Biomedical subjects

A Ilebekk

Publications and source records attributed to A Ilebekk.

At least 19 recordsLinked to original sources

PubMed1992

Oxygen free radical injury and Gs mediated signal transduction in the stunned porcine myocardium.

OBJECTIVE: The aim was to investigate involvement of oxygen free radicals and any changes in the Gs mediated beta adrenergic signalling system of stunned porcine myocardium. METHODS: Myocardial stunning was induced in eight pentobarbitone anaesthetised pigs by brief occlusions of the distal left anterior descending coronary artery for periods of up to 10 min. Segment length function was measured in the ischaemic region and in a control region supplied by the circumflex artery. Left ventricular biopsies were obtained from the two regions 1 h after the last occlusion for ultrastructural and biochemical studies. Timolol has been used to prevent arrhythmia during ischaemia. RESULTS: At the time when biopsies were obtained, percent systolic shortening was reduced to 58% in the region subjected to ischaemia and was only minimally reduced in the control region. In the biopsies from the stunned region: (1) electron microscopy showed mild and reversible intracellular changes in the stunned myocardium; (2) the activities of superoxide dismutase and glutathione peroxidase were decreased by 66% and 52%, respectively; (3) the content of malondialdehyde was increased by 49%; (4) neither density nor affinity of beta adrenoceptors showed any changes; (5) there were no alterations in messenger RNA encoding for the alpha subunit of the stimulatory guanine nucleotide binding protein (Gs), demonstrated by northern and dot-blot hybridisations; (6) ELISA technique utilising a specific antipeptide antibody showed no quantitative change in Gs; (7) the activity of adenyl cyclase was unchanged. CONCLUSIONS: Even though the stunned porcine myocardium showed substantial evidence of free radical injury, the beta adrenergic signalling system was intact.

Adenylyl Cyclases↗

PubMed1992

Myocardial potassium balance associated with regional ischaemia in the pig: effects of beta-adrenoceptor blockade, duration of ischaemia and preceding ischaemic periods.

The effects of beta-adrenoceptor blockade, duration of ischaemia and preceding ischaemic periods on ischaemia-induced changes in myocardial K+ balance were studied in 12 open-chest pigs. Coronary venous blood was directed through a shunt from the coronary sinus to the right atrium. Continuous recordings of arterial, shunt blood [K+] and shunt flow enabled us to compute myocardial K+ balance during and after consecutive 2-, 2-, 5-, 10- and 2-min periods of regional ischaemia separated by 30 min of reperfusion. beta-adrenoceptor blockade (propranolol 1 mg kg-1 i.v.) given between the first and second ischaemic period did not alter the effects of 2 min ischaemia on myocardial K+ balance. Total K+ losses induced by 2, 5 and 10 min of ischaemia were 67.1 (40.6-93.3), 106.7 (69.4-176.8) and 192.2 (117.7-332.6) mumol 100 g-1, respectively. Thus, the plateau observed in extracellular [K+] between 2 and 10 min of regional ischaemia could, at least partly, be explained by continuous drainage of K+ from ischaemic myocardium into the surrounding normally perfused tissue. The total K+ loss induced by the second and last 2-min ischaemic period were 67.1 (40.6-93.3) and 35.6 (23.1-53.6) mumol 100 g-1 (P less than 0.001), respectively. This reduction shows that ion homeostasis during ischaemia was greatly changed in myocardium which had been 'preconditioned' and 'stunned' by 5 plus 10 min of ischaemia. Total amount, maximal rate and duration of post-ischaemic K+ reuptake increased with the duration of the preceding ischaemia. Moreover, K+ re-uptake after 2 min of ischaemia and the number of sarcolemmal Na/K pumps ([3H]ouabain binding), were normal in stunned myocardium. From these observations we conclude that progressive stimulation of the Na/K-pump occurred when ischaemia was prolonged from 2 to 10 min, and that Na/K-pump function was preserved in stunned myocardium.

Adrenergic beta-Antagonists↗

PubMed1992

Calcium-induced net potassium uptake of pig hearts in vivo.

