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Michael Axelsson

Publications and source records attributed to Michael Axelsson.

10 recordsLinked to original sources
PubMed2006

Central venous pressure and mean circulatory filling pressure in the dogfish Squalus acanthias: adrenergic control and role of the pericardium.

Subambient central venous pressure (Pven) and modulation of venous return through cardiac suction (vis a fronte) characterizes the venous circulation in sharks. Venous capacitance was estimated in the dogfish Squalus acanthias by measuring the mean circulatory filling pressure (MCFP) during transient occlusion of cardiac outflow. We tested the hypothesis that venous return and cardiac preload can be altered additionally through adrenergic changes of venous capacitance. The experiments involved the surgical opening of the pericardium to place a perivascular occluder around the conus arteriosus. Another control group was identically instrumented, but lacked the occluder, and was subjected to the same pharmacological protocol to evaluate how pericardioectomy affected cardiovascular status. Routine Pven was negative (-0.08+/-0.02 kPa) in control fish but positive (0.09+/-0.01 kPa) in the pericardioectomized group. Injections of 5 microg/kg body mass (Mb) of epinephrine and phenylephrine (100 microg/kg Mb) increased Pven and MCFP, whereas isoproterenol (1 microg/kg Mb) decreased both variables. Thus, constriction and relaxation of the venous vasculature were mediated through the respective stimulation of alpha- and beta-adrenergic receptors. Alpha-adrenergic blockade with prazosin (1 mg/kg Mb) attenuated the responses to phenylephrine and decreased resting Pven in pericardioectomized animals. Our results provide convincing evidence for adrenergic control of the venous vasculature in elasmobranchs, although the pericardium is clearly an important component in the modulation of venous function. Thus active changes in venous capacitance have previously been underestimated as an important means of modulating venous return and cardiac performance in this group.

Adrenergic Agonists↗
PubMed2006

Adrenergic control of venous capacitance during moderate hypoxia in the rainbow trout (Oncorhynchus mykiss): role of neural and circulating catecholamines.

Central venous blood pressure (P(ven)) increases in response to hypoxia in rainbow trout (Oncorhynchus mykiss), but details on the control mechanisms of the venous vasculature during hypoxia have not been studied in fish. Basic cardiovascular variables including P(ven), dorsal aortic blood pressure, cardiac output, and heart rate were monitored in vivo during normoxia and moderate hypoxia (P(W)O(2) = approximately 9 kPa), where P(W)O(2) is water oxygen partial pressure. Venous capacitance curves for normoxia and hypoxia were constructed at 80-100, 90-110, and 100-120% of total blood volume by transiently (8 s) occluding the ventral aorta and measure P(ven) during circulatory arrest to estimate the mean circulatory filling pressure (MCFP). This allowed for estimates of hypoxia-induced changes in unstressed blood volume (USBV) and venous compliance. MCFP increased due to a decreased USBV at all blood volumes during hypoxia. These venous responses were blocked by alpha-adrenoceptor blockade with prazosin (1 mg/kg body mass). MCFP still increased during hypoxia after pretreatment with the adrenergic nerve-blocking agent bretylium (10 mg/kg body mass), but the decrease in USBV only persisted at 80-100% blood volume, whereas vascular capacitance decreased significantly at 90-110% blood volume. In all treatments, hypoxia typically reduced heart rate while cardiac output was maintained through a compensatory increase in stroke volume. Despite the markedly reduced response in venous capacitance after adrenergic blockade, P(ven) always increased in response to hypoxia. This study reveals that venous capacitance in rainbow trout is actively modulated in response to hypoxia by an alpha-adrenergic mechanism with both humoral and neural components.

Adrenergic alpha-Antagonists↗
PubMed2006

Venous responses during exercise in rainbow trout, Oncorhynchus mykiss: alpha-adrenergic control and the antihypotensive function of the renin-angiotensin system.

The role of the alpha-adrenergic system in the control of cardiac preload (central venous blood pressure; P(ven)) and venous capacitance during exercise was investigated in rainbow trout (Oncorhynchus mykiss). In addition, the antihypotensive effect of the renin-angiotesin system (RAS) was investigated during exercise after alpha-adrenoceptor blockade. Fish were subjected to a 20-min exercise challenge at 0.66 body lengths s(-1) (BL s(-1)) while P(ven), dorsal aortic blood pressure (P(da)) and relative cardiac output (Q) was recorded continuously. Heart rate (f(H)), cardiac stroke volume (SV) and total systemic resistance (R(sys)) were derived from these variables. The mean circulatory filling pressure (MCFP) was measured at rest and at the end of the exercise challenge, to investigate potential exercise-mediated changes in venous capacitance. The protocol was repeated after alpha-adrenoceptor blockade with prazosin (1 mg kg(-1)M(b)) and again after additional blockade of angiotensin converting enzyme (ACE) with enalapril (1 mg kg(-1)M(b)). In untreated fish, exercise was associated with a rapid (within approx. 1-2 min) and sustained increase in Q and P(ven) associated with a significant increase in MCFP (0.17+/-0.02 kPa at rest to 0.27+/-0.02 kPa at the end of exercise). Prazosin treatment did not block the exercise-mediated increase in MCFP (0.25+/-0.04 kPa to 0.33+/-0.04 kPa at the end of exercise), but delayed the other cardiovascular responses to swimming such that Q and P(ven) did not increase significantly until around 10-13 min of exercise, suggesting that an endogenous humoral control mechanism had been activated. Subsequent enalapril treatment revealed that these delayed responses were in fact due to activation of the RAS, because resting P(da) and R(sys) were decreased further and essentially all cardiovascular changes during exercise were abolished. This study shows that the alpha-adrenergic system normally plays an important role in the control of venous function during exercise in rainbow trout. It is also the first study to suggest that the RAS may be an important modulator of venous pressure and capacitance in fish.

Adrenergic alpha-Antagonists↗
PubMed2006

An intravital microscopy method permitting continuous long-term observations of ovulation in vivo in the rabbit.

BACKGROUND: A method for intravital microscopy of the rabbit ovary was developed to enable observations of real-time changes during ovulation in vivo. The aim was to correlate these events to biochemical events at specific stages of ovulation. METHODS: Virgin, female rabbits were primed with equine chorionic gonadotrophin (CG) (30-100 IU) then HCG (100 IU) 2 days later to induce ovulation. During anaesthesia, the right ovary was surgically exteriorized and submerged in an organ chamber with a microscopy lens positioned close to the ovary. Continuous video recordings were performed. RESULTS: Initial equine CG priming experiments revealed the highest ovulation rate, without premature luteinization, after 30 IU equine CG. This priming protocol subsequently demonstrated follicular ruptures 11.5-14 h after HCG. Numbers of ovulations from the exteriorized and contralateral non-exteriorized ovary were similar. The sequence of typical features of ovulation was: shutdown of microcirculation in the follicular apex, formation of petechiae in the follicular wall and a cone-shaped structure over the future rupture site, marked bleeding in connection with follicular rupture and a fairly steady extrusion velocity of granulosa cells and the oocyte. CONCLUSION: This method captured a sequence of structural changes during ovulation. It could be combined with blood and follicular fluid sampling for biochemical analysis and could be used in studies on biochemical reactions in relation to specific changes in the follicular structure during ovulation.

Animals↗
PubMed2005

Cardiac preload and venous return in swimming sea bass (Dicentrarchus labrax L.).

