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Biomedical subjects

M Axelsson

Publications and source records attributed to M Axelsson.

At least 55 records · Page 3Linked to original sources
PubMed1995

Effects of swimming and environmental hypoxia on coronary blood flow in rainbow trout.

Previous studies have suggested that trout cardiac performance is highly dependent on coronary blood flow during periods of increased activity or hypoxia. To examine the relationship between coronary perfusion and cardiac performance in swimming trout, cardiac output (Q), coronary blood flow (qcor), and dorsal aortic blood pressure were measured in rainbow trout (Oncorhynchus mykiss) during normoxia and hypoxia (PO2 approximately 9 kPa). In normoxic trout, stepwise changes in cardiovascular variables were observed as the swimming speed was incrementally increased from 0.15 body lengths (bl)/s to 1.0 bl/s. At 1.0 bl/s, qcor and cardiac power output had both increased by approximately 110%, and coronary artery resistance (Rcor) had decreased by 40%. During hypoxia, resting qcor was 35% higher, and Rcor was 20% lower, compared with normoxic values. In hypoxic swimming trout, the maximum changes in qcor (155% increase) and Rcor (50% decrease) were recorded at 0.75 bl/s. In contrast, cardiac power output and Q increased by an additional 40 and 20%, respectively, as swimming speed was increased from 0.75 to 1.0 bl/s. The results indicate that 1) increases in qcor parallel changes in cardiac power output; 2) during hypoxia there are compensatory increases in cardiac performance and coronary perfusion; and 3) the scope for increasing qcor in swimming trout is approximately 150%. In addition, results from preliminary experiments suggest that beta-adrenergic, but not cholinergic, mechanisms are involved in the regulation of coronary blood flow during exercise.

Animals↗
PubMed1995

The role of the pericardium and the effects of adrenaline and changes in oxygen tension on the performance of an in situ perfused crocodile heart

An in situ perfused crocodile (Crocodylus porosus) heart preparation was used to examine the mechanical responses of the heart to increases in adrenaline concentration, to a decrease in oxygen tension and to opening of the pericardium. Starling and power curves were constructed before and after these experimental manipulations. Increasing adrenaline concentration in the perfusate from 5 nmol l-1 to 0.5 µmol l-1 produced a significant increase in heart rate and a decrease in stroke volume, leaving cardiac output unchanged. With maximal adrenergic stimulation, the left ventricle was able to generate greater power outputs at high right aortic output pressures; however, the right ventricle showed a decrease in performance with increasing output pressure. Decreasing the PO2 of the perfusate to 10 kPa resulted in a significant bradycardia. Both the flow and pressure-generating capabilities of the perfused heart preparation were reduced, although the heart was able to maintain low work levels at this PO2. Opening the pericardium permitted greater movement/expansion of the cardiac chambers and resulted in an increase in heart rate. Higher flows were generated at low filling pressures during the input pressure challenge as a result of an increase in the sensitivity of the Starling response.

Journal Article↗
PubMed1994

Neuropeptides in the Australian lungfish Neoceratodus forsteri: effects in vivo and presence in autonomic nerves.

The Australian lungfish Neoceratodus forsteri is one of the few extant species of a phylogenetically ancient group. Immunohistochemistry showed the presence of galanin-, vasoactive intestinal polypeptide (VIP)-, neurotensin-, substance P-, and calcitonin gene-related peptide (CGRP)-like immunoreactivities in nerve fibers in the heart, lung, and gut, with a coexistence of VIP-, galanin-, and somatostatin-like immunoreactivity in the lung and galanin- and somatostatin-like immunoreactivity in the gut. About 20% of the substance P-immunoreactive fibers in gut and lung contained CGRP-like material. Major vessels showed a sparse innervation. In free-swimming unanesthetized fish, neurotensin (1 nmol/kg), galanin (1 nmol/kg), and bombesin (10 nmol/kg) reduced the heart rate. In two specimens tested, the effect of neurotensin was partially antagonized by atropine. Galanin and bombesin reduced and cholecystokinin 8 (CCK-8-S) increased blood flow to the lung. Neurotensin decreased, CCK-8-S increased, and substance P had no effect on dorsal aortic pressure, and all three decreased flow to the gut. It can be concluded from the present study that the general vertebrate pattern of cardiovascular and visceral nervous control by several neuropeptides is present also in Neoceratodus.