To determine whether the catecholamine-induced myocardial potassium uptake could be mimicked by increasing extracellular and intracellular calcium concentrations in vivo, we measured changes in myocardial potassium balance in nine anaesthetized open-chest pigs with PVC-valinomycin electrodes in arterial and coronary sinus blood. CaCl2 infusion (200-400 mumol min-1) into the left coronary artery increased coronary sinus blood calcium concentration from 2.29 (2.19-2.42) to 4.63 (3.76-5.67) mmol l-1 (median, 95% confidence interval, P = 0.01) indicating a similar increment in myocardial extracellular calcium concentration. The contractility measure LV dP/dt increased 95 (76-147) %, indicating a substantial increment in intracellular calcium concentration. During the CaCl2 infusion coronary sinus potassium concentration declined to a nadir 0.12 (0.09-0.17) mmol l-1 below baseline (P = 0.008) whereas arterial concentration remained unchanged. Peak myocardial potassium uptake was 18 (7-32) mumol min-1 100 g-1 and occurred 150 (110-195) s after start of infusion. The response remained unaltered after adrenoceptor blockade by prazosin and propranolol. Prolonged CaCl2 infusion caused a net myocardial potassium loss which was accompanied by metabolic and haemodynamic indications of myocardial ischaemia. These findings are consistent with enhanced Na-K pump activity in the intact beating pig heart in response to increased extracellular and intracellular calcium concentrations.

Animals↗

PubMed1992

Passive effect of reduced cardiac function on splanchnic intravascular volume.

It has been hypothesized that lowered cardiac output due to heart failure results in passive redistribution of intravascular volume from the peripheral circulation to the central circulation and that this redistribution acts to support cardiac output. To test this hypothesis, acute heart failure was induced by rapid atrial pacing to raise heart rate from 148 +/- 6 to 232 +/- 1 beats/min for 5 min, while splanchnic intravascular volume was assessed with radionuclide imaging in eight anesthetized pigs that had undergone prior carotid denervation and vagotomy. Cardiac output decreased from 3,350 +/- 410 to 2,170 +/- 290 ml/min (P less than 0.001), mean arterial pressure decreased from 103 +/- 5 to 84 +/- 4 mmHg (P less than 0.001), left atrial pressure increased from 5.9 +/- 0.6 to 10.8 +/- 0.9 mmHg (P less than 0.001), right atrial pressure increased from 2.4 +/- 0.5 to 4.8 +/- 0.9 mmHg (P less than 0.001), total splanchnic intravascular volume did not change (0 +/- 2 ml), splenic intravascular volume decreased 11 +/- 3% (P less than 0.001), hepatic intravascular volume increased 12 +/- 2% (P less than 0.001), and mesenteric intravascular volume did not change (-3 +/- 2%). Thus, when cardiac output is lowered with pacing-induced acute heart failure, lowered perfusion pressure acts to lower splenic intravascular volume and increased central venous pressure acts to increase hepatic intravascular volume; however, total splanchnic intravascular volume does not decrease to support cardiac filling and cardiac output.

Animals↗

PubMed1992

Characteristics and development of myocardial stunning in the pig.

Regional left ventricular function associated with consecutive ischemic periods of 2, 2, 5, 10, and 2 min was recorded by ultrasonic technique in pentobarbital-anesthetized pigs. All systolic and diastolic derangements first appeared after 5 min of ischemia, and all worsened after 10 min of ischemia. Percent systolic segment length shortening reached nadirs 23 (17-29)% (P less than 0.001) and 54 (45-65)% (P less than 0.001) below baseline 30 min after 5 and 10 min of ischemia. During reperfusion all recorded systolic and diastolic variables transiently recovered and then deteriorated with a closely similar time course. This covariance indicates that systolic and diastolic derangements are causally related, and because diastolic compliance was preserved in stunned myocardium we conclude that all derangements largely result from reduced systolic tension development. Transient postischemic hypercontractility followed all occlusions and was not attenuated by beta-blockade and not mimicked by hyperemia alone. Postischemic hypercontractility was greatly enhanced in stunned myocardium, and we hypothesize that more pronounced and sustained postischemic elevation of intracellular Ca2+ concentration explains this observation.

