are found after alpine long-distance cycling (230 km distance). CONCLUSIONS: This study proves that there is slow-twitch skeletal muscle fiber damage after prolonged strenuous endurance exercise and short-distance downhill running. Exhaustive endurance exercise involving downhill running and short-distance downhill running lead to more pronounced injury than strenuous endurance exercise involving concentric actions. From our results there is no reason for suggesting that prolonged intense exercise may induce myocardial injury in symptom-less athletes without cardiac deseases.

Adult↗
PubMed1997

Muscular adaptation and strength during the early phase of eccentric training: influence of the training frequency.

We investigated the effects of different training frequencies on maximum isometric voluntary contraction (MVC) force and plasma concentrations of muscle proteins during the early phase of eccentric training. MVC and plasma concentrations of creatine kinase (CK) and slow-twitch skeletal (cardiac beta-type) myosin heavy chain (MHC) fragments were measured before and 4 and 7 d after performing the first and last training task. Training tasks, which comprised 70 high-force eccentric contractions involving the thigh muscles (single leg), were performed under supervision in three groups (A, B, C) at the beginning and at the end of the study period (7 wk). In addition, groups A (N = 10) and B (N = 10) trained during the study period starting 1 wk after the first training task. Group A performed one training task once a week for 5 wk and group B (N = 10) twice a week for 2 wk and three times a week during the subsequent 3 wk. In all three groups the first training task resulted in delayed CK and MHC peaks and decrements in MVC, which were comparable (P > 0.05). Only training regimen B resulted in a significant increase in the MVC. Compared with the first training task training regimens, A and B significantly (P < 0.01) reduced the increase in serum muscle protein and muscle function impairment. The responses to the last training task did not differ significantly between groups A and B. In group C the responses after the second training task did not differ significantly from those observed after the first task. Our results suggest that, compared with group A, additional eccentric exercise in group B is the essential basis for the increase in muscle strength during the early phase of eccentric training without further benefits for muscular adaptation. In group C we found no muscular adaptation.

Adaptation, Physiological↗
PubMed1997

Gender difference in myogenic tone of rat arterioles is due to estrogen-induced, enhanced release of NO.

The characteristics of arteriolar myogenic responses of female rats have not been investigated. Thus experiments were conducted on isolated gracilis muscle arterioles (approximately 55 microm diameter) of four groups of 12-wk-old rats: male rats, female rats, ovariectomized female rats with no estrogen replacement (OV), and ovariectomized female rats with estrogen replacement (OV + E2, 50 microg/kg s.c. injection of 17beta-estradiol benzoate every 48 h). Diameter changes in response to increases in perfusion pressure from 20 to 140 mmHg and to various concentrations of substance P (SP, 10(-9)-5 x 10(-8) M) and sodium nitroprusside (SNP, 10(-8)-10(-6) M) were measured before and after administration of N(omega)-nitro-L-arginine (L-NNA, 10(-4) M), an inhibitor of NO synthase. Arteriolar diameters of male and OV female rats were significantly less at 60-140 mmHg pressure than those of normal female and OV + E2 female rats (at 80 mmHg, 45.4 +/- 1.8 and 43.1 +/- 2.2 vs. 58.4 +/- 1.6 and 57.3 +/- 1.3%). L-NNA elicited a significantly greater downward shift of pressure-diameter curves in arterioles of normal female and OV + E2 female rats than in arterioles of male and OV female rats (28.6 +/- 4.6 and 30.6 +/- 4.7 vs. 13.2 +/- 0.9 and 10.4 +/- 2.6%). Dilations of arterioles from normal female and OV +/- E2 female rats to SP were significantly greater (by 50-60%) than those from male and OV female rats (20.8 +/- 1.8 and 22.3 +/- 1.9 vs. 13.8 +/- 1.4 and 13.8 +/- 0.6% at 10(-8) M). L-NNA did not affect dilations to SNP but significantly reduced the dilation of arterioles in all groups to SP, more so in arterioles of male and OV female rats than in arterioles of the other two groups. We conclude that pressure-induced myogenic constriction of arterioles of female rats is less pronounced than that of male rats; this is, most likely, due to the enhanced release and/or activity of NO related to the presence of estrogen.

Animals↗
PubMed1997

Release of nitric oxide and prostaglandin H2 to acetylcholine in skeletal muscle venules.