Animals↗
PubMed1994

THE INTRINSIC PROPERTIES OF AN IN SITU PERFUSED CROCODILE HEART

An in situ perfused crocodile (Crocodylus porosus) heart preparation was developed to investigate the effects of input and output pressure on cardiac dynamics and to determine the conditions that lead to a right-to-left cardiac shunt. The pericardium was kept intact, both the left and right atria were perfused and all three outflow tracts (right aortic, left aortic and pulmonary) were cannulated, enabling pressures and flows to be monitored. The perfused heart preparation had an intrinsic heart rate of 34 beats min-1 and generated a physiological power output. Both the left and right sides of the heart were sensitive to filling pressure. Increasing the filling pressure to both atria resulted in an increase in stroke volume and cardiac output (Frank­Starling effect). Increasing the filling pressure to the right atrium also had a positive chronotropic effect. Large right ventricular stroke volumes initiated a right-to-left shunt, despite the left aorta having a pressure 1.5 kPa higher than the pulmonary output pressure. The left ventricle was able to maintain its output and stroke volume up to an output pressure of approximately 8 kPa. However, the right ventricle was significantly weaker. Right ventricular output and stroke volume showed a marked decrease when the output pressure was increased above 5 kPa. A right-to-left shunt occurred when pulmonary output pressure was increased. Surprisingly, a shunt occurred into the left aorta before the pressure in the pulmonary artery became greater than that in the left aorta. Once the pressure in the pulmonary artery exceeded the left aortic pressure, pulmonary artery flow ceased and right ventricular output was solely via the left aorta. A right-to-left shunt could also be initiated by increasing the filling pressure to the left atrium.

Journal Article↗
PubMed1994

BLOOD PRESSURE CONTROL IN THE ANTARCTIC FISH PAGOTHENIA BORCHGREVINKI

The mechanisms of cardiovascular control in the Antarctic fish Pagothenia borchgrevinki were investigated during rest and swimming exercise using pharmacological tools to reveal the nature of the control systems involved. Simultaneous and continuous recordings of ventral and dorsal aortic blood pressure, heart rate and ventral aortic blood flow (cardiac output) were made using standard cannulation procedures and a single-crystal Doppler flowmeter. Exercise produced a clear and consistent decrease in dorsal aortic blood pressure caused by a decrease in systemic vascular resistance. At the same time, ventral aortic blood pressure increased owing to the combined effects of a markedly increased cardiac output (by about 80 %) and branchial vasoconstriction. Judged from the effects of the alpha-adrenoceptor antagonist prazosin, control of the branchial vasculature involves an alpha-adrenoceptor-mediated vasoconstriction, in addition to more traditional cholinergic vasoconstrictor and ss-adrenoceptor-mediated dilatory mechanisms. The range of heart rates is large, from 3-4 beats min-1 in individual fish during hypertensive bradycardia to about 28 beats min-1 after atropine treatment. Both chronotropic and inotropic effects are responsible for a marked increase in cardiac output during exercise. The increase in blood pressure caused by adrenaline injection was due largely to an increase in cardiac output, while direct effects on the systemic vasculature were small and transient. The increase in cardiac output, in turn, was due solely to an adrenergic stimulation of stroke volume. A barostatic bradycardia, often seen in other vertebrates in response to adrenaline injection, was absent and it is possible that a decrease in heart rate was offset by direct adrenergic stimulation of the heart. Angiotensin II (Ang II) produced consistent hypertension by systemic vasoconstriction. In contrast to the effects of adrenaline injection, the hypertension caused by Ang II was accompanied by a marked bradycardia. This could be abolished by atropine, suggesting a cholinergic vagal reflex of the type found in other vertebrates. Angiotensin I also caused an elevated blood pressure, and this effect was abolished by the angiotensin converting enzyme inhibitor enalapril, demonstrating elements of an angiotensin-related cardiovascular control system.

Journal Article↗
PubMed1994

EVIDENCE OF REGULATORY MECHANISMS FOR THE DISTRIBUTION OF BLOOD BETWEEN THE ARTERIAL AND THE VENOUS COMPARTMENTS IN THE HAGFISH GILL POUCH

Of the extant vertebrate animals, the hagfishes are generally considered to be the group which diverged first from the ancestral vertebrate lineage, although molecular sequence analysis has recently suggested that they form a monophyletic group with lampreys (Stock and Whitt, 1992). The circulatory system of hagfishes has features that have been described as 'primitive' (Burggren et al. 1985), but their gills are effective gas exchangers. The gills are contained within discrete muscular pouches, and the anatomy of the blood system and ventilatory ducts has an ideal countercurrent arrangement (Mallatt and Paulsen, 1986; Elger, 1987). Reite (1969) first reported effects of catecholamines and other drugs on the branchial vasculature of hagfish. Recent studies of both perfused gills in situ and of blood flow in vivo have suggested that blood flow through the gills of hagfish is under tonic control by catecholamines (Axelsson et al. 1990; Forster et al. 1992). In teleosts, several studies have shown that adrenergic control mechanisms are involved in the distribution of blood between the arterio-arterial and the arterio-venous pathways of the gill vasculature (see Nilsson, 1983). Anatomical and ultrastructural studies have demonstrated the existence of similar pathways in hagfish (Cole, 1925; Mallatt and Paulsen, 1986; Elger, 1987). The experiments reported here demonstrate that, in the hagfish gill pouch, both adrenaline and isoprenaline can increase the proportion of fluid leaving via the efferent arterial route, at the expense of the venous outflow. Hagfish (Eptatretus cirrhatus Forster) were collected off Motunau, North Canterbury, New Zealand, and held in seawater aquaria until used. The masses of the 11 animals used in these experiments ranged from 680 to 1720 g with a mean of 1140±110 g (s.e.m.). Animals were anaesthetized in a 0.4 % solution of benzocaine in sea water. The hagfish were opened ventrally to expose the gills and their blood supply. Individual gill pouches were prepared for perfusion studies.

Journal Article↗
PubMed1994

CARDIOVASCULAR RESPONSES TO SCYLIORHININ I AND II IN THE RAINBOW TROUT, ONCORHYNCHUS MYKISS, IN VIVO AND IN VITRO

Changes in cardiac output, heart rate, dorsal aortic blood pressure and coeliac artery blood flow were measured in unrestrained rainbow trout, Oncorhynchus mykiss, following injections of the elasmobranch tachykinins scyliorhinin I and II. The resistance in the coeliac vascular bed and the total systemic vasculature were calculated from blood pressure and flow. In addition, isolated tails were perfused to investigate the effect of the peptides on the somatic vasculature. Scyliorhinin I (SCY I) produced a biphasic change in the coeliac vascular resistance: an initial decrease was followed by an increase. The decrease in coeliac vascular resistance was accompanied by a decrease in the total systemic vascular resistance, leading to an increased cardiac output. The ensuing increase in coeliac vascular resistance caused a slight increase in blood pressure. In the perfused tail, SCY I produced a marked increase in the somatic vascular resistance. Scyliorhinin II (SCY II) decreased the systemic vascular resistance, causing an increase in cardiac output. SCY II also caused a late increase in the coeliac vascular resistance, which led to hypertension and bradycardia. In vitro, SCY II produced a biphasic response in which an initial decrease in the somatic resistance was followed by a larger increase. The results demonstrate that exogenous SCY I and II are vasoactive peptides that act by different mechanisms in the rainbow trout cardiovascular system. Their actions also differ from the actions of substance P previously observed in the cod, Gadus morhua, and possibly involve a neural reflex.

Journal Article↗
PubMed1994

Coronary hemodynamics in elasmobranchs and teleosts.

Until recently, direct measurements of coronary blood flow in fishes had not been made. This review presents and compares in vivo measurements of coronary flow recorded from the school shark, Galeorhinus australis, and the coho salmon, Oncorhynchus kisutch. In both species, the coronary blood flow was phasic and strongly influenced by the cardiac cycle. Coronary blood flow in the school shark was more severely compromised by the cardiac cycle with a short retrograde flow occurring during systole. In the coho salmon, there was an anterograde coronary blood flow throughout the cardiac cycle. Differences in coronary hemodynamics are discussed in relation to differences in the myoarchitecture of the school shark and coho salmon hearts. The regulation of coronary blood flow through changes in vascular resistance (vasoactivity of the coronary vessels) is also discussed.

Animals↗
PubMed1993

Respiratory and cardiovascular responses to hypoxia in the Australian lungfish.

Simultaneous measurements of pulmonary blood flow (qPA), coeliacomesenteric blood flow (qCoA), dorsal aortic blood pressure (PDA), heart rate (fH) and branchial ventilation frequency (fv) were made in the Australian lungfish, Neoceratodus forsteri, during air breathing and aquatic hypoxia. The cholinergic and adrenergic influences on the cardiovascular system were investigated during normoxia using pharmacological agents, and the presence of catecholamines and serotonin in different tissues was investigated using histochemistry. Air breathing rarely occurred during normoxia but when it did, it was always associated with increased pulmonary blood flow. The pulmonary vasculature is influenced by both a cholinergic and adrenergic tonus whereas the coeliacomesenteric vasculature is influenced by a beta-adrenergic vasodilator mechanism. No adrenergic nerve fibers could be demonstrated in Neoceratodus but catecholamine-containing endothelial cells were found in the atrium of the heart. In addition, serotonin-immunoreactive cells were demonstrated in the pulmonary epithelium. The most prominent response to aquatic hypoxia was an increase in gill breathing frequency followed by an increased number of air breaths together with increased pulmonary blood flow. It is clear from the present investigation that Neoceratodus is able to match cardiovascular performance to meet the changes in respiration during hypoxia.

Animals↗
PubMed1993

Coronary blood flow in vivo in the coho salmon (Oncorhynchus kisutch).

The effects of adrenergic agonists on dorsal aortic blood pressure, cardiac output, and coronary blood flow were studied in unrestrained coho salmon, Oncorhynchus kisutch. Resting coronary blood flow was 0.43 ml.min-1.kg body mass-1, which represented 1.1% of cardiac output or approximately 0.5 ml.min-1.g-1 compact ventricular mass calculated on 40% of total ventricle mass. Coronary blood flow was phasic and continuous throughout the cardiac cycle; flow seems to be affected by the ventricular contraction, with a peak flow occurring during diastole and a nadir in early systole. Epinephrine injections into the dorsal aorta resulted in a rapid increase in coronary blood flow in association with a rapid increase in dorsal aortic blood pressure. Subsequently there was also a slower increase in coronary vascular resistance, which could be blocked by phentolamine, indicating an alpha-adrenergic vasoconstriction. Isoprenaline injection produced an increase in coronary blood flow and a large reduction in coronary vascular resistance. The coronary vasodilatation was blocked by propranolol, indicating that it may be partly due to a beta-adrenergic vasodilatation. Preliminary results showed a marked increase in coronary blood flow associated with exposure to environmental hypoxia.

Animals↗
PubMed1992

Cardiovascular responses to hypoxia in the hagfish, Eptatretus cirrhatus.

Simultaneous measurements of cardiac output (Q), blood pressures and blood gases were made in the hagfish, Eptatretus cirrhatus, during exposure to hypoxia. The partial pressure of oxygen in the medium (PIO2) was reduced from 20.7 kPa to 8.0 kPa and then lowered to 5.3 kPa. At a PIO2 of 5.3 kPa there was a 40% increase in Q. Part of the increase may have been due to the increased activity of the animal at low PIO2. In recovery, when the animals were inactive, Q continued to rise to 160% of the control values. At 5.3 kPa, oxygen consumption (as determined by the Fick principle) fell to 29% of the normoxic value and was associated with increased branchial vascular resistance (Rg) and an increased diffusion limitation of the gills (Ldiff). Adrenaline increased heart rate and aortic blood pressures. Increased Rg and Ldiff could be provoked in normoxia by the injection of the beta-adrenergic blocking drug propranolol. We suggest that catecholamines may be involved in the tonic control of gill vasomotor tone.

Animals↗
PubMed1992

Cardiovascular responses of the red-blooded antarctic fishes Pagothenia bernacchii and P. borchgrevinki.

The aim of this study was to investigate cardiac performance and cardiovascular control in two red-blooded nototheniid species of antarctic fishes, Pagothenia bernacchii (a benthic fish) and P. borchgrevinki (a cryopelagic fish), and to make comparisons with existing information on haemoglobin-free antarctic teleosts. In quiescent P. bernacchii at 0 degrees C ventral aortic pressure (PVA) was 3.09 kPa and cardiac output (Q) was 17.6 ml min-1 kg-1, with a heart rate (fH) of 10.5 beats min-1 and stroke volume of 1.56 ml kg-1. Following atropine treatment, Q was maintained but heart rate increased and stroke volume decreased. Resting heart rate resulted from an inhibitory cholinergic tone of 80.4% and an excitatory adrenergic tone of 27.5%. The intrinsic heart rate was 21.7 beats min-1 at 0 degrees C. In quiescent P. borchgrevinki at 0 degrees C, PVA was 3.6 kPa, Q was 29.6 ml min-1 kg-1 and stroke volume was 2.16 ml kg-1. The resting heart rate in P. borchgrevinki of 11.3 beats min-1 resulted from an inhibitory cholinergic tone of 54.5% and an excitatory adrenergic tone of 3.2%. The intrinsic heart rate was 23.3 beats min-1. P. bernacchii maintained Q during a progressive decrease in water oxygen tension from 20 to 6.7 kPa, but fH was increased significantly. Thus, although there is cholinergic control of the heart, no hypoxic bradycardia was observed. Recovery from hypoxia was associated with increases in Q and fH; stroke volume returned to control values. PVA declined in recovery as total vascular resistance decreased. Hypoxic exposure following atropine treatment resulted in progressive increases in PVA, Q and stroke volume; fH decreased during the recovery period. Hypoxic exposure in P. borchgrevinki produced similar cardiovascular responses to those observed in P. bernacchii. During an acute increase in water temperature from 0 to 5 degrees C, P. bernacchii regulated Q and total vascular resistance. Stroke volume decreased as fH increased. The intrinsic heart rate had a Q10 of 1.96 over this temperature range. P. bernacchii maintained chronotropic inhibition up to a temperature of 2.5-3.0 degrees C. However, by 5 degrees C this chronotropic inhibition of the heart rate was lost. Infusion of adrenaline into the ventral aorta of P. bernacchii resulted in significant increases in Q, fH, PVA and total vascular resistance. Infusion of adrenaline after atropine treatment caused similar cardiovascular changes without the change in fH. P. borchgrevinki could sustain swimming in a water tunnel at approximately 1 body length per second for 6-10 min.(ABSTRACT TRUNCATED AT 400 WORDS)

Acclimatization↗
PubMed1991

Gut blood flow in the estuarine crocodile, Crocodylus porosus.

Simultaneous recordings of blood flow in the right and left aorta and carotid and coeliac artery were made in the crocodile, Crocodylus porosus at rest and during various stimuli. In resting animals the right aorta and carotid artery flow profiles resembled the recordings obtained in the caiman (Axelsson et al. 1989a), with an anterograde blood flow throughout the cardiac cycle. As in the caiman, the left aorta flow profile was complex with both anterograde and retrograde blood flow during the cardiac cycle, and a net left aorta blood flow near zero at rest. The coeliac artery blood flow profile did not show the complex pattern seen in the upper aorta, immediately suggesting that most of the coeliac artery blood originates elsewhere. We believe that coeliac artery blood flow in the resting animal derives from the right aorta via the abdominal anastomosis between the two aortas. Feeding induced an increase in the coeliac artery and left aorta blood flow, probably due to a decrease in visceral vascular resistance, and hence coeliac arterial and the left aorta blood pressure, which facilitates blood flow (from right to left aorta) through the foramen of Panizza. During short 'fright dives', heart rate fell and there was a decrease in the recorded blood flows: carotid artery blood flow did not decrease to the same extent as the RAo and coeliac artery flow, indicating some capacity for redistribution of blood to the cephalic circuits during diving. Similarly, a near-unimpaired carotid artery blood flow was maintained after adrenaline injection. Substance P increased the coeliac artery blood flow and produced a right-to-left cardiac shunt, probably by construction of the pulmonary vasculature.

Alligators and Crocodiles↗
PubMed1991

Effects of exercise, hypoxia and feeding on the gastrointestinal blood flow in the Atlantic cod Gadus morhua.

Cardiac output, ventral and dorsal aortic blood pressure, heart rate, and coeliac and mesenteric artery blood flow were recorded simultaneously in the Atlantic cod, Gadus morhua L., at rest, during exercise, during hypoxia and after feeding. In the resting unfed animals, coeliac artery blood flow was 4.1 +/- 0.8 ml min-1 kg-1 and mesenteric artery blood flow was 3.5 +/- 1.1 ml min-1 kg-1 (mean +/- S.E.M., N = 10); together, these flows represent approximately 40% of the cardiac output. Exercise or exposure to hypoxia resulted in increased visceral vascular resistance, leading to reductions in the coeliac and mesenteric artery blood flows. Coeliac and mesenteric blood flows were increased 24 h after feeding and the coeliac and systemic vascular resistances decreased in comparison with the prefeeding values. Phentolamine did not affect the gastrointestinal artery blood flow, but produced a significant decrease in the mesenteric and systemic vascular resistance. Treatment with bretylium and phentolamine revealed differences between the coeliac and the mesenteric vasculature regarding the control mechanisms during hypoxia and during exercise and feeding. During hypoxia, an adrenergic control of the gastrointestinal vasculature with both nervous and humoral components was found, whereas during exercise and after feeding an additional non-adrenergic mechanism controlling gut blood flow was demonstrated.

Animals↗