Biomedical subjects

J Thorvaldson

Publications and source records attributed to J Thorvaldson.

At least 19 recordsLinked to original sources

PubMed1994

[Percutaneous transluminal angioplasty in the treatment of arteriosclerosis of the lower extremities].

With the introduction of balloon catheters in 1974, dilatation of arteriosclerotic stenoses has become an important treatment for this condition. During the years 1979-88, 368 such procedures were performed in 270 patients. Two patients (0.7%) died from complications. In 8%, revascularisation was unsuccessful. Long occlusions appeared especially difficult to recanalize. 81% of the patients were improved by the treatment. The long term results were best in the iliac segment with 5-year patency of 90% after dilatation of short stenoses (< 4 cm) and 65% after dilatation of longer stenoses. In the femoropopliteal segment, the 5-year patency rates were 65% and 50% respectively. Results after recanalisation of occlusions were poor. Percutaneous transluminal angioplasty is an important supplement to surgery, applying mainly to patients with limited arteriosclerosis and moderate symptoms.

Adult↗

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↗

PubMed1985

Determinants of pulmonary blood volume. Effects of acute changes in airway pressure.

To examine the effects of airway pressure (AWP) on pulmonary blood volume (PBV) at various pulmonary vascular pressures and flows, experiments were performed in anaesthetized, open-chest dogs. The AWP was raised by elevating end-expiratory pressure, and PBV was calculated as the product of electromagnetic aortic flow and pulmonary mean transit time for ascorbate (polarographic method). When AWP was raised from 3 to 13 mmHg, changing lung conditions from zone 3 [left atrial pressure (LAP) higher than AWP] to zone 2 (AWP higher than LAP), PBV decreased by 14.5 +/- 6.2%. When LAP was raised above 7 mmHg at constant pulmonary arterial pressure (PAP), PBV increased under zone 2 but not under zone 3 conditions. During blood volume expansion to LAP 15 mmHg, PBV rose by 30-50% and became equal at AWP of 4 and 14 mmHg, whereas the pulmonary vascular resistance remained 40% higher at high AWP. These data suggest that PAP, LAP and AWP regulate PBV by acting on compliant vessels surrounding the alveoli. Under zone 2 conditions with collapsed aveolar capillaries, elevation of LAP results in re-expansion of the alveolar capillaries, and PBV is restored without a rise in PAP. Under zone 3 conditions, a rise in LAP cannot increase PBV without raising PAP, explaining why PBV remains constant when PAP is kept constant.

Airway Resistance↗

PubMed1984

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.

Angioplasty, Balloon↗

PubMed1984

Determinants of pulmonary blood volume. Effects of acute changes in pulmonary vascular pressures and flow.

To examine the effects of pulmonary vascular pressures and flow on pulmonary blood volume (PBV), experiments were performed at constant heart rate and zone 3 conditions (mean left atrial pressure (LAP) above airway pressure) in six anesthetized, open-chest dogs. PBV was calculated as the product of electromagnetic aortic flow and pulmonary mean transit time for ascorbate, obtained without blood withdrawal by polarographic recording of aortic ascorbate changes. In three series of experiments LAP was raised similarly in three steps, from 4.5 to 14.8 mmHg: by mitral constriction which reduced pulmonary blood flow, by blood volume expansion which more than doubled pulmonary blood flow, or by a combination of the two procedures which kept pulmonary blood flow constant. In all three series, LAP and mean pulmonary arterial pressure (PAP) rose in proportion, but PBV was better correlated to PAP (r = 0.87 +/- 0.02) than to LAP (r = 0.66 +/- 0.09). These experiments suggest that PAP is the most important factor in determining PBV under zone 3 conditions, whether PAP is raised by increasing pulmonary blood flow or by mitral constriction.

Animals↗

PubMed1983

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 alpha- and beta-adrenergic stimulation, phenylephrine, an alpha-adrenergic agonist, and norepinephrine, an alpha- and beta-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 beta-adrenergic blockade by propranolol, normalization of preload reduced the pressure response by 2/3 during both phenylephrine and norepinephrine infusions. Thus, during alpha-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 beta-adrenergic stimulation is as important as alpha-adrenergic stimulation for the pressure response.

Adrenergic alpha-Agonists↗

PubMed1983

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.

Adrenergic beta-Agonists↗

PubMed1982

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 mesenteric arteries and was sensitive to changes in pressure in the inferior vena cava, did not contribute to the cardiac response to aortic occlusion.

Animals↗

PubMed1982

Mechanism of blood pressure elevation during angiotensin infusion.

The mechanism of increased preload and its contribution to the rise in blood pressure during intravenous angiotensin infusion were studied in anesthetized dogs. In open-chest dogs angiotensin increased mean aortic blood pressure by 58 +/- 12 mmHg. Left ventricular end-diastolic dimension, measured as myocardial chord length (MCL) by ultrasonic technique, increased by 7 +/- 1%. By inflating a balloon in the inferior vena cava, end-diastolic MCL was reduced to control value and the rise in mean aortic blood pressure was almost halved to 32 +/- 10 mmHg above control value. A similar preload effect was recorded in closed-chest dogs using end-diastolic left ventricular pressure as an estimate of left ventricular volume. During angiotensin infusion to the upper body only, end-diastolic MCL did not increase. When redistribution of the splanchnic blood volume was prevented, the effect of angiotensin on end-diastolic MCL was reduced to 1/3. Angiotensin reduced liver but not splenic dimension measured by ultrasonic technique. We conclude that about half of the rise in blood pressure during angiotensin infusion is due to increased end-diastolic volume caused by blood redistribution. About 2/3 of this increase in preload is due to redistribution from the splanchnic bed, mainly from the liver.

Angiotensin II↗

PubMed1982

Dynamics of the interventricular septum and free ventricular walls during blood volume expansion and selective right ventricular volume loading in dogs.

To examine whether the right ventricle responds differently to blood volume expansion and selective right ventricular volume loading, segment lengths in the interventricular septum and the free walls of both ventricles and right ventricular septal-to-free-wall-distance were measured by an ultrasonic technique in open-chest dogs. Blood volume expansion increased segment lengths at all recording sites in proportion to stroke volume. Selective right ventricular volume loading induced by opening a shunt between the pulmonary artery and the superior vena cava increased right ventricular stroke volume by 40-80%; end-diastolic segment length and myocardial shortening increased in the septum and free wall of the right ventricle whereas left ventricular stroke volume and segment length decreased. Comparison of data obtained before and after opening of the shunt indicated that changes in myocardial dynamics of the right ventricle and septum accounted for approximately 30% of the increase in right ventricular stroke volume. However, both end-diastolic dimension and systolic shortening of the right ventricular septal-to-free-wall distance were larger during right ventricular volume loading than during blood volume expansion. Thus, most of the increase in stroke volume during selective right ventricular volume loading is caused by a change in the configuration of the right ventricle.

Animals↗

PubMed1981

[Splenic cysts].

Explore the source record for details and available documents.

Adult↗

PubMed1981

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.

Animals↗

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↗