Biomedical subjects

J W Heslinga

Publications and source records attributed to J W Heslinga.

13 recordsLinked to original sources

PubMed2001

Microvascular pressure measurement reveals a coronary vascular waterfall in arterioles larger than 110 microm.

Pressure-flow relationships at the entrance of the coronary circulation in the diastolic myocardium exhibit a zero-flow pressure intercept (P(int)). We tested whether this intercept is the same throughout the vascular bed. Microvascular pressure-flow relationships were therefore measured in vessels of various sizes of the maximally dilated vasculature of perfused unstimulated papillary muscle using the servo-null technique. From these relationships, P(int) were calculated with nonlinear regression. The P(int) at the level of the septal artery (diameter, 150-250 microm) was 23.2 +/- 4.4 cmH2O (n = 12). In arterioles with a diameter range between 24 and 110 microm, P(int) was 1.7 +/- 0.5 cmH2O (n = 6, P < 0.01), significantly lower than in the septal artery but significantly higher than zero, and not dependent on vessel size. In venules with the same diameters, P(int) was 1.1 +/- 1.1 cmH2O (n = 4), which was not different from zero. We conclude that, in the dilated vascular bed of the papillary muscle, two vascular waterfalls are found. The first waterfall is located in arterioles between 150 and 110 microm. The second waterfall is probably located in the small postcapillary venules.

Animals↗

PubMed1998

Perfusion-induced changes in cardiac contractility depend on capillary perfusion.

The perfusion-induced increase in cardiac contractility (Gregg phenomenon) is especially found in heart preparations that lack adequate coronary autoregulation and thus protection of changes in capillary pressure. We determined in the isolated perfused papillary muscle of the rat whether cardiac muscle contractility is related to capillary perfusion. Oxygen availability of this muscle is independent of internal perfusion, and perfusion may be varied or even stopped without loss of function. Muscles contracted isometrically at 27 degrees C (n = 7). During the control state stepwise increases in perfusion pressure resulted in all muscles in a significant increase in active tension. Muscle diameter always increased with increased perfusion pressure, but muscle segment length was unaffected. Capillary perfusion was then obstructed by plastic microspheres (15 microns). Flow, at a perfusion pressure of 66.6 +/- 26.2 cmH2O, reduced from 17.6 +/- 5.4 microliters/min in the control state to 3.2 +/- 1.3 microliters/min after microspheres. Active tension developed by the muscle in the unperfused condition before microspheres and after microspheres did not differ significantly (-12.8 +/- 29.4% change). After microspheres similar perfusion pressure steps as in control never resulted in an increase in active tension. Even at the two highest perfusion pressures (89.1 +/- 28.4 and 106.5 +/- 31.7 cmH2O) that were applied a significant decrease in active tension was found. We conclude that the Gregg phenomenon is related to capillary perfusion.

Animals↗

PubMed1997

Reoxygenated effluent of Tyrode-perfused heart affects papillary muscle contraction independent of cardiac perfusion.

OBJECTIVE: We determined, via a bioassay, if inotropic factors are released in the coronary circulation of the rat heart and if changes in cardiac perfusion change papillary muscle inotropy. METHODS: An isolated isometrically contracting rat papillary muscle (n = 5, acceptor) was superfused with Tyrode or with reoxygenated coronary venous effluent from an isolated isovolumically beating rat heart (donor) at 27 degrees C, which was perfused with Tyrode according to Langendorff. The superfusion solution in the muscle bath was exchanged completely in 90 s. During coronary venous effluent superfusion, the flow of the heart (donor) was changed in steps. RESULTS: The peak force of the papillary muscle (acceptor) was unaffected by a change from Tyrode to coronary venous effluent superfusion, but time to half relaxation (RT 1/2) significantly increased by 23.0 +/- 9.0% (mean +/- s.d.) and positive dF/dtmax significantly decreased by 14.6 +/- 4.7%. These twitch characteristics were unaffected by changes in coronary perfusion while in the heart isovolumic developed left ventricular pressure did increase with perfusion (the Gregg phenomenon). CONCLUSIONS: Factors that affected papillary muscle contractility are released into the coronary circulation, but their effect is independent of the magnitude of coronary perfusion.

Animals↗

PubMed1997

Perfusion-induced changes in cardiac contractility and oxygen consumption are not endothelium-dependent.

