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Biomedical subjects

J Thorvaldson

Publications and source records attributed to J Thorvaldson.

10 recordsLinked to original sources
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

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↗
PubMed1989

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.

Adrenergic alpha-Agonists↗
PubMed1988

Cardiac function in open-chest dogs after left to right ventricular shunting and right coronary artery occlusion.

Patients with acquired ventricular septal defect (VSD) after myocardial infarction have a particularly bad prognosis if right ventricular function is severely impaired. The significance of an ischaemic right ventricular free wall on cardiac function during interventricular shunting was examined in open-chest dogs. An external interventricular shunt could be opened and closed at will, and by occlusion of the right coronary artery (RCA), a part of the right ventricular free wall was rendered ischaemic. Aortic flow decreased by 8 +/- 2% when the shunt was opened in the presence of a normal right ventricle, and by 16 +/- 2% (difference: P less than 0.05) in the presence of right ventricular ischaemia. Aortic flow fell by 19 +/- 3% when the RCA was occluded. Right ventricular dyskinesia was demonstrated after occlusion of RCA, by recording segment lengths in the right ventricular free wall. The dyskinesia was aggravated when the shunt was opened. The left ventricle exerted a 'negative' work on the ischaemic right ventricular free wall. Retention of blood in the right ventricle, with a subsequent decline in left ventricular filling and an almost unchanged interventricular shunting of blood, explain why aortic flow fell more when the shunt was opened in the presence of right ventricular ischaemia.

Animals↗
PubMed1987

Rhabdomyoma of the heart with intrapericardial expansion.

A rare case of a rhabdomyoma originating from the surface of the right atrium in a 20-year-old female is reported. The tumor showed electrical activity and caused both outflow obstruction and tamponade symptoms. It was successfully removed by a right-sided thoracotomy. The clinical course, diagnostic investigations, and the therapeutical approach of this rare lesion are discussed.

Adult↗
PubMed1986

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.

Adrenergic beta-Agonists↗
PubMed1979

Cardiac performance: optimal heart rate for maximal cardiac output.

To determine optimal heart rate for the maximal cardiac output at various levels of inotropy and blood volume, the relationship between heart rate (HR) and stroke volume (SV) was examined in anaesthetized dogs during right atrial pacing. Myocardial inotropy was raised by intravenous infusion of isoproterenol, a stimulator of adrenergic beta-receptors, and reduced by propranolol, an inhibitor of adrenergic beta-receptors. Circulating blood volume was increased by saline infusion. Within the range of optimal heart rate, SV and HR were inversely related: SV = k (HR0-HR), where k indicates the relationship between changes in SV and HR. The intercept with the HR axis is HR0. At constant HR a rise in inotropy increased SV and a fall in inotropy reduced SV. These changes in SV were eual at every HR, and k was therefore constant. In contrast, blood volume expansion increased SV more at low than at high HR (k increased), but HR0 was not significantly changed. Calculated maximal cardiac output: k.HR02/4, and optimal heart/rate: HR0/2, agreed with observations when maximal cardiac output was raised from 1900 to 4500 ml/min by increasing blood volume and inotropy. Optimal HR was not influenced by changes in blood volume, but was increased from 160 to 200 beats/min by increasing inotropy. We conclude that the optimal heart rate and the maximal cardiac output can be predicted from the linear relationship between SV and HR during right atrial pacing.

Adrenergic beta-Agonists↗
PubMed1979

Myocardial ischemia. Relationship between local flow, function and ST-segment elevation.

The significance of reductions in local myocardial flow on mechanical function and intramural electrocardiograms (ECG) was studied in anesthetized open-chest dogs. Local dimensional changes in the anterior wall of the left ventricle were recorded by ultrasonic technique. By platinum electrodes in the same region, both intramural ECG and hydrogen tension were recorded. Local flow was calculated from hydrogen desaturation curves. At approx. 25% flow reduction (constriction of the left anterior descending coronary artery (LAD)) local enddiastolic dilation and reduced systolic shortening appeared. Significant ST-segment elevation first appeared with flow reduction of 50%. After complete LAD-occlusions, enddiastolic dilation appeared within 20 sec, ST-segment elevation 40 sec later. It is concluded that mechanical and electrical events can be dissociated during acute myocardial ischemia: enddiastolic dilation and reduced systolic shortening are more sensitive indicators of moderate reductions in myocardial tissue flow than ST-segment elevation.

Animals↗
PubMed1976

Left ventricular function during acute elevation of aortic blood pressure in dogs.

Cardiac responses to mechanical constriction of the aorta proximal and distal to the arch arteries and to intravenous infusion of angiotensin were examined in open-chest atropinized dogs during continuous recording of left ventricular and aortic dimensions by means of ultrasonic elements. Proximal constriction reduced stroke volume by 18% both before and during isoproterenol infusion without changing left ventricular end-diastolic pressure, dimensions, or contractility, (dP/dt)IP; angiotensin induced less pronounced increments in stroke volume and end-diastolic volume. By combining proximal constriction with saline-dextran infusion, stroke volume and end-diastolic volume increased as during distal constriction. These results indicate that differences in preload account for the differences in stroke volume responses to proximal and distal aortic constriction. We propose that increased preload is caused by redistribution of blood from capacitance vessels rather than retention secondary to cardiac decompensation.

Angiotensin II↗