The role of endothelium in regulating venular resistance is not well characterized. Thus we aimed to elucidate the endothelium-derived factors involved in the mediation of responses of rat gracilis muscle venules to acetylcholine (ACh) and other vasoactive agents. Changes in diameter of perfusion pressure (7.5 mmHg)- and norepinephrine (10(-6) M)-constricted venules (approximately 225 microns in diam) to cumulative doses of ACh (10(-9) to 10(-4) M) and sodium nitroprusside (SNP, 10(-9) to 10(-4) M), before and after endothelium removal or application of various inhibitors, were measured. Lower doses of ACh elicited dilations (up to 42.1 +/- 4.7%), whereas higher doses of ACh resulted in smaller dilations or even constrictions. Endothelium removal abolished both ACh-induced dilation and constriction. In the presence of indomethacin (2.8 x 10(-5) M), a cyclooxygenase blocker, or SQ-29548 (10(-6) M), a thromboxane A2-prostaglandin H2 (PGH2) receptor antagonist, higher doses of ACh caused further dilation (up to 72.7 +/- 7%) instead of constriction. Similarly, lower doses of arachidonic acid (10(-9) to 10(-6) M) elicited dilations that were diminished at higher doses. These reduced responses were, however, reversed to substantial dilation by SQ-29548. The nitric oxide (NO) synthase blocker, N omega-nitro-L-arginine (L-NNA, 10(-4) M), significantly reduced the dilation to ACh (from 30.6 +/- 5.5 to 5.4 +/- 1.4% at 10(-6) M ACh). In contrast, L-NNA did not affect dilation to SNP. Thus ACh elicits the release of both NO and PGH2 from the venular endothelium.

Acetylcholine↗
PubMed1997

Skeletal troponin I as a marker of exercise-induced muscle damage.

The utility of skeletal troponin I (sTnI) as a plasma marker of skeletal muscle damage after exercise was compared against creatine kinase (CK), myoglobin (Mb), and myosin heavy chain (MHC) fragments. These markers were serially measured in normal physical education teacher trainees after four different exercise regimens: 20 min of level or downhill (16% decline) running (intensity: 70% maximal O2 uptake), high-force eccentric contractions (70 repetitions), or high-force isokinetic concentric contractions of the quadriceps group (40 repetitions). Eccentrically biased exercise (downhill running and eccentric contractions) promoted greater increases in all parameters. The highest plasma concentration were found after downhill running (median peaks: 309 U/l CK concentration (-CK-)), 466 microgram/l Mb concentration (-Mb-), 1,021 microU/l MHC concentration (-MHC-), and 27.3 microgram/l sTnI concentration ([sTnI]). Level running produced a moderate response (median peaks: 178 U/l -CK-, 98 microgram/l -Mb-, 501 microU/l -MHC-, and 6.6 microgram/l [sTnI]), whereas the concentric contraction protocol did not elicit significant changes in any of the markers assayed. sTnI increased and peaked in parallel to CK and stayed elevated (>2.2 microgram/l) for at least 1-2 days after exercise. In contrast to MHC, sTnI is an initial, specific marker of exercise-induced muscle injury, which may be partly explained by their different intracellular compartmentation with essentially no (MHC <0.1%) or a small soluble pool (sTnI: median 3.4%).

Adult↗
PubMed1997

Estrogen maintains nitric oxide synthesis in arterioles of female hypertensive rats.

We hypothesized that in female spontaneously hypertensive rats (SHR), estrogen moderates the dysfunction of arterioles by preserving nitric oxide synthesis. To this end, we conducted experiments on isolated gracilis muscle arterioles (approximately 55 microns in diameter) of 12-week-old (SHR divided into four groups: females (fSHR), ovariectomized females (fSHR-OV), ovariectomized females with estrogen replacement (fSHR-OV+ES, 50 micrograms/kg SC 17 beta-estradiol benzoate every 48 hours), and males (mSHR). Arteriolar diameter in the presence of perfusion pressures of 60, 80, 100, and 120 mm Hg were obtained, and diameter changes were measured (at 80 mm Hg) in response to various concentrations of substance P (10(-9) to 5 x 10(-8) mol/L), sodium nitroprusside (10(-8) to 10(-6) mol/L), and A23187 (5 x 10(-8) to 10(-6) mol/L). The pressure-induced diameter of mSHR and fSHR-OV arterioles was significantly less (by approximately 10%) than that of fSHR and fSHR-OV+ES arterioles. N omega-nitro-L-arginine (10(-4) mol/L), a nitric oxide synthase inhibitor, elicited a significant decrease in basal arteriolar diameter of fSHR (by approximately 19%) and fSHR-OV+ES (by approximately 17%), thereby eliminating the differences in tone among the various groups. Dilations of fSHR and fSHR-OV+ES arterioles to substance P were significantly greater (by 140% at a concentration of 5 x 10(-8) mol/L) than those of mSHR and fSHR-OV arterioles, whereas dilations to sodium nitroprusside were not different among the groups. A23187 (a nitric oxide releaser) elicited dilations in arterioles of fSHR (5.9 +/- 1.5%, 13.0 +/- 1.8%, and 19.2 +/- 2.1%) and fSHR-OV+ES (4.3 +/- 1.0%, 10.3 +/- 2.4%, and 15.0 +/- 4.0%) but constrictions in those of mSHR (-7.5 +/- 1.6%, -25.3 +/- 39%, and -36.9 +/- 4.1%) and fSHR-OV (-2.6 +/- 1.7%, 7.4 +/- 3.3%, and -11.5 +/- 6.1%). We conclude that estrogen in fSHR is responsible for the preservation of nitric oxide synthesis in skeletal muscle arterioles, resulting in a greater modulation of pressure-induced myogenic tone than in mSHR and maintenance of nitric oxide-mediated dilations.

Animals↗