Contributions of blood drainage from the liver,spleen and intestines to cardiac effects of aortic occlusion in the dog

By occluding the descending thoracic aorta, blood transferred from the lower to the upper part of the body increases left ventricular end-diastolic volume and maintains stroke volume despite a rise in systolic left ventricular pressure (LVP) of about 60 mmHg. Seventy percent of the blood drained stems from the splanchnic circulation. To examine which splanchnic organs contribute to the cardiac effects, selective occlusions were performed during ultrasonic measurements of spleen and liver dimensions and left ventricular myocardial chord length (MCL) in atropinized, open-chest dogs. Drainage of 15±2 ml from the spleen accounted for 18±4% of the increase in end-diastolic MCL, whereas liver dimensions remained unaltered. Similar results were obtained during aortic occlusion at high inotropy (isoproterenol infusion). it was ascertained by occlusion of the coeliac and mesenteric arteries that about 50% of the cardiac response to aortic occlusion was due to drainage from the intestines and the aorta. Liver blood volume could be reduced by combined occlusion of the aorta and portal vein or coeliac and mesentenc arteries and was sensitive to changes in pressure in the inferior vena cava, but did not contribute to the cardiac response to aortic occlusion.     

Cardiac effects of splanchnic and non-splanchnic blood volume redistribution during aortic occlusions in dogs

Translocation of blood from the lower body dilates the left ventricle during occlusion of the descending thoracic aorta and by increased activation of the Frank-Starling mechanism, stroke volume is maintained despite raised aortic blood pressure. The contributions from the splanchnic and non-splanchnic blood volumes to the left ventricular dilation were examined by ultrasonic measurements of myocardial chord length (MCL) in atropinized open-chest dogs. End-diastolic MCL rose by 2.5±0.9% during abdominal suprarenal aortic occlusion, draining blood from the non-splanchnic region, and by 7.4±1.7% during thoracic aortic occlusion draining blood from both splanchnic and non-splanchnic regions. Systolic left ventricular pressure rose by 16±3 mmHg and 76±12 mmHg, respectively. End-diastolic MCL rose by 6.0±1.2% during combined thoracic aortic and abdominal infrahepatic vena cava occlusion draining blood solely from the splanchnic region and further by 2.5±0.8% by blood drained from the non-splanchnic region after release of the vena cava occlusion. Similar results were obtained using a shunt permitting selective drainage first from the non-splanchnic region during thoracic aortic occlusion. Blood translocation from the non-splanchnic region maintains cardiac output during abdominal aortic occlusion. During occlusion of the thoracic aorta, drainage from the splanchnic region accounts for about 70% of the increase in end-diastolic MCL.     

Factors contributing to blood pressure elevation during norepinephrine and phenylephrine infusions in dogs

To examine the factors contributing to the rise in systemic blood pressure during α- and β- adrenergic stimulation, phenylephrine, an α-adrenergic agonist, and norepinephrine, an α- and β-adrenergic agonist, were infused intravenously to anesthetized dogs until mean aortic blood pressure was raised equally by 40–60 mmHg. Changes in preload were estimated by changes in left ventricular end-diastolic pressure or segment length recorded by an ultrasonic technique. By obstructing the inferior vena cava (IVC), the increase in preload could be reduced to control level during phenylephrine and norepinephrine infusions without altering peripheral resistance (mean aortic blood pressure/cardiac output). Normalization of preload reduced the pressure response by 2/3 during phenylephrine infusion and by 1/4 during norepinephrine infusion. However, after β-adrenergic blockade by propranolol, normalization of preload reduced the pressure response by 2/3 during both phenylephrine and norepinephrine infusions. Thus, during α-adrenergic stimulation, the increase in preload is a more important factor than the increase in peripheral resistance. Norepinephrine raised stroke volume by 24±5%. When the increase in stroke volume was prevented by IVC obstruction, the pressure response to norepinephrine was halved. Thus, during norepinephrine infusion the rise in stroke volume caused by β-adrenergic stimulation is as important as α-adrenergic stimulation for the pressure response.     

Angiotensin II infusion during β-adrenergic stimulation by isoproterenol. Effects on hepatic,splenic and cardiac blood volumes and on the magnitude and distribution of cardiac output in the dog

The cardiac and peripheral vascular adjustments to angiotensin II (0.1–0.2 μg kg^-1 min^-1 i.v.) during high β-adrenergic activity by a continuous isoproterenol infusion (0.2–0.3 μg kg^-1 min^-1 i.v.) were examined in anaesthetized, atropinized dogs. Hepatic, splenic and left ventricular (LV) volume changes were estimated by an ultrasonic-technique, and the blood flow distribution was measured by injecting radioactive microspheres and by electromagnetic flowmetry on the caval veins, the hepatic artery and the portal vein. During isoproterenol infusion, angiotensin II increased the systolic LV pressure by 45 ± 3 mmHg and the stroke volume by 17 ± 6 %. Concomitantly, the hepatic and splenic blood volumes declined by 29 ± 4 and 14 ± 6 ml, respectively, and the LV end-diastolic segment length increased by 3 ± 1 %. The flow through the inferior caval vein increased by 39 ± 9%, whereas the superior vena caval flow remained unchanged. The hepatic arterial flow more than doubled. Thus, at high inotropy by isoproterenol infusion, angiotensin II relocates blood from the liver and the spleen towards the heart. By activating the Frank-Starling mechanism, cardiac output is increased and conducted through the lower body, especially through the hepatic artery, because of the poor autoregulation of flow through this vessel.,     

Cardiopulmonary blood volume during acute blood pressure elevations in dogs

During aortic blood flow obstructions and angiotensin infusion blood may be accumulated in the heart and the lungs because of retention or redistribution of blood from compliant regions. We measured the cardiopulmonary blood volume (CPBV) when left ventricular systolic pressure was raised by about 50 mmHg by angiotensin infusion and by balloon inflation in the ascending and descending thoracic aorta, at control inotropy and during isoproterenol infusion, in 6 anesthetized, closed-chest dogs. CPBV was calculated from determinations of cardiac output (thermodilution) and the interventricular mean transit time of ascorbate (polarographic determination). Angiotensin always increased CPBV, but the rise was greater at high than at control inotropy (16.5 +/- 4.4% and 5.1 +/- 1.2%). Balloon inflation in the descending thoracic aorta increased CPBV similarly at high and control inotropy (11.1 +/- 2.4% and 16.6 +/- 4.0%) whereas CPBV was unaltered or fell during inflation in the ascending aorta at both inotropic levels. Right and left ventricular end-diastolic pressures rose only during angiotensin infusion and balloon inflation in the descending thoracic aorta. By balloon inflation, cardiac output only fell during blood flow obstruction in the ascending aorta. Thus, an increase in CPBV during these interventions is not due to retention but is caused by redistribution of blood towards the heart.     

Cardiac performance: independence of adrenergic inotropic and chronotropic effects

During right atrial pacing in open-chest anesthetized dogs, the relationships between reduction in stroke volume and rise in heart rate were identical in control experiments, during intravenous infusion of isoproterenol, and after blockade of adrenergic beta-receptors by propranolol. To examine the mechanism of this constant relationship, left ventricular volume was estimated by continuous recordings of myocardial chord length (MCL) between ultrasonic elements inserted into the anterior ventricular wall. Diastolic filling curves were curtailed by raising heart rate and end-diastolic MCL was reduced. At constant heart rate, end-diastolic MCL was not altered by isoproterenol infusion, except for a slight rise at heart rates exceeding 220 beats/min. End-systolic MCL, however, was reduced, accounting for larger stroke volume during isoproterenol than during propranolol infusion. The reduction in end-systolic MCL was constant at all heart rates examined. Hence, chronotropic changes influence end-diastolic volume and inotropic changes influence end-systolic volume; their effects on stroke volume regulation are, therefore, virtually independent.     

Mechanisms of left ventricular filling during increased preload and inotropy

To examine the factors contributing to left ventricular filling, experiments were performed in anesthetized, open-chest dogs with intact or mechanically constricted mitral ostium. Stroke volume was raised either by increasing left ventricular end-diastolic volume (preload) by blood volume expansion or by infusing isoproterenol, a beta-adrenergic agonist. In all experimental settings, stroke volume rose in proportion (r greater than 0.9) to the pressure time product (PTP = integral of the diastolic atrio-ventricular (A-V) pressure difference). During saline infusion atrial distention and contraction increased atrial pressure more than ventricular pressure whereas diastolic filling time (DFT) was not lengthened. Peak mitral and peak aortic flow rose almost equally. During isoproterenol infusion at constant heart rate (atrial pacing), the increase in PTP was mainly caused by a longer DFT. When heart rate was allowed to rise, DFT was reduced and the A-V pressure difference increased because of a greater reduction in ventricular than in atrial pressure in early diastole. Thus, the A-V pressure difference is generated in different ways by raising preload and inotropy with and without changes in heart rate.     

Cardiac performance: independent effects of inotropy and preload at high heart rate.

Linear relationships between stroke volume (SV) and heart rate (HR) were observed during right atrial pacing in open-chest dogs at control inotropy, during intravenous isoproterenol infusion and during blood volume expansion by saline infusion at HR exceeding 150 beats/min. The slope of these relationships remained constant during variations in inotropy, but rose during blood volume expansion. Myocardial chord lengths in the anterior left ventricular wall were continuously recored by ultrasonic technique to estimate left ventricular volume. When heart rate was increased, end-diastolic volume decreased more rapidly after than before blood volume expansion, explaining the increased slope of the SV/HR relationship. The end-diastolic volume and the SV/HR relationship were not influenced by changes in inotropy. After blood volume expansion by 57 +/- 13%, control end-diastolic volume was reestablished by increasing heart rate 84 +/- 20 beats/min. At identical end-diastolic volume, SV was equal at different HR. Thus, the effects on SV of changes in preload and inotropy are separable during right atrial pacing, and SV is independent of HR at constant preload and adrenergic stimulation.     

Modification of regional myocardial performance caused by blood withdrawal and infusion in acute ischaemic canine heart

The effect of changes in preload on regional myocardial motion in acute ischaemia was examined by miniature ultrasonic gauges after left anterior descending coronary artery occlusion in eight open chest dogs with the pericardium preserved. Left ventricular end-diastolic pressure was varied by blood withdrawal and infusion. When preload changed, isovolumetric shortening in the non-ischaemic region was inversely related to that in the ischaemic region. When preload decreased, stroke volume decreased and was accompanied by a decrease in end-diastolic length and ejection shortening in the non-ischaemic region together with an increase in isovolumetric bulging in the ischaemic region. When preload increased, these variables changed in opposite directions. These results indicate that in acute ischaemia: (1) changes in isovolumetric shortening in the non-ischaemic and ischaemic regions were related with each other when the level of volume expansion varied, and suggest that; (2) stroke volume is affected by end-diastolic length, ejection shortening in the non-ischaemic region and isovolumetric bulging in the ischemic region.     

Angiotensin causes vasoconstriction during hemorrhage in baroreceptor-denervated dogs

The participation of angiotensin II (ANG II) in the maintenance of arterial blood pressure during hypotensive hemorrhage was examined in unanesthetized, baroreceptor-denervated dogs. When mean aortic blood pressure was reduced to 69.0 +/- 2.2 mmHg, plasma renin activity increased from 0.6 +/- 0.3 ng ANG I X ml-1 X h-1 during the prehemorrhage control period to 4.5 +/- 1.6. Twenty minutes after the hemorrhage, mean aortic blood pressure rose to 78.9 +/- 3.1 mmHg. Subsequent infusion of the angiotensin II antagonist saralasin (5.2-14.0 micrograms X kg-1 X min-1) decreased mean aortic pressure to 59.6 +/- 3.3 mmHg. When 5% dextrose was infused in place of saralasin, mean aortic pressure was 79.3 +/- 4.3 mmHg. The lower aortic blood pressure caused by saralasin infusion was the result of a significant decrease in total peripheral resistance. Resistance was 10.3 +/- 3.2 mmHg X l-1 X min lower during saralasin infusion than during dextrose infusion. We conclude that baroreceptor reflexes are not essential for the elevation of plasma renin activity during hemorrhage. In baroreceptor-denervated dogs subjected to hypotensive hemorrhage, the increased formation of ANG II has a vasoconstrictor action that contributes to the maintenance of arterial blood pressure.     

Effect of increased α-adrenergic activity on the blood pressure/cardiac output relationship in dogs

The relationship between mean aortic blood pressure (MAP) and cardiac output (CO) was examined in anaesthetized, open-chest dogs during variations in pre-load with and without α-adrenergic stimulation with phenylephrine. When phenylephrine increased MAP to 200 mmHg, CO fell greatly and could not be increased by volume expansion. Left ventricular ultrasonic measurements and pressure recordings showed that the Frank-Starling mechanism was maximally activated. During vena cava obstruction CO and MAP fell proportionally. At a lower infusion rate of phenylephrine, MAP increased to 160 mmHg without a great reduction of CO. As in control experiments without phenylephrine infusion, CO could be increased by dextran/saline infusion and lowered about 20% below control by vena cava obstruction with no significant change in MAP; by further caval obstruction CO and MAP fell in proportion. Phenylephrine did not alter the relationship between aortic baroreceptor activity and MAP. The same MAP/CO relationships were obtained before and after bilateral vagotomy and nephrectomy. Caval obstruction and pacing tachycardia resulted in similar MAP/CO relationships despite different effects on left ventricular end-diastolic pressure. Thus, phenylephrine infusion may raise MAP to 200 mmHg but no cardiac reserve is left. During reduction of CO by caval obstruction, peripheral vascular resistance remains constant despite varying baroreceptor activity. At the lower infusion rate of phenylephrine, raising MAP to 160 mmHg, peripheral vascular resistance is constant at low CO, but at high CO the vasoconstrictive effect of phenylephrine is counteracted by a vasodilatory mechanism which seems to be flow-dependent.     

Effect of increased alpha-adrenergic activity on the blood pressure/cardiac output relationship in dogs

The relationship between mean aortic blood pressure (MAP) and cardiac output (CO) was examined in anaesthesized, open-chest dogs during variations in pre-load with and without alpha-adrenergic stimulation with phenylephrine. When phenylephrine increased MAP to 200 mmHg, CO fell greatly and could not be increased by volume expansion. Left ventricular ultrasonic measurements and pressure recordings showed that the Frank-Starling mechanism was maximally activated. During vena cava obstruction CO and MAP fell proportionally. At a lower infusion rate of phenylephrine, MAP increased to 160 mmHg without a great reduction of CO. As in control experiments without phenylephrine infusion, CO could be increased by dextran/saline infusion and lowered about 20% below control by vena cava obstruction with no significant change in MAP; by further caval obstruction CO and MAP fell in proportion. Phenylephrine did not alter the relationship between aortic baroreceptor activity and MAP. The same MAP/CO relationships were obtained before and after bilateral vagotomy and nephrectomy. Caval obstruction and pacing tachycardia resulted in similar MAP/CO relationships despite different effects on left ventricular end-diastolic pressure. Thus, phenylephrine infusion may raise MAP to 200 mmHg but no cardiac reserve is left. During reduction of CO by caval obstruction, peripheral vascular resistance remains constant despite varying baroreceptor activity. At the lower infusion rate of phenylephrine, raising MAP to 160 mmHg, peripheral vascular resistance is constant at low CO, but at high CO the vasoconstrictive effect of phenylephrine is counteracted by a vasodilatory mechanism which seems to be flow-dependent.     

Angiotensin II infusion during beta-adrenergic stimulation by isoproterenol. Effects on hepatic, splenic and cardiac blood volumes and on the magnitude and distribution of cardiac output in the dog

The cardiac and peripheral vascular adjustments to angiotensin II (0.1-0.2 microgram kg-1 min-1 i.v.) during high beta-adrenergic activity by a continuous isoproterenol infusion (0.2-0.3 microgram kg-1 min-1 i.v.) were examined in anaesthetized, atropinized dogs. Hepatic, splenic and left ventricular (LV) volume changes were estimated by an ultrasonic technique, and the blood flow distribution was measured by injecting radioactive microspheres and by electromagnetic flowmetry on the caval veins, the hepatic artery and the portal vein. During isoproterenol infusion, angiotensin II increased the systolic LV pressure by 45 +/- 3 mmHg and the stroke volume by 17 +/- 6%. Concomitantly, the hepatic and splenic blood volumes declined by 29 +/- 4 and 14 +/- 6 ml, respectively, and the LV end-diastolic segment length increased by 3 +/- 1%. The flow through the inferior caval vein increased by 39 +/- 9%, whereas the superior vena caval flow remained unchanged. The hepatic arterial flow more than doubled. Thus, at high inotropy by isoproterenol infusion, angiotensin II relocates blood from the liver and the spleen towards the heart. By activating the Frank-Starling mechanism, cardiac output is increased and conducted through the lower body, especially through the hepatic artery, because of the poor autoregulation of flow through this vessel.     

Cardiac end-diastolic dilation during acute blood pressure elevation is inotropy dependent

To examine if the degree of left ventricular (LV) end-diastolic dilation during an acute blood pressure elevation is inotropy dependent, the descending thoracic aorta was occluded before and during a continuous isoproterenol infusion into the left coronary artery in 10 open-chest pigs. The increase in peak LV systolic pressure and in LV tension-time-index induced by aortic occlusion, were equal before and during the isoproterenol infusion. Left and right ventricular (RV) segment lengths were continuously recorded in the free walls of both ventricles, by an ultrasonic technique. A slight fall in LV end-diastolic segment length by the intracoronary isoproterenol infusion was corrected by an i.v. saline infusion. Left ventricular end-diastolic volume was therefore equal at both levels of inotropy when the aorta was occluded, and the heart rate was kept constant by right atrial pacing. At control inotropy, aortic occlusion induced a rise in LV end-diastolic segment length; 6.0 (4.0-8.2)% (median and 95% confidence interval), compared with the smaller (P less than 0.05) increase of 3.8 (2.6-5.5)% during isoproterenol infusion. The end-systolic segment length increased more (P less than 0.01) at control inotropy than during intracoronary isoproterenol infusion: 10.9 (6.9-14.4)% and 4.1 (1.5-7.4)%, respectively. In the RV, both end-diastolic and end-systolic segment length increased slightly during aortic occlusion but only at control inotropy. Thus during an acute blood pressure elevation, the end-diastolic and end-systolic ventricular volumes are better maintained at high than at control inotropy.     

The responses of left ventricular end-systolic pressure-diameter relationship to acute pressure overload induced by aortic constriction

The aim was to investigate the responses of the left ventricular (LV) end-systolic pressure-diameter relationship (ESPDR) to acute pressure overload. ESPDRs were made by 2-min ascending and descending aortic constrictions before and after administration of propranolol and atropine sulphate (both 0.2 mg kg^-1 i.v.) in eight open-chest dogs with the pericardium preserved. LV anterior-posterior diameter was measured with ultrasonic crystals. In the ascending aortic constriction, end-diastolic pressure (EDP) and end-diastolic diameter (EDD) were unchanged and ESPDR shifted to the left. In the descending aortic constriction, EDP and EDD increased from 6.8±0.7 to 8.8±0.9mmHg (P < 0.01) and from 32.7±1.4 to 34.5+1.6 mm (P < 0.05) and ESPDR shifted to the right. After administration of propranolol and atropine sulphate, cases having smaller changes in EDD during 2 min constriction (0.3+0.3 mm in all cases of ascending, 0.3 + 0.2 mm in four cases of descending aorta) showed a leftward shift of ESPDR. The remaining four cases of descending aortic constriction with larger changes in EDD (1.8 + 0.8 mm, P < 0.05) showed a rightward shift of ESPDR. An inverse curvilinear correlation was found between percentage changes in EDD and in the slopes. These results suggest that the responses in ESPDR to acute pressure overload were determined by not only changes in the contractile state but also the interplay between adaptation to acute pressure overload (the Anrep effect) and preload.     

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 μg 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< 0.005), portal vein pressure decreased by 1.0 ± 0.3 mmHg (P< 0.01), IVC pressure increased by 0.2 ± 0.1 mmHg (P< 0.01), hepatic arterial flow increased by 10 ± 6 ml min^-1 (NS), portal vein flow decreased by 89 ± 20 ml min^-1 (P< 0.005), splenic segment length (SSL) decreased by 0.52 ± 0.11 mm (P< 0.005) (control 12.49 ± 1.27) (measured with ultrasonic crystals) and hepatic segment length (HSL) increased by 0.29 ± 0.06 mm (P< 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< 005). 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.     

Extent of utilization of the Frank-Starling mechanism in conscious dogs

The extent to which an increase in preload increases left ventricular (LV) end-diastolic (ED) diameter (D) was studied in seven conscious dogs instrumented with ultrasonic D transducers and miniature LV pressure (P) gauges. Preload was elevated by three techniques: 1) volume loading with saline infusion, 2) induction of global myocardial ischemia by constricting the left main coronary artery, and 3) infusion of methoxamine. These three interventions increased LVEDP to over 30 mmHg from a control of 10 +/- 1 mmHg. With volume loading, LVEDD rose by only 1.55 +/- 0.39 mm from a control of 44.08 +/- 1.08 mm; with ischemia LVEDD rose by only .96 +/- .29 mm from a control of 42.55 +/- 2.18 mm, while with methoxamine LVEDD rose by only 1.34 +/- 0.38 mm from a control of 43.89 +/- 2.07 mm. In contrast, in the open-chest, anesthetized dog, LVEDD was greatly reduced and volume expansion resulted in a profound increase in LVEDD. Thus, the Frank-Starling mechanism is not an important controlling mechanism in the normal, reclining, conscious animal, since LVEDD appears to be near maximal at rest and does not increase substantially despite striking increases in LVEDP.     

Influence of α-adrenergic receptor stimulation on splanchnic intravascular volume in conscious humans

The influence of selective α-adrenergic receptor stimulation on total splanchnic intravascular volume and blood volume in individual splanchnic organs in humans has not been previously examined. The present study employed a previously validated quantitative radionuclide imaging technique, involving a gamma camera and Tc-99m labeled erythrocytes, to measure changes in total splanchnic, hepatic, splenic, and extrahepatosplenic volume during a 20-minute phenylephrine infusion (30–120 μ min^-1 iv). Changes in total splanchnic volume were estimated from changes in total splanchnic radioactivity, blood radioactivity, and estimated in vivo tissue attenuation. Radionuclide-estimated total splanchnic volume increased 477±96 ml (P < 0.0003) at the end of phenylephrine infusion. Hepatic volume increased 25±5% (P < 0.0003), splenic volume decreased 46±7% (P < 0.0003), and extrahepatosplenic volume decreased 15±2% (P < 0.0003). Systolic and diastolic arterial pressures increased from 119±4 to 138 ± 5 mmHg (P < 0.0003) and from 83+1 to 96 ± 2 mmHg (P < 0.0003), respectively. Heart rate decreased from 62±2 to 51±3 bpm (P < 0.0003). Thus, in man, selective α-adrenergic receptor stimulation is associated with an increase in splanchnic intravascular volume that is due to an increase in hepatic volume and occurs despite decreases in splenic and extrahepatosplenic volumes. This increase in total splanchnic volume would be associated with a decrease in venous return from the splanchnic vasculature to the right heart which would act to decrease cardiac output.     

Arterial pressure-flow relations in the awake standing dog.

The transient circulatory changes following paced heart rate increase are reported from 133 trials with 6 unanesthetized dogs with chronically implanted monitoring devices for heart rate, cardiac output, aortic blood pressure, and mean right atrial pressure. In 62 trials with 2 of the dogs, pulmonary artery, and left ventricular end-diastolic pressure, as well as left ventricular dP/dt were also studied. The sequence of changes in pressures and flows is analyzed in terms of probable underlying mechanisms, particularly with respect to the nature of vascular resistances. The rise in aortic pressure and flow during the first 3 s of paced heart rate increase, before arterial stretch receptor reflexes become active, is more consistent with an effective downstream pressure of about 49 mmHg, presumably at the arteriolar level, than with an effective downstream pressure close to 0 mmHg at the right atrial level. In the pulmonary circulation where vascular reflex effects are less prominent, the pattern of pulmonary arterial pressure and flow for the entire 30 s of observation is consistent with an effective downstream pressure of 9 mmHg, presumably at the alveolar or pulmonary arteriolar level, rather than at the level of the left ventricular end-diastolic pressure.     

Dynamics of the interventricular septum and free ventricular walls during selective left ventricular volume loading in dogs

A previous study suggested that a change in the position of the interventricular septum played an important role in regulating cardiac performance during selective right ventricular volume loading. In the present study the cardiac response to selective left ventricular volume loading induced by a shunt between the subclavian artery and the left atrium was examined in anesthetized open-chest dogs. Opening the shunt increased left and reduced right ventricular stroke volume, particularly after blood volume expansion. The end-diastolic transseptal pressure difference increased. Myocardial segment length in the septum and free walls of both ventricles and the distances between the septum and the free walls were measured by an ultrasonic technique. Comparisons at similar left ventricular stroke volume with the shunt open and closed showed that the Frank-Starling mechanisms of the free wall of the left ventricle and the septum were stimulated less with the shunt open. At similar right ventricular stroke volume the end-diastolic dimension of the right ventricular free wall was larger with the shunt open. The distance decreased across the right ventricle and increased across the left ventricle when the shunt was open. We conclude that a change in the position of the septum improves left and reduces right ventricular performance during selective left ventricular volume loading.