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Biomedical subjects

F Kiil

Publications and source records attributed to F Kiil.

At least 73 records · Page 4Linked to original sources
PubMed1984

Site and magnitude of the tubular inhibitory effect of expanding the extracellular volume in dogs.

Ethacrynic acid inhibits energy-requiring transcellular NaCl reabsorption without affecting NaHCO3 reabsorption. Acetazolamide inhibits NaHCO3 and most of the remaining NaCl reabsorption in the proximal tubules (bicarbonate-dependent reabsorption) but raises distal transcellular NaCl reabsorption. After administration of both diuretics, the remaining bicarbonate-dependent and transcellular reabsorptions become constant until glomerular filtration rate (GFR) is almost halved. The inhibitory effect of expanding the extracellular volume (ECV) until plasma volume and GFR increased 30-40% was examined in anesthetized dogs. Examinations at comparable GFR obtained by altering arterial perfusion pressure showed that the inhibitory effect of ECV expansion was attenuated by administering acetazolamide. Ethacrynic acid amplified the inhibitory effect which for sodium and chloride reabsorption amounted to 6-7% of the filtered load at comparable GFR. An inhibitory effect of ECV expansion of bicarbonate reabsorption was disclosed only after raising plasma bicarbonate concentration. Thus, the small inhibitory effect of massive ECV expansion is confined to proximal tubular bicarbonate-dependent reabsorption and is of the same magnitude as previously demonstrated in experiments of similar design by raising plasma pH by only 0.07 unit. Since ouabain inhibits transcellular NaCl reabsorption, a natriuretic hormone is more likely to be an inhibitor of carbonic anhydrase than of Na,K-ATPase.

Absorption↗
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↗
PubMed1984

Glomerulotubular balance and prostaglandin synthesis.

We have tested a hypothesis proposed to explain glomerulotubular balance (GTB) as a consequence of variations in prostaglandin synthesis. Arachidonic acid (40 micrograms x kg-1 x min-1) infused into the renal artery of anesthetized dogs raised renal blood flow (RBF) by 41 +/- 5% in hydropenic and by 24 +/- 11% in volume-expanded dogs, but the absolute changes were similar. The infusion of arachidonic acid after the administration of indomethacin (10 mg x kg-1) had no effect on RBF. Arachidonic acid infusion increased the excretion of sodium and chloride in hydropenic dogs but not after the administration of ethacrynic acid in volume-expanded dogs. During continued infusion of ethacrynic acid, the glomerular filtration rate (GFR) was lowered by suprarenal aortic constriction and raised by carotid constriction. A linear relationship between electrolyte reabsorption and GFR (GTB) was observed when GFR was varied between 20 and 110% of control. GTB and tubular reabsorption at comparable GFR were not significantly altered during arachidonic acid infusion or after indomethacin administration. In all experimental settings, bicarbonate, chloride, and sodium reabsorption were altered in molar ratios of 1:2:3 during variations in GFR. We conclude that GTB is independent of variations in prostaglandin synthesis.

Animals↗
PubMed1983

Compensatory cardiac mechanisms evoked by septal ischemia in dogs.

To examine the cardiac responses to selective septal ischemia, the septal artery was occluded intermittently in anesthetized open-chest dogs. Myocardial segment length was recorded continuously by an ultrasonic technique in the interventricular septum and the right and left ventricular free walls. At left ventricular end-diastolic pressure of 3.0 +/- 0.6 mm Hg, occlusion of the septal artery increased left ventricular end-diastolic segment length by 3.9 +/- 0.9% and stroke volume was maintained. After blood volume expansion to a left ventricular end-diastolic pressure of 7.2 +/- 1.4 mm Hg, occlusion of the septal artery did not increase end-diastolic dimensions and stroke volume decreased significantly but by less than 10%. At all levels of blood volume expansion, occlusion of the septal artery did not alter significantly the end-systolic segment length of the free wall of the left ventricle and the dimensions of the free wall of the right ventricle. The distance between the septum and the right ventricular free wall was unchanged in end-diastole and reduced in end-systole after occlusion of the septal artery. These observations indicate paradoxical movement of the ischemic septum. The ischemic septum seems to act as a passive diaphragm pump on the right ventricle without activation of the Frank-Starling mechanism in uninjured areas. In the left ventricle, the Frank-Starling mechanism is fully exploited with unaltered end-systolic dimensions of the uninjured myocardium because of the systolic bulging of the ischemia septum.

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↗
PubMed1983

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

A previous study suggests 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.

Animals↗
PubMed1983

Segmental distribution of vascular resistances during ureteral occlusion. The vasoconstrictive effects of angiotensin and CaCl2 differ from those of catecholamines and renal nerve stimulation.

UNLABELLED: Examinations of renal autoregulation and renin release suggest that alpha-adrenergic agonists, in contrast to other vasoconstrictors, preferentially constrict the preglomerular arteries. To examine this hypothesis, experiments were performed in anesthetized dogs during ureteral occlusion. At a ureteral pressure (UP) of 100 mmHg the afferent arterioles are dilated and mechanical constriction of the renal artery does not alter intrarenal vascular resistances. Whereas angiotensin and CaCl2 infused into the renal artery reduced renal blood flow (RBF) by 25-30% without reducing UP, renal nerve stimulation reduced RBF and UP in proportion. During angiotensin and catecholamine infusion, measurements of UP and intrarenal venous pressure permitted calculations of preglomerular, efferent vascular and intrarenal venous resistances. Until RBF was reduced by 25%, angiotensin raised both preglomerular and efferent vascular resistances, whereas norepinephrine and the alpha-adrenergic agonists, phenylephrine and methoxamine, raised preglomerular more than efferent vascular resistance. When RBF was reduced by more than 25%, all vasoconstrictors showed a similar pattern with large increments both in preglomerular and efferent vascular resistances. CONCLUSIONS: Humoral and nervous stimulation of alpha-adrenergic receptors reduce glomerular capillary pressure by preferentially constricting the preglomerular arteries and may affect renal autoregulation and renin release by reducing the transmural pressure of the afferent arterioles.

Adrenergic alpha-Agonists↗
PubMed1983

Evidence for bicarbonate-dependent magnesium reabsorption.

During ethacrynic acid administration about 50% of the filtered load of magnesium is reabsorbed. To examine whether the remaining component of magnesium reabsorption is bicarbonate-dependent, i.e. varies with factors known to alter passive reabsorption, experiments were performed in anesthetized dogs. During ethacrynic acid administration MgCl2 infusion raised the plasma concentration of magnesium (PMg) from 0.64 +/- 0.05 to 3.06 +/- 0.27 mM and doubled magnesium reabsorption. The infusion of acetazolamide at high PMg reduced bicarbonate reabsorption by 41 +/- 3% and magnesium reabsorption by 31 +/- 16%. When plasma pH was reduced to 7.04 +/- 0.02 and increased to 7.83 +/- 0.02 by altering PCO2 at a constant plasma bicarbonate concentration of 31.2 +/- 0.8 mM, magnesium and bicarbonate reabsorption were correlated (r = 0.82). The infusion of mannitol, which acts by reducing passive solute transport without affecting bicarbonate reabsorption, halved magnesium reabsorption. By combining mannitol and acetazolamide infusions, only 6 +/- 4% of the filtered magnesium was still reabsorbed. These results indicate that the reabsorption of magnesium remaining after the infusion of ethacrynic acid and after raising PMg varies with changes in PCO2 and is inhibited by the infusion of acetazolamide and mannitol as expected for bicarbonate-dependent passive reabsorption.

Acetazolamide↗
PubMed1983

Conditions for augmentation of renin release by theophylline.

Isoproterenol, dopamine, glucagon and dibutyryl cyclic AMP (DB-cAMP) increase renin release at low but not at control blood pressure. These findings suggest that autoregulated afferent arteriolar dilation is a prerequisite of renin release mediated by intracellular generation of cyclic AMP. To examine this hypothesis further the effects on renin release of theophylline, which would maintain high intracellular concentration of cAMP by inhibiting phosphodiesterase, were studied in anesthetized dogs. After inhibiting beta-adrenergic stimulation with propranolol, theophylline increased renin release significantly from 0.7 +/- 0.2 to 1.8 +/- 0.7 micrograms/min at control blood pressure and from 23 +/- 4 to 41 +/- 5 micrograms/min at a renal perfusion pressure of about 50 mmHg. The greater effect at low blood pressure occurred despite adjustment of the infusion rate of theophylline to keep arterial plasma concentration of theophylline unaltered. Isoproterenol infusion at low blood pressure raised renin release from 41 +/- 11 to 76 +/- 19 micrograms/min before and 54 +/- 13 to 108 +/- 31 micrograms/min during continuous infusion of theophylline. The renin release response to infusion of theophylline at low blood pressure was not enhanced by DB-cAMP infusion. We conclude that arteriolar dilation provides a condition for stimulation of renin release during the theophylline infusion. Theophylline infusion may augment the effect of isoproterenol on renin release by delaying the intracellular degradation of cAMP.

Animals↗
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

Energetics of tubular sodium reabsorption sensitive to ethacrynic acid and ouabain.

Ouabain reduces renal oxygen consumption more extensively than ethacrynic acid despite similar natriuretic effects. Therefore, ethacrynic acid, which does not inhibit Na-K-ATPase, might stimulate energy metabolism unrelated to net sodium reabsorption. Experiments were performed on anesthetized dogs that had received isotonic saline intravenously corresponding to 10% of body wt and acetazolamide (100 mg.kg-1 i.v.). Subsequent infusion of ouabain in nine dogs (120 nmol.kg-1 intrarenally) reduced sodium reabsorption and oxygen consumption in parallel, giving a delta Na/delta O2 ratio of 18.0 +/- 1.1. With ethacrynic acid (3 mg.kg-1 i.v.) in six other dogs the delta Na/delta O2 ratio averaged 24.5 +/- 1.4. In a third group of five dogs, ouabain administered after ethacrynic acid reduced sodium reabsorption and oxygen consumption to the same levels as when ouabain was given alone. Thus, the high oxygen consumption remaining after ethacrynic acid can be inhibited by ouabain. We propose that ethacrynic acid generates a futile cycling of sodium by Na-K-ATPase across the basolateral cell membrane that is not apparent as net sodium reabsorption and is stopped by ouabain.U

Absorption↗
PubMed1982

Conditions for enhancement of renin release by isoproterenol, dopamine, and glucagon.

Isoproterenol infusion increases renin release at low but not at control blood pressure. To examine whether this effect is dependent on arteriolar dilation and is specific for agonists of beta-adrenoceptors, responses to intrarenal infusion of isoproterenol (0.2 micrograms.kg body wt-1.min-1), glucagon (0.1 micrograms.kg body wt-1.min-1), and dopamine (1 micrograms.kg body wt-1.min-1) were compared at control and low or high ureteral pressure, which also dilates the renal arterioles. During renal arterial constriction, renin release was equal at two perfusion pressures below the range of autoregulation and was 76 +/- 24 micrograms/min higher during isoproterenol than during propranolol administration. Intravenous infusion of isoproterenol gave qualitatively similar results. Intrarenal infusion of glucagon and dopamine increased renin release by 13 +/- 3 and 22 +/- 12 micrograms/min, respectively; enhancement of renin release was also present after propranolol administration. During ureteral occlusion, intrarenal infusion of isoproterenol, dopamine, and glucagon increased renin release from 30-40 micrograms/min by 78 +/- 11, 13 +/- 3, and 31 +/- 10 micrograms/min, respectively. At control blood and ureteral pressure, the effects on renin release of infusing isoproterenol, dopamine, or glucagon were small or absent. Thus, isoproterenol, dopamine, amd glucagon enhance renin release when the arterioles are dilated by renal arterial constriction or ureteral occlusion.

Animals↗