OBJECTIVE: Are substances released from rat coronary endothelial cells responsible for the increase in contractility and oxygen consumption (Gregg phenomenon) seen with an increase in cardiac perfusion? METHODS: In an isovolumically contracting, Langendorff, crystalloid perfused rat heart (n = 6) at 27 degrees C, coronary flow was changed (from 4.4 to 15.4 ml.min-1.gww(-1)) before and after the endothelium was made dysfunctional by Triton X-100. Vascular endothelium and smooth muscle function were tested with bradykinin (BK, 1 microM, an endothelium-dependent dilator) and papaverine (PAP, 1 microM, an endothelium-independent dilator) in a preconstricted vascular bed (vasopressin, VP, 3 nM). RESULTS: Before Triton X-100, coronary resistance (at constant flow) decreased significantly in response to BK and to PAP. After Triton X-100 treatment the dilatory response to BK was abolished while the PAP response was still present, suggesting endothelial dysfunction with intact smooth muscle function. Due to Triton X-100 treatment, coronary resistance increased significantly. Therefore coronary flow changes were also applied during a similar increase in coronary resistance induced by VP infusion (3 nM) before Triton X-100 treatment. During control, developed left ventricular pressure (dev Plv) increased with 68 +/- 21% and oxygen consumption (VO2) increased with 122 +/- 25% in response to the maximal increase in coronary flow. During increased coronary resistance with and without functional endothelium, dev Plv increased by 57 +/- 16 and 64 +/- 22%, respectively, and VO2 increased by 126 +/- 21 and 103 +/- 20%, respectively, in response to the maximal increase in flow. These changes were not significantly different from control. CONCLUSION: The results suggest that the arterial endothelium is not involved in the Gregg phenomenon.

Animals↗

PubMed1997

Effects of contraction, perfusion pressure, and length on intramyocardial pressure in rat papillary muscle.

If intramyocardial pressure (IMP) is the pressure that causes coronary flow to stop, i.e., "backpressure," then it should be equal to the zero-flow perfusion pressure intercept (Pzf). Therefore we determined Pzf and IMP at zero flow (IMPzf) in papillary muscles suspended isometrically in a bath, superfused with a well-oxygenated Tyrode solution (27 degrees C), and perfused with Tyrode solution via the septal artery. For the IMP (servo-null) measurements, we used unbeveled glass micropipettes with a tip diameter of 3-4 microns. During diastolic arrest and systolic contracture (2 mM Ba21), perfusion pressure steps were applied, and the corresponding flow and IMP values were recorded. Fitting of the relationships, yielded Pzf and IMPzf. In the diastolically arrested muscle, perfusion pressure affected IMP. Pzf was much higher in systolically contracted muscle than in diastolically arrested muscle. The IMPzf in both conditions was significantly smaller than Pzf. Thus, even in this preparation with no ventricular pressure, IMP increases during contraction. We conclude that IMP arises from contraction per se but is not the pressure that causes the flow to stop.

Animals↗

PubMed1996

Intramyocardial pressure measurements in the isolated perfused papillary muscle of rat heart.

The intramyocardial pressure (IMP) plays a role in the interaction between heart contraction and coronary flow. In order to measure IMP we developed the isolated perfused papillary muscle. The papillary muscle was suspended in a muscle bath with oxygenated Tyrode's solution. Perfusion with Tyrode's solution took place via the septal artery. Diastolic intramyocardial pressure was measured with micropipettes with a tipdiameter of 3 to 4 microns in combination with the servo-null technique. After an equilibration period of at least a half hour where the muscle was perfused with a perfusion pressure of 40 cmH2O and stimulated with 0.2 Hz the IMP measurements started. Pressure changes resulting from changes in perfusion pressure and injection of ink via the pipette made it possible to distinguish between interstitial and vascular localization. No leakage along the shaft of the pipette to the outside was found. Perfusion caused interstitial edema in the muscle so that the cross-sectional area (CSA) of myocytes relative to total muscle CSA decreased from 71% in non-perfused muscle to 51% in perfused muscle. Interstitial edema increased approximately from 10% to 30%. The amount of edema was reduced by rapid pacing (3.3 Hz) as judged from decreased muscle diameter and a lower IMP. It is concluded that reliable IMP measurements can be made in the isolated papillary muscle and that increased filling of the interstitium increases its pressure.

Animals↗

PubMed1996

Perfusion-induced changes in cardiac O2 consumption and contractility are based on different mechanisms.