Adrenergic beta-Antagonists↗

PubMed1992

Role of adenosine for reactive hyperemia in normal and stunned porcine myocardium.

The role of adenosine for reactive hyperemia in normal and stunned myocardium was examined in 16 open-chest barbiturate-anesthetized pigs. Interstitial adenosine concentration was reduced or enhanced by intracoronary infusion of adenosine deaminase or the nucleoside transport inhibitor R 75231, respectively. In normal myocardium, adenosine deaminase reduced volume of hyperemia (Doppler flowmetry) after a 30-s left anterior descending coronary artery (LAD) occlusion by 20% (6-34%; P < 0.05), whereas R 75231 increased volume of hyperemia by 15% (2-24%; P < 0.05). Adenosine deaminase reduced volume of hyperemia after a 2-min LAD occlusion by 27% (13-37%; P < 0.001), whereas R 75231 increased volume of hyperemia by 66% (53-159%; P < 0.001). Adenosine deaminase and R 75231 did not affect maximal hyperemia. Volume of hyperemia after a 2-min LAD occlusion was reduced in stunned myocardium (%systolic segment length shortening reduced by approximately 45%, ultrasonic technique) but not further altered by either adenosine deaminase or R 75231. These findings show that adenosine contributes to reactive hyperemia after 30-120 s of ischemia in normal myocardium and indicate that the reduced reactive hyperemia in stunned myocardium is due to reduced accumulation of adenosine during ischemia.

Adenosine↗

PubMed1991

Frequency dependent myocardial potassium fluxes during beta adrenergic stimulation of intact pig hearts.

STUDY OBJECTIVE: The aim was to determine the frequency dependent myocardial potassium fluxes of intact pig hearts at control inotropy and during beta adrenergic stimulation. DESIGN - Atrial pacing rate was suddenly raised and decreased by 50 beats.min-1 at control inotropy and during infusion of isoprenaline, 2.5 nmol.min-1, into the left coronary artery. EXPERIMENTAL MATERIAL: Nine anaesthetised pigs (21-33 kg) were instrumented for electric pacing of the right atrium and metabolic and haemodynamic recordings. MEASUREMENTS AND MAIN RESULTS: Myocardial potassium balance was measured by PVC-valinomycin electrodes in the left atrial cavity and in a shunt (with flow meter) diverting blood from the coronary sinus to the right atrium. Isoprenaline raised net myocardial potassium flux following the change in pacing rate from 19(14-23) to 38(32-46) mumol.100 g-1.min-1 (median, 95% confidence interval, difference: p = 0.03). The corresponding myocardial potassium flux per beat increased from 0.38(0.29-0.45) to 0.80(0.63-0.97) mumol.100 g-1 (p = 0.03). Accumulated potassium flux increased from 9(8-11) to 17(11-27) mumol.100 g-1, respectively (p = 0.03). CONCLUSIONS: In intact hearts beta adrenergic stimulation doubles the frequency dependent myocardial potassium flux. This component constitutes 22-25% of the ouabain inhibitable potassium flux at both levels of inotropy.

Animals↗

PubMed1991

Reduced prostaglandin release from the stunned porcine heart--significance for attenuated reactive hyperaemia.