Cardiac preload (central venous pressure, P(CV), mean circulatory filling pressure (MCFP), dorsal aortic blood pressure (P(DA)) and relative cardiac output (Q) were measured in sea bass (Dicentrarchus labrax) at rest and while swimming at 1 and 2 BL s(-1). MCFP, an index of venous capacitance and the upstream venous pressure driving the return of venous blood to the heart, was measured as the plateau in Pcv during ventral aortic occlusion. Compared with resting values, swimming at 1 and 2 BL s(-1) increased Q (by 15+/-1.5 and 38+/-6.5%, respectively), P(CV) (from 0.11+/-0.01 kPa to 0.12+/-0.01 and 0.16+/-0.02 kPa, respectively), MCFP (from 0.27+/-0.02 kPa to 0.31+/-0.02 and 0.40+/-0.04 kPa, respectively) and the calculated pressure gradient for venous return (DeltaP(V), from 0.16+/-0.01 kPa to 0.18+/-0.02 and 0.24+/-0.02 kPa, respectively), but not P(DA). In spite of an increased preload, the increase in Q was exclusively mediated by an increased heart rate (f(H), from 80+/-4 beats min(-1) to 88+/-4 and 103+/-3 beats min(-1), respectively), and stroke volume (Vs) remained unchanged. Prazosin treatment (1 mg kg(-1) Mb) abolished pressure and flow changes during swimming at 1 BL s(-1), but not 2 BL s(-1), indicating that other control systems besides an alpha-adrenoceptor control are involved. This study is the first to address the control of venous capacitance in swimming fish. It questions the generality that increased Q during swimming is regulated primarily through Vs and shows that an increased cardiac filling pressure does not necessarily lead to an increased Vs in fish, but may instead compensate for a reduced cardiac filling time.

Animals↗
PubMed2004

Intrinsic autoregulation of cardiac output in rainbow trout (Oncorhynchus mykiss) at different heart rates.

Intrinsic regulation of the heart in teleosts is partly driven by central venous pressure, which exerts a modulatory role on stroke volume according to the well-known Frank-Starling mechanism. Although this mechanism is well understood from heart perfusion studies, less is known about how this mechanism operates in vivo, where heart rate varies markedly. We used zatebradine, a bradycardic agent, to attain resting heart rates in surgically instrumented animals. A dose of zatebradine of 2.79+/-0.47 mg l(-1) decreased heart rate by half, from 44.4+/-4.19 beats min(-1) to 22.1+/-1.9 beats min(-1). Zatebradine had no significant effect on the peripheral vasculature and no inotropic effects, so was a suitable pharmacological agent with which to manipulate heart rate. When heart rate halved, cardiac output dropped to 87.5+/-4.6% of the control value, due to the concomitant increase in stroke volume to 165+/-13%. In vivo recordings of venous pressure at varying heart rates indicated that the partial compensation in cardiac output was possible through an increase in pressure in the sinus venosus, from -0.06+/-0.04 kPa at a control heart rate of 58.3+/-3.5 beats min(-1) (N=10) to 0.07+/-0.05 kPa after injection of zatebradine (4 mg kg(-1)). The operation of the so-called time-dependent autoregulatory mechanism was further demonstrated in perfused hearts. The positive pressures recorded in the sinus venosus at low heart rates coincident with non-invasive measurements in trout suggest that atrial filling in trout is more dependent on the build-up of pressure in the venous circulation (vis-à-tergo filling) than a suction mechanism during ventricular contraction (vis-à-fronte filling).

Animals↗
PubMed2003

Ventricular haemodynamics in Python molurus: separation of pulmonary and systemic pressures.

Vascular pressure separation by virtue of a two-chambered ventricle evolved independently in mammals and birds from a reptilian ancestor with a single ventricle, and allowed for high systemic perfusion pressure while protecting the lungs from oedema. Within non-crocodilian reptiles, ventricular pressure separation has only been observed in varanid lizards and has been regarded as a unique adaptation to an active predatory life style and high metabolic rate. The systemic and pulmonary sides of the ventricle in Python molurus are well separated by the muscular ridge, and a previous study using in situ perfusion of the heart revealed a remarkable flow separation and showed that the systemic side can sustain higher output pressures than the pulmonary side. Here we extend these observations by showing that systemic blood pressure P(sys) exceeded pulmonary pressure P(pul) almost seven times (75.7+/-4.2 versus 11.6+/-1.1 cm H(2)O). The large pressure difference between the systemic and pulmonary circulation persisted when P(sys) was altered by infusion of sodium nitroprusside or phenylephrine. Intraventricular pressures, measured in anaesthetised snakes, showed an overlap in the pressure profile between the pulmonary side of the ventricle (cavum pulmonale) and the pulmonary artery, while the higher pressure in the systemic side of the ventricle (cavum arteriosum) overlapped with the pressure in the right aortic arch. This verifies that the pressure differences originate within the ventricle, indicating that the large muscular ridge separates the ventricle during cardiac contraction.

Animals↗
PubMed2002

Intracardiac flow separation in an in situ perfused heart from Burmese python Python molurus.

The heart of non-crocodilian reptiles has two separate atria that receive blood from the systemic and pulmonary circulations. The ventricle is not fully divided, but is compartmentalised into two chambers (cavum dorsale and cavum pulmonale) by a muscular ridge that runs from the apex to the base of the ventricle. The muscular ridge is small in turtles, but is well developed in varanid lizards and many species of snakes. These anatomical differences correlate with an effective blood flow separation in varanid lizards, whereas turtles can exhibit very large cardiac shunts. Very little is known about the cardiac shunt patterns in other groups of reptiles. Here we characterise cardiac performance and flow dynamics in the Burmese python (Python molurus) using an in situ perfused heart preparation. The pericardium remained intact and the two atria were perfused separately (Ringer solution), and the two systemic and the pulmonary outflows were independently cannulated. Right and left atrial filling pressures and ventricular outflow pressures of the pulmonary and systemic vessels could be manipulated independently, permitting the establishment of large experimental intraventricular pressure gradients across the muscular ridge. The maximal power output generated by the systemic side of the ventricle exceeded the maximal power output that was generated by the cavum pulmonale that perfuse the pulmonary circulation. Furthermore, systemic flow could be generated against a higher outflow pressure than pulmonary flow. Perfusate entering the right atrium was preferentially distributed into the pulmonary circulation, whereas perfusate into the left atrium was distributed to the systemic circulation. Our study indicates that the well-developed muscular ridge can separate the cavum systemic and pulmonary sides of the heart to prevent mixing of systemic and pulmonary flows. Therefore, the heart of Python appears to exhibit a large degree of ventricular flow separation as previously described for varanid lizards. We speculate that the ventricular separation has evolved in response to the need of maintaining high oxygen delivery while protecting the pulmonary circulation from oedema as result of high vascular pressures.

Animals↗
PubMed2002

Post-prandial blood flow to the gastrointestinal tract is not compromised during hypoxia in the sea bass Dicentrarchus labrax.

The hypothesis that the increase in post-prandial splanchnic blood flow will be reduced during hypoxia to prioritise blood flow to other organs was tested by measuring cardiac output and gut blood flow during a stepwise hypoxic challenge (five steps, from 20.6 to 3.9 kPa, 5 min of exposure to each level) before and after feeding (equivalent to 2.9% of body mass). Splanchnic blood flow, both absolute and relative to cardiac output, increased after feeding. Mean post-prandial gut blood flow increased by 71% (from 9.6+/-1.6 to 14.9+/-1.6 ml min(-1) kg(-1), means +/- S.E.M.). Before feeding, gut blood flow was 24.0% of cardiac output, and this increased significantly 24 h after feeding to 34.0%. The absolute post-prandial increase in gut blood flow (5.3+/-0.9 ml min(-1) kg(-1)) was paralleled by an increase in cardiac output (5.4+/-2.1 ml min(-1) kg(-1)). Hypoxia decreased gut blood flow significantly from 9.6+/-1.6 to 3.7+/-1.1 ml min(-1) kg(-1), corresponding to a decrease in relative gut blood flow from 24 % to 13%. Contrary to our initial hypothesis, and although post-prandial absolute blood flow decreases during hypoxia, the relative proportion of cardiac output reaching the gut did not decrease (34.6% pre-hypoxia versus 26.7% during hypoxia), unlike the situation in non-feeding fish. We propose that, following feeding, relative gut blood flow is maintained because splanchnic hyperaemia occurs as a result of the release of local factors; consequently the reflex vasoconstriction of the gastrointestinal vasculature during hypoxia is not as effective in decreasing gut blood flow as it was before feeding because local hyperaemia out-competes the reflex regulation.

Animal Feed↗