Increased cardiac perfusion results in increased oxygen consumption (VO2) and increased contractility (Gregg phenomenon) in the isolated heart. We investigated whether these two aspects of the Gregg phenomenon are related to coronary flow or arterial pressure. Coronary flow and, thus, arterial pressure were changed in the reference state and during vasoconstriction (3 nM vasopressin) in the Langendorff-perfused rat heart contracting isovolumically (ventricular balloon) at 27 degrees C (n = 5). All hearts showed an increase in developed isovolumic left ventricular pressure (measure of contractility) and in VO2 with increased perfusion. Developed left ventricular pressure depended primarily on arterial pressure, so its relationship with coronary flow was shifted by vasoconstriction. Conversely, VO2 primarily depended on coronary flow, so its relationship with arterial pressure was shifted with vasoconstriction. By use of vasoconstriction (decreased vascular radii), the effects of arterial pressure and wall shear stress (proportional to arterial pressure x radius) should be separable, but the results did not reach significance. Thus contractility is related to arterial pressure or shear stress, whereas VO2 is related to coronary flow. We conclude that the two aspects of the Gregg phenomenon are based on different mechanisms.

Animals↗

PubMed1995

Growth and immobilization effects on sarcomeres: a comparison between gastrocnemius and soleus muscles of the adult rat.

The effects of growth and limb immobilization on muscle mass, total physiological cross-section (PC), the number of sarcomeres in series and the length of sarcomere components were investigated in the soleus muscle (SOL) and compared to previously obtained data on gastrocnemius (GM) muscles of rats between age 10 and 16 weeks. For SOL this period of growth was reflected in an increased muscle mass and PC. No such increases were found for GM. In contrast, immobilization caused severe atrophy of fibres of both muscles. Compared to the value at the start of the immobilization, it was found that the fast twitch muscle (GM) atrophied more than the typically slow twitch one (SOL). The number of sarcomeres in series within fibres increased after growth and decreased after immobilization of SOL. For fibres of GM no such changes were observed. Muscle architecture is proposed as an important factor for the explanation of the results concerning the number of sarcomeres in series and those arranged in parallel. Due to the difference in muscle architecture, GM being more pennate than SOL, during growth, it is thought that increases in bone length affect the length of fibres of SOL more than those of GM. During immobilization, atrophy of fibres of GM was sufficient for the muscle length adaptation to meet the muscle length change induced by immobilization but in SOL, atrophy had to be accompanied by decreases in the number of sarcomeres in series to achieve adequate muscle length adaptation.

Animals↗

PubMed1995

Mean sarcomere length-force relationship of rat muscle fibre bundles.

To study how sarcomere length inhomogeneities and the duration of activation affect sarcomere length-force characteristics of muscle, the mean sarcomere length-force relationship was determined for twitches and at 100 and 300 ms during tetanic activation for rat extensor digitorum longus and gastrocnemius medialis muscle fibre bundles. Mean sarcomere length is the mean length of all sarcomeres within the fibre, calculated by dividing fibre length by the number of sarcomeres in series in the fibre. The twitch mean sarcomere length-force relationship is shifted to larger sarcomere lengths (optimum mean sarcomere length = 2.69 microns) compared to the relationships determined at 100 or 300 ms of tetanic activation (optimum mean sarcomere length = 2.38 microns), which were the same. It is shown that the normalized Gordon et al. rationale results in a large overestimate of force (at most 68% of force at a sarcomere length of 1.60 microns) for mean sarcomere lengths between 1.4 and 2.0 microns, and in an underestimate of force between 2.3 and 3.0 microns. It is concluded that modelling skeletal mammalian muscle length-force relationships can be improved by using mean sarcomere length-force relations of mammalian fibres instead of the normalized rationale of Gordon et al. derived from a selected homogeneous part of frog fibre.

Animals↗

PubMed1993

Muscle length-force characteristics in relation to muscle architecture: a bilateral study of gastrocnemius medialis muscles of unilaterally immobilized rats.

