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Biomedical subjects

F Kiil

Publications and source records attributed to F Kiil.

At least 109 records · Page 6Linked to original sources
PubMed1979

Cardiac performance: independent effects of inotropy and preload at high heart rate.

Linear relationships between stroke volume (SV) and heart rate (HR) were observed during right atrial pacing in open-chest dogs at control inotropy, during intravenous isoproterenol infusion and during blood volume expansion by saline infusion at HR exceeding 150 beats/min. The slope of these relationships remained constant during variations in inotropy, but rose during blood volume expansion. Myocardial chord lengths in the anterior left ventricular wall were continuously recored by ultrasonic technique to estimate left ventricular volume. When heart rate was increased, end-diastolic volume decreased more rapidly after than before blood volume expansion, explaining the increased slope of the SV/HR relationship. The end-diastolic volume and the SV/HR relationship were not influenced by changes in inotropy. After blood volume expansion by 57 +/- 13%, control end-diastolic volume was reestablished by increasing heart rate 84 +/- 20 beats/min. At identical end-diastolic volume, SV was equal at different HR. Thus, the effects on SV of changes in preload and inotropy are separable during right atrial pacing, and SV is independent of HR at constant preload and adrenergic stimulation.

Animals↗
PubMed1979

Coupling of NaHCO3 and NaCl reabsorption in dog kidneys during changes in plasma PCO2.

To study the relationship between proximal tubular reabsorption of bicarbonate, sodium, and chloride, the effects of changes in plasma PCO2 were examined in anesthetized dogs. Distal tubular reabsorption was inhibited by ethacrynic acid; plasma bicarbonate concentration was kept constant at 33.4 +/- 0.3 mM; glomerular filtration rate (GFR) was varied over a wide range to examine glomerulotubular balance (constant fractional reabsorption). Hypercapnia (PCO2, 112.0 +/- 2.5 mmHg) increased bicarbonate reabsorption by about 30%, and hypocapnia (PCO2, 19.8 +/- 0.6 mmHg) decreased reabsorption of bicarbonate by more than 50% and altered reabsorption of sodium, chloride, and bicarbonate in the molar ratios 2.7:1.6:1, respectively. During hypercapnia the range of glomerulotubular balance was extended to a GFR 125% of control. During hypocapnia glomerulotubular balance was present only at GFR below 50% of control; reabsorption of bicarbonate sodium, and chloride was constant at GFR exceeding 50% of control. During metabolic acidosis hypercapnia had no significant effect on reabsorption of bicarbonate, sodium, and chloride. These observations support the hypothesis that bicarbonate reabsorption is the main driving force for osmotic reabsorption of water and NaCl in the proximal tubules.

Acidosis↗
PubMed1979

Role of preload and inotropy in stroke volume regulation at constant heart rate.

The relationship between preload and inotropy on left ventricular function was studied in anaesthetized open-chest dogs, by measuring left ventricular dimensions and stroke volume before and during saline infusion at different levels of inotropy. Left ventricular dimensions were continuously estimated by recording myocardial chord length (MCL) in the anterior wall of the left ventricle by ultrasonic technique. The effects of isoproterenol, a stimulator of adrenergic beta-receptors (high inotropy), and propranolol, an inhibitor of adrenergic beta-receptors (low inotropy), were examined during right atrial pacing at constant heart rate averaging 161 +/- 5 beats/min. Stroke volume was varied within the range 9.0 +/- 1.7 ml to 28.6 +/- 3.2 ml by increasing inotropy and preload. To increase preload, saline was infused intravenously until end-diastolic MCL increased by about 10% and left ventricular end-diastolic pressure was higher than 10 mmHg. At constant heart rate and blood volume, both before and during saline infusion, end-diastolic MCL was not influenced by isoproterenol or propranolol administration. End-systolic MCL was reduced by raising inotropy. The difference between end-diastolic and end-systolic MCL, the systolic myocardial shortening (MS), increased during saline infusion; the relative increase in MS was the same at high and low inotropy. On average, MS was more than 50% longer at high than at low inotropy, both before and after saline infusion. Thus, left ventricular end-diastolic volume is increased by saline infusion and end-systolic volume is reduced by increasing inotropy. Preload and inotropy exert independent effects on stroke volume.

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

Re-examination of the dose-reponse relationship for the renal effect of acetozolamide.

To examine the effect of acetazolamide on tubular reabsorption of bicarbonate, plasma concentrations of bicarbonate, potassium and PCO2 were kept constant in volume expanded dogs. Intravenous infusion of acetazolamide reduced glomerular filtration rate (GFR) at all dose levels; after a dose of 30 mg/kg body wt GFR was reduced by about 30% and was not reduced further by increasing the infused dose of acetazolamide up to 500 mg/kg body wt. When control GFR was restored by raising systemic blood pressure, increments in filtered and excreted bicarbonate were not significantly different. At control GFR a linear relationship was obtained between bicarbonate reabsorption and log dose when acetazolamide was administered intravenously in doses ranging between 0.3 and 500 mg/kg body wt (r = 0.93). We conclude that a log dose-reponse relationship applies over a 25 times larger dose range than previously assumed.

Absorption↗
PubMed1978

Factors limiting renal proximal tubular reabsorption at high glomerular filtration rate.

To examine the factors limiting proximal reabsorption, distal reabsorption was inhibited by continuous infusion of ethacrynic acid in anaesthetized dogs. During combined infusion of ethacrynic acid and 0.9% saline, autoregulation of renal blood flow is impaired and glomerular filtration rate (GFR) can be varied by lowering or raising renal perfusion pressure. During lowering of GFR reabsorption of bicarbonate, chloride and sodium varied in proportion to reduction in GFR (glomerulotubular balance), but during elevation of GFR the increase in the filtered load of all three ions was excreted and a maximal rate of reabsorption was approached. Administration of acetazolamide reduced the reabsorption of bicarbonate, chloride and sodium in the ratio 1:2:3, whether GFR was at control, reduced (74% of control) or increased (124% of control). Renal blood flow was 80--90% greater at high than at low GFR. These observations indicate that bicarbonate concentration increases along the proximal tubules during elevation of GFR, until plasma bicarbonate concentration is approached at the distal end of the proximal tubules. From then on, bicarbonate reabsorption cannot be further raised by increasing GFR. Proximal tubular sