Fredrik Kiil

Local Dimensional Changes of the Myocardium Measured by Ultrasonic Technique

Pairs of ultrasonic elements (piezo-electric ceramics of lead zirconate titanate) were implanted in the myocardium with 0.8–1.2 cm between the elements. Measurements of mural thickness or distance variations along the muscle layers, myocardial chord length (MCL), were performed in anesthetized and conscious dogs. Mural thickness varied reciprocally to MCL during the heart cycle, both with amplitudes of 8—15 per cent of end-diastolic lengths. Shortening usually started in the apical and interventricular parts, whereas shortening of the myocardium close to the base was often delayed. This asynchrony may reflect differences in end-diastolic myocardial fibre lengths. During the isovolumic phase, dimensional changes were small or absent. Comparative measurements with mercury-in-rubber gauges revealed that the considerable isovolumic expansion produced by this technique was an artefact due to stretching of the muscle fibres by the gauges.

Local regulation of vascular cross section during changes in femoral arterial blood flow in dogs.

Diameters of the exposed femoral artery of anesthetized dogs were continuously measured with ultrasonic elements of lead zirconate titanate. In 13 of 16 dogs vascular diameters increased following a sudden increment in arterial blood flow induced by the injection of vasodilating agents (acetylcholine, histamine) peripheral to the recording level, by opening an arteriovenous shunt, or after tetanic stimulation of the sciatic nerve. The dilatation response occurred despite slight reductions in femoral blood pressure, and was present after ganglionic blockade, blockade of alpha and beta receptors with phenoxybenzamine and propranolol, atropinization and injection of an antihistamine. The dilatation response was also observed after transsection of the femoral artery distal to the recording level and is therefore not dependent on the retrograde propagation of nervous or myogenous impulses along the vascular wall.

Influence of plasma potassium concentration on the capacity for sodium reabsorption in the diluting segment of the kidney

A previous study showed that sodium reabsorption and heat production in the outer medulla and cortex increased during saline loading until 15-20% of the filtered sodium was excreted. To examine if the capacity for energy-requiring transcellular sodium reabsorption is altered by changes in plasma potassium concentration, renal heat production and sodium reabsorption were measured in anaesthetized dogs during hypokalemia, normokalemia and hyperkalemia. A rise in plasma potassium concentration from 1.8 to 4 mmol/l was associated with a 50% increase in both outer medullary heat production and sodium reabsorption in dogs which received acetazolamide to avoid changes in proximal tubular reabsorption; cortical metabolism increased only slightly. In contrast, no change in tubular reabsorption of sodium was observed during intravenous infusion of KC1 to hypokalemic dogs which had not received acetazolamide. Under this condition an increase in sodium reabsorption in the diluting segment is counteracted by a reducti...

Mechanism of renin release during acute ureteral constriction in dogs.

The relationship between renal arterial pressure and renin release was examined in anesthetized dogs during complete or partial ureteral constriction. During complete ureteral occlusion ureteral pressure rose to 95 ± 4 mm Hg and renin release increased from 1.7 ± 0.7 to 22.3 ± 3.1 &mgr;g/min; renal blood flow (RBF) was not significantly changed. Renin release was not further increased during subsequent renal arterial constriction; RBF fell in proportion to perfusion pressure, indicating maximum autoregulated arteriolar dilation. During partial ureteral constriction to a ureteral pressure of 65 ± 6 mm Hg, renin release was moderately raised but release mechanisms became fully stimulated when renal arterial pressure was reduced to 104 ± 3 mm Hg. By further constriction of the renal artery, RBF fell in proportion to perfusion pressure and renin release remained high and constant. In control experiments without ureteral constriction, renal arterial pressure had to be reduced to below 65 ± 8 mm Hg to fully stimulate renin release (22.0 ±3.8 jug/min which is not different from 22.3 ±3.1 &mgr;g/min during ureteral occlusion). During partial ureteral constriction, saline infusion (0.9% NaCl at 40 ml/min) raised urine flow, sodium excretion, renal pelvic pressure, and renin release. Thus, the stimulatory effect on renin release of a rise in ureteral pressure exceeded the inhibitory effect of increased sodium excretion. This observation, together with maximum renin release coinciding with complete arteriolar dilation during various combinations of renal arterial and ureteral constriction, is compatible with the conclusion that arteriolar dilation is the predominating stimulus to renin release during ureteral constriction.

Principles of active sodium reabsorption in the kidney

(1978). Principles of active sodium reabsorption in the kidney. Scandinavian Journal of Clinical and Laboratory Investigation: Vol. 38, No. 7, pp. 597-602.

Cardiac Response to Increased Aortic Pressure Changes in Output and Left Ventricular Pressure Pattern at Various Levels of Inotropy

The cardiac effects of raising aortic pressure were studied in thoracotomized dogs, in conscious dogs after implantation of aortic flowmeters, and in anesthetized, intact dogs Mean aortic blood pressure was raised 50–100 mm Hg either by mechanical constriction of the ascending or descending aorta or by intravenous (i.v.) infusion of angiotensin. Reflex bradycardia was avoided by administration of atropine, but the directional changes in cardiac output were similar before and after atropinization. Stroke volume remained unchanged or decreased when aortic pressure was raised in control experiments and after blockade of β-adrenergic receptors with propranolol. In contrast, the response to a similar pressure increase during continuous infusion of a stimulator of adrenergic β-receptors (isoproterenol i.v. at 3–4 μg per minute) was an increase in stroke volume averaging 27.5 per cent in thoracotomized and 20 per cent in conscious dogs. This response was characterized by maintained peak flow, slightly increased ...

Effect of Acetazolamide on Glomerulotubular Balance and Renal Metabolic Rate

Mathisen, O., Raeder, M., Sejersted, O. M. & Kiil, F. Effect of Acetazolamide on Glomerulotubular Balance and Renal Metabolic Rate. Scand. J. clin. Lab. Invest. 36, 617–625, 1976.Glomerulotubular balance, defined as proportionality between filtered and re-absorbed sodium during inhibition of sodium reabsorption in the thick ascending limb of Henles loop (diluting segment), was examined in anaesthetized dogs by gradual reduction of renal arterial pressure. In control experiments, glomerulotubular balance applied over the whole range of glomerular filtration rate (GFR) examined but was absent after acetazolamide administration (30 mg/kg body wt) at GFR above 50 % of control. Hence, the inhibitory effect of acetazolamide varied with GFR. At control GFR, acetazolamide reduced tubular sodium reabsorption by 32 ±2%, chloride reabsorption by 34 ±3%, and bicarbonate reabsorption by 52±2%; no significant effect was observed at GFR below 50% of control. For each bicarbonate ion, three sodium ions and two chloride ...

Potentiation of Renin Release by Combining Renal Arterial Constriction and β -Adrenergic Stimulation

Intrarenal mechanisms for renin release can be activated by reducing renal arterial pressure until renal blood flow (RBF) falls, but renin release is not further raised by reducing arterial pressure below the range of autoregulation of RBF. To examine whether the renin release evoked by reduction of renal arterial pressure is influenced by adrenergic stimulation, isoproterenol or propranolol was administered in anesthetized dogs at control pressure (120-140 mm Hg) and after constricting the renal artery to a low pressure (50-60 mm Hg), well below the range of autoregulation of RBF. Infusion of isoproterenol into the renal artery (0.2 μg/min per kg body weight) increased renin release from 1.8 ± 0.5 μg/min (mean ± S.E.M.) to 8.9 ± 1.7 μg/min at control pressure and from 31.9 ± 3.2 μg/min to 54.3 ± 5.0 μg/min at low pressure. Thus, isoproterenol raised renin release more (P < 0.05) at low (δRR = 22.4 ± 2.9 μg/min) than at normal renal arterial pressure (δRR = 7.1 ± 1.6 μg/min). Similar results were obtained...

Relationship Between Local Myocardial Dimensions and Left Ventricular Volume in Dogs

Ultrasonic elements inserted parallel to the surface of the anterior wall of the left ventricle in open-chest dogs were used to determine myocardial distances (MCL). During saline loading with and without administration of isoproterenol, end-systolic and end-diastolic MCL were compared with the corresponding ventricular volumes (ESV and EDV), estimated by thermodilution technique. In individual experiments, correlation coefficients for the relationship between MCL3and ventricular volumes ranged from 0.91 to 0.99. It is concluded that stroke volume can be analyzed in terms of end-systolic and end-diastolic MCL, and that the thermodilution technique correctly determines ESV/EDV.

Characteristics of transcellular NaCl reabsorption in the kidney

To examine the characteristics of transcellular, energy-requiring NaCl reabsorption, increased delivery of tubular fluid of different bicarbonate and chloride composition to the outer medulla was achieved by infusion of acetazolamide (30 mg/kg body wt) or 0.9% NaCl in anaesthetized dogs. As an index of energy-requiring NaCltransport, cortical and outer medullary metabolism were determined by the heat production technique. Outer medullary metabolism was correlated to sodium excretion but not to chloride excretion. A rise in sodium excretion up to 20-25% of the filtered load during hydropenia was associated with a 70-80% increase in outer medullary metabolism. Further increments in sodium excretion induced by increasing systemic blood pressure and thereby increasing glomerular filtration rate or by infusing 2.9% NaCl did not significantly increase either reabsorption of sodium or cortical and outer medullary metabolism. By infusion of furosemide (2mg/kg body wt) sodium reabsorption and outer medullary heat production could be reduced below control values. These experiments show that sodium rather than chloride determine transcellular NaCl reabsorption. The maximal capacity of this reabsorption system is approached first at sodium excretion rates beyond the physiological range. Calculations based on clearance studies and heat production measurements, before and after furosemide infusion, indicate that transcellular NaCl reabsorption accounts for more than half of the NaCl reabsorption in the kidney.