The geometry of rat gastrocnemius medialis muscle (GM) was studied at different muscle lengths. In addition, the number of sarcomeres in series within fibres was estimated. For muscles of immobilized legs (i.e. GM was held at in vivo smallest length) as well as those of the contralateral legs, comparison was made with controls of similar age. Immobilization periods of 4 and 6 weeks were used. For immobilized GM muscles, the number of sarcomeres in series was lower only within distal fibres after 4 weeks of immobilization. Aponeuroses were 25% shorter after both immobilization periods and no differences were found for fibre and aponeurosis angle. For GM of contralateral legs no difference with respect to controls was found regarding the number of sarcomeres in series. Aponeuroses were approximately 15% shorter and the fibre and the aponeurosis angle were also smaller. Based on these geometrical differences, it was expected that both experimental muscles should exert force over a smaller range of muscle length than controls. However, for immobilized muscles a similar range of length was found for which a possible explanation could be the more compliant aponeurosis. For contralateral muscle a 2-mm larger length range as well as a change of distribution of optimal fibre length with respect to optimal muscle length was found. For immobilized muscles indications of a distribution of optimal fibre lengths were also found but these did not differ from those of the controls. The results for contralateral muscles would indicate that the distribution may be changed under the influence of an altered use of the limb and that this may be an important factor determining the length range of active force generation.

Animals↗

PubMed1992

Unilateral immobilization affects contralateral rat gastrocnemius muscle architecture.

In order to study the effects of unilateral short length immobilization on the contralateral gastrocnemius muscle (GM), length measurements were conducted on photographs taken in the active condition (tetanic plateau). Comparison of geometry of experimental and control muscles was made at optimum muscle length. The results show that a process occurred in the muscle which can be ascribed predominantly in terms of atrophy. This atrophy did not reach a maximum after 4 weeks but gradually increased in time. The altered conditions imposed on the muscle changed its architecture. It was shown that variables of the contralateral GM muscle are not representative of those of normally used muscles and should therefore not be used as control muscles for the determination of immobilization effects.

Adaptation, Physiological↗

PubMed1992

Effects of short length immobilization of medial gastrocnemius muscle of growing young adult rats.

Effects of four and six weeks of immobilization at short length of gastrocnemius muscle on its architecture at optimum muscle length and length-force characteristics were studied. In general, immobilization effects were similar after 4 and 6 weeks. Smaller physiological cross-sectional area and lower muscle force were found as a consequence of immobilization. Muscle and aponeurosis were shorter. This was shown to be quantitatively related to atrophy i.e. smaller fibre diameter. Despite this atrophy no effects of immobilization on fibre and aponeurosis angles could be shown. Adaptation of the number of sarcomeres in series was found exclusively in distal fibres after 4 weeks of immobilization. No significant effects were found for proximal fibres of muscles at this time nor for any fibres after 6 weeks of immobilization. The effects of immobilization on muscle architecture did not affect the length range of active force exertion. It is concluded that muscle length adaptation as a consequence of short length immobilization is not related to adaptation of number of sarcomeres in series but to the occurrence of atrophy. It is also concluded that atrophy of pennate muscles does not have to be accompanied by a lower fibre and aponeurosis angle. Comparison of immobilized and control group rats indicates that the effects of immobilization can be characterized as a combination of retarded development of several variables and the influence of atrophy and its consequences.

Adaptation, Physiological↗

PubMed1990

Effects of growth on architecture and functional characteristics of adult rat gastrocnemius muscle.

Changes of architecture of adult rat gastrocnemius medialis muscle (GM) due to growth were studied in relation to length-force characteristics. Myofilament lengths were unchanged, indicating constant sarcomere length-force characteristics. Number of sarcomeres within fibers was unchanged as a consequence of growth, allowing persistence of differences between proximal and distal fibers in all age groups. Distal fiber length at muscle optimum length was shorter for the 14- than for the 10- and 16-week age groups despite a lack of difference of number of sarcomeres. This is indicative of a shift of optimum length. Some evidence for the occurrence of distribution of fiber optimum lengths with respect to muscle optimum length was found in other age groups as well, albeit of a smaller magnitude. Muscle and aponeurosis length increased substantially with growth. Functional effects of increased aponeurosis lengths were increased contributions to muscle length changes by the aponeurosis, allowing smaller fiber contributions in older animals. Fiber angle increased approximately 5 degrees with growth. Despite the differences of architecture indicated above, muscle length range between optimum length and active slack length was constant. This was probably caused by widening of this length range in the youngest age group by variations of architecture within the muscle. It is concluded that adaptation of aspects of muscle architecture is an important mechanism for adult muscle growth in rat GM. Of these aspects regulation of muscle length seems a dominant factor.

Aging↗