STUDY OBJECTIVE: Since both reactive hyperaemia and membrane phospholipids are altered even after short lasting ischaemic periods, the release of PGE2 and PGI2 in the basal state and during early reperfusion was examined to determine whether it was changed in the stunned myocardium. The effect of prostaglandin synthesis inhibition on reactive hyperaemia was also examined. DESIGN: The distal left anterior descending coronary artery was occluded for brief periods and coronary flow was recorded by Doppler flowmetry. In subgroups: (1) a shunt was established draining the ischaemic region for determination of myocardial prostaglandin release associated with 2 min of ischaemia before and after a 10 min occlusion; (2) prostaglandin synthesis was blocked between two 2 min occlusions by infusing indomethacin into the left anterior descending artery; and (3) segment lengths were measured in the left anterior descending artery region subjected to consecutive periods of 2, 10, and 2 min of ischaemia, and in a control region. EXPERIMENTAL MATERIAL: 21 pentobarbitone sodium anaesthetised pigs, weight 21-30 kg, were used. MEASUREMENTS AND MAIN RESULTS: 30 min after the 10 min occlusion, systolic shortening was reduced by 38(18-57)% (median +95% confidence interval; p less than 0.05). Concomitantly, basal PGE2 and PGI2 release was reduced by 69(30-77)% (p less than 0.05) and 58(7-81)% (p less than 0.05), respectively. During early reperfusion after 2 min of ischaemia, PGE2 release was reduced by 53(17-86)% (p less than 0.05) after development of stunning, whereas PGI2 release remained unaltered. Blockade of prostaglandin synthesis did not affect reactive hyperaemia either in normal or in stunned myocardium. CONCLUSIONS: Prostaglandin release from the stunned myocardium is reduced. Since indomethacin did not affect reactive hyperaemia, the attenuated PGE2 release during early reperfusion in stunned myocardium cannot explain the concomitant reduction in reactive hyperaemia.

6-Ketoprostaglandin F1 alpha↗

PubMed1991

Right and left atrial diameters during incremental atrial pacing in pigs.

The relationship between right and left atrial diameters and heart rate was examined in 14 open-chest barbiturate-anesthetized pigs by an ultrasonic technique. The maximal atrial diameter was read at the top of the v wave, which decreased in both atria when heart rate was increased from 124 (118-130) to 159 (156-160) (median and 95% confidence interval) beats/min. Right and left atrial maximal diameter fell significantly from 25.7 (23.6-32.6) to 24.9 (22.9-29.5) mm and from 30.8 (25.1-37.2) to 29.8 (23.4-36.3) mm, respectively, when heart rate was increased from 124 to 180 (177-182) beats/min. At higher pacing frequencies, both right and left atrial maximal diameter progressively increased, and at 220 (216-221) beats/min the maximal diameter regained the values obtained at 124 beats/min. The minimal atrial diameter, which was read at the end of the a wave, remained unchanged at heart rates below 180 beats/min but rose significantly at higher rates. Our findings indicate progressively reduced atrial filling with increasing heart rate and hampered atrial emptying and atrial distension at the highest heart rates.

Animals↗

PubMed1991

Release of atrial natriuretic factor during selective cardiac alpha- and beta-adrenergic stimulation, intracoronary Ca2+ infusion, and aortic constriction in pigs.

The effects of alpha- and beta-adrenergic stimulation on release of atrial natriuretic factor (ANF) were examined in seven anesthetized, open-chest pigs. The alpha-adrenergic agonist phenylephrine (28.0 micrograms/min) and the beta-adrenergic agonist isoproterenol (0.3 micrograms/min) were infused into the proximal part of the circumflex coronary artery to stimulate the left atrial adrenoceptors without concomitant changes in left and right atrial filling pressures (v wave). Isoproterenol reduced plasma immunoreactive ANF (irANF) by 15 +/- 7 pg/ml (20%) from 76 +/- 10 pg/ml despite a rise in left atrial systolic pressure (a wave). A comparable rise in left atrial systolic pressure, induced by intracoronary infusion of calcium chloride (8.0 mg/min), increased plasma irANF by 33 +/- 10 pg/ml (53%) from 62 +/- 7 pg/ml. Phenylephrine increased plasma irANF by 9 +/- 4 pg/ml (14%) from 66 +/- 10 pg/ml without altering right and left atrial pressures. A rise in left atrial filling pressure of 3.2 +/- 0.5 mm Hg, induced by constricting the ascending aorta, increased plasma irANF by 83 +/- 35 pg/ml (141%) from 59 +/- 11 pg/ml. This increase was nine times that during phenylephrine infusion. In conclusion, alpha-adrenergic stimulation increases and beta-adrenergic stimulation inhibits ANF release by a direct action on the atrial myocytes. The direct effects of alpha- and beta-adrenergic stimulation on ANF release in vivo are small compared with the effect of a moderate rise in atrial filling pressure.

Animals↗

PubMed1990

Changes in cardiac dynamics by opening an interventricular shunt in dogs.

Changes in right and left ventricular (RV, LV) dynamics caused by an interventricular shunt were examined in open-chest dogs. At a pulmonary to systemic blood flow ratio of 1.7 +/- 0.2 pulmonary flow increased by 53 +/- 13%, whereas aortic flow decreased by 9 +/- 2%. Shunt flow was continuous from the left to the right ventricle throughout the cardiac cycle, but 72 +/- 4% took place during the LV ejection phase. Peak systolic LV pressure declined by 6 +/- 3 mm Hg, LV end-diastolic segment length (SL) rose, and systolic shortening of the SL increased. Peak systolic RV pressure rose from 28 +/- 3 to 36 +/- 3 mm Hg and RV end-diastolic and end-systolic SL rose almost equally. Accordingly, RV systolic SL shortening did not rise despite the substantial augmentation in RV outflow. The transseptal end-diastolic pressure gradient did not rise, while the transseptal peak systolic gradient decreased when the shunt was opened. Similarly directed alterations were observed when the shunt was opened at different preloads and when the shunt flow was varied. Local work in the anterior wall of the right ventricle (calculated from the RV pressure SL loop) rose by 26 +/- 4%, whereas RV stroke work (product of mean systolic right ventricular pressure and pulmonary flow) rose by 57 +/- 12%; difference, P less than 0.05. LV stroke work and local work in anterior LV free wall rose in proportion when the shunt was opened.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Coronary reactivity in the porcine heart after short lasting myocardial ischaemia: effects of duration of ischaemia and myocardial stunning.

STUDY OBJECTIVE: The aim was to characterise reactive hyperaemia and endothelium dependent (ADP) and independent (adenosine) vasodilatation after ischaemic periods of increasing duration, and in the stunned myocardium. DESIGN: The left anterior descending coronary artery was occluded 5-7 cm distal from its origin for consecutive periods of 2, 2, 5, 10, and 2 min separated by 30 min of reperfusion. Coronary flow was continuously measured by Doppler flowmetry proximal to the occlusion site. ADP and adenosine were infused into the left coronary artery proximal to the flowprobe. EXPERIMENTAL MATERIAL: 11 domestic pigs, weight 25-36 kg, were used. MEASUREMENTS AND MAIN RESULTS: In the stunned myocardium maximal reactive hyperaemia after 2 min of ischaemia was preserved, whereas all other variables describing reactive hyperaemia were diminished: time to maximal hyperaemia by 40% (p less than 0.01), duration of hyperaemia by 44% (p less than 0.001), volume of hyperaemia by 53% (p less than 0.001), and repayment of flow debt by 43% (p less than 0.001). The vasodilating effects of ADP and adenosine (dose-response curves) were not altered after development of stunning. CONCLUSIONS: Preserved maximal hyperaemia and vasodilation during ADP and adenosine infusion, but reduced volume of hyperaemia, indicate normal coronary reactivity but diminished release in the stunned myocardium of the vasodilator(s) responsible for the prolonged postischaemic flow increase.

Adenosine↗

PubMed1990

Regulation of splanchnic organ size during muscarinic receptor stimulation in the anaesthetized pig.

To determine the mechanisms responsible for changes in splanchnic organ size during muscarinic receptor stimulation, acetylcholine was infused at 5 micrograms kg-1 min-1 in 11 anaesthetized pigs which had previously undergone carotid denervation and cervical vagotomy. Blood pressure decreased by 42 +/- 4 mmHg (P less than 0.005), portal vein pressure decreased by 1.0 +/- 0.3 mmHg (P less than 0.01), IVC pressure increased by 0.2 +/- 0.1 mmHg (P less than 0.01), hepatic arterial flow increased by 10 +/- 6 ml min-1 (NS), portal vein flow decreased by 89 +/- 20 ml min-1 (P less than 0.005), splenic segment length (SSL) decreased by 0.52 +/- 0.11 mm (P less than 0.005) (control 12.49 +/- 1.27) (measured with ultrasonic crystals) and hepatic segment length (HSL) increased by 0.29 +/- 0.06 mm (P less than 0.005) (control 13.94 +/- 1.16). Aortic constriction to decrease the splanchnic distending pressure by an amount comparable to that achieved with the acetylcholine-associated decrease in portal flow caused a similar decrease in SSL and increase in HSL. Graded constriction of the portal vein or IVC, to increase SSL or HSL respectively, in the presence and absence of acetylcholine demonstrated no change in splenic or hepatic compliance with acetylcholine. Ligation of the splenic vasculature reduced the acetylcholine-associated HSL increase from 0.41 +/- 0.09 to 0.20 +/- 0.07 mm (P less than 0.05). Acetylcholine infused directly into the portal vein did not alter HSL. Atropine abolished all acetylcholine-associated haemodynamic changes. Thus, muscarinic receptor stimulation does not appear to act directly on splanchnic capacity vessels. Splenic dimension decreases due to a decrease in splanchnic flow and pressure, and hepatic dimension increases due to an increase in IVC pressure and redistribution of volume from the spleen.

Acetylcholine↗

PubMed1990

Variations in left ventricular volume alter myocardial oxygen consumption more at low than at high inotropy.

Variations in left ventricular (LV) wall tension during changes in LV end-diastolic volume significantly affect myocardial oxygen consumption (MVO2). In the present study we examined if the reduction in MVO2 per beat accompanying a decline in LV end-diastolic volume at constant LV systolic pressure (LVSP) is dependent on the level of myocardial inotropy. In six anaesthetized open-chest pigs, the blood volume was expanded by i.v. infusion of a Ringer solution. At constant heart rate (by atrial pacing) and LVSP (by adjustments of a proximal aortic snare), LV end-diastolic volume was reduced in steps by withdrawals of blood. This procedure was performed at high inotropy (during a continuous intracoronary infusion of isoproterenol, 0.40 +/- 0.08 micrograms min-1), and at low inotropy (after i.v. injection of 3.4 +/- 0.2 mg propranolol). LVSP was about 25 mmHg higher at high than at low inotropy. The fall in LV tension was therefore greater during blood volume reductions at high than at low inotropy because the fall in LV end-diastolic volume was almost identical and was initiated from the same level at both high and low inotropy. Nevertheless, the slope of the MVO2/LV end-diastolic volume relationship was significantly (P less than 0.05) less steep at high (1.26 +/- 0.30 mumol 100 g-1 mm-1) than at low inotropy (2.06 +/- 0.48 mumol 100 g-1 mm-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Influence of angiotensin on total intravascular capacity in the anaesthetized pig.

The present study examined the influence of angiotensin on total intravascular capacity. In eight anaesthetized pigs, splenectomy, carotid sinus denervation and cervical vagotomy were performed. Blood was drained from the venae cavae to an extracorporeal reservoir and returned to the right atrium at a constant rate so that changes in total intravascular volume could be recorded as the inverse of changes in reservoir volume. Angiotensin administration at 0.2 microgram kg-1 min-1 i.v. for 5 min was associated with a decrease in total intravascular volume of 57 +/- 6 ml (P less than 0.05) and an increase in aortic pressure from 96 +/- 5 to 119 +/- 6 mmHg (P less than 0.05). With subsequent angiotensin administration in five of the animals, the responses were not attenuated. In five of the animals, angiotensin was associated with a decrease in intravascular volume of 72 +/- 8 ml (P less than 0.05) before abdominal evisceration and 33 +/- 13 ml (P less than 0.05) after evisceration. These responses were significantly different from each other. In four of these eviscerated animals, angiotensin was associated with a decrease in intravascular volume of 35 +/- 17 ml (P less than 0.05) before ligation of all four limbs and a decrease of 36 +/- 4 ml (P less than 0.05) after limb ligation. Thus, angiotensin acts directly to decrease total intravascular volume. The decrease is due to decreases in both splanchnic and extrasplanchnic volume. The extrasplanchnic volume decrement is not due to decreases in skeletal muscle or cutaneous tissue intravascular capacity in the limbs.

Angiotensin II↗

PubMed1990

Isoprenaline augments total myocardial K+ influx of the in-situ beating porcine heart.

To determine the total rate of K+ flux into myocardial cells of the in-situ beating heart and how this influx is affected by beta-adrenoceptor stimulation, we measured 42K+ content in myocardial biopsies taken at intervals after an intra-atrial infusion of 42K+ before and during an i.v. isoprenaline infusion (20 micrograms min-1) in six anaesthetized, open-chest pigs. Determination of the total K+ influx during beta-adrenoceptor stimulation was initiated 10 min after the start of isoprenaline infusion, when the transient net myocardial K+ uptake had subsided. Total K+ influx increased from a control value of 414 +/- 42 to 1086 +/- 246 mumol 100 g-1 min-1 during isoprenaline infusion. A quantitatively smaller increase in K+ influx carried by the Na(+)-K+ pump has previously been demonstrated during isoprenaline infusion. Left ventricular dP/dt rose from 1350 +/- 146 to 4833 +/- 150 mmHg s-1, stroke volume remained unchanged, but heart rate and peak left ventricular systolic pressure rose as expected, by 52 +/- 4 and 32 +/- 4% respectively during isoprenaline stimulation. All haemodynamic parameters, total plasma K+ concentration and plasma 42K+ activity remained stable throughout each experimental period. The number of ouabain binding sites was 65.5 +/- 1.0 before and 66.9 +/- 1.6 nmol 100 g-1 during isoprenaline infusion (difference n.s.). The present data indicate that not only the K+ influx carried by the ouabain-sensitive Na(+)-K+ pump but also the influx through ouabain-insensitive pathways is increased during beta-adrenoceptor stimulation of the in-situ beating pig heart.

Animals↗

PubMed1990

Effects of increased splenic arterial flow and venous pressure on splenic red cell accumulation.

The importance of increments in splenic venous pressure (SVP) and splenic arterial flow (SAF) for splenic red cell accumulation was estimated in 14 anesthetized dogs with the spleen in situ by arterial and splenic venous hematocrit measurements and continuous ultrasonic recording of splenic diameter (SD). A 10-mmHg increase in SVP by 4 min of splenic venous constriction reduced SAF by 32 +/- 5%, increased SD by 5.1 +/- 0.8%, and transiently reduced splenic venous hematocrit, measured every 10 s, from 35.4 +/- 1.4 to a minimum of 29.2 +/- 1.8%. A 10-mmHg rise in SVP by 4 min of saline infusion increased SAF by 178 +/- 25% and SD by 16.1 +/- 3.0%, and splenic venous hematocrit declined more rapidly and to a lower value than arterial hematocrit. Blood volume expansion with saline or blood at constant, 10-mmHg elevated SVP confirmed that splenic red cell accumulation was greater during blood volume expansion than during splenic venous constriction. We conclude that the spleen accumulates red cells when SVP is raised. At constant, elevated SVP splenic red cell accumulation is flow dependent.

Animals↗

PubMed1990

Influence of atrial natriuretic factor on intravascular volume displacement in pigs.

The present study was undertaken to quantitate the influences of transcapillary fluid loss, urine output, and the capacity vessels on volume displacement toward and away from the right heart during atrial natriuretic factor (ANF) administration. In eight anesthetized pigs undergoing carotid denervation, cervical vagotomy, and splenectomy, blood was drained from the venae cavae to an extracorporeal reservoir and returned to the right atrium at a constant rate so that volume displacement toward and away from the heart could be recorded as change in reservoir volume. Human ANF-(99-126) (0.1 micrograms.kg-1.min-1) for 15 min was associated with a decrease in reservoir volume of 2.7 +/- 0.4 ml/kg (P less than 0.05), which resulted from a decrease in total blood volume of 8.6 +/- 1.0 ml/kg (P less than 0.05) and a displacement from the capacitance vasculature of 5.9 +/- 1.3 ml/kg (P less than 0.05). Since urine output increased only slightly, virtually all of the total blood volume decrement was due to a displacement of fluid into the extravascular space. Thus ANF acts to displace volume away from the right heart. The displacement is due almost entirely to an increase in transcapillary fluid loss; however, volume displacement from the capacity vessels to the right heart partially counteracts this transcapillary influence.

Animals↗