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Biomedical subjects

O Stokland

Publications and source records attributed to O Stokland.

27 records · Page 2Linked to original sources
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↗
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

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↗
PubMed1981

Myocardial function of the interventricular septum. Effects of right and left ventricular pressure loading before and after pericardiotomy in dogs.

We examined the function of the interventricular septum in six open-chest dogs by inserting piezoelectric crystals into the interventricular septum. Continuous ultrasonic recordings showed that the changes in myocardial chord length (MCL) in the septum and free walls of the right and left ventricle were similar during saline infusion and during pericardiotomy. End-diastolic MCL and myocardial shortening during ejection (MS) rose in the septum and free walls of both ventricles during saline infusion as end-diastolic MCL and MS in the septum and free walls of the ventricles, and reduced end-diastolic pressures by 1-2 mm Hg. The responses to aortic and pulmonary artery constrictions were similar before and after pericardiotomy. When aortic constriction had raised free left ventricular systolic pressure by about 60 mm Hg, end-diastolic MCL increased in the septum and free left ventricular wall, whereas end-diastolic MCL and MS of the free right ventricular wall fell. Pulmonary artery constriction increased end-diastolic MCL in the free right ventricular wall and reduced end-diastolic MCL and MS in the septum and free left ventricular wall. Thus, the myocardium, including the interventricular septum, is uniformly expanded during saline infusion and pericardiotomy. The interventricular septum behaves as part of the left ventricle during aortic and pulmonary artery constriction. The pericardium imposes a restraint on the interventricular septum and free walls of the ventricles during volume loading, but not during pressure loadings, because dilation of one ventricle is associated with shrinkage of the other.

Animals↗
PubMed1980

Mechanism of hemodynamic responses to occlusion of the descending thoracic aorta.

To examine left ventricular responses to aortic occlusion, changes in end-diastolic volume (EDV) and end-systolic volume (ESV) were estimated by ultrasonic recordings of myocardial distances in atropinized open-chest dogs. During aortic occlusion EDV and ESV increased equally, systolic left ventricular pressure (LVP) rose by 86 +/- 8 mmHg, and blood flow more than doubled in the superior vena cava and fell by 90% in the inferior vena cava. During combined occlusion of aorta and inferior vena cava, systolic LVP and superior vena cava flow did not rise above control and EDV declined. By infusing 25 +/- 2 ml/kg body wt of blood during combined occlusion, the effects of aortic occlusion could be reproduced; control values before blood infusion were reestablished by withdrawal of only one-third of the infused volume, indicating a shunt line along the spinal column. Thus during aortic occlusion, transfer of blood accounts for the rise in EDV and increased activation of the Frank-Starling mechanism; increased afterload raises ESV as much as EDV in anesthetized dogs not subjected to sympathetic stimulation. Consequently, stroke volume is maintained and systolic LVP increased.

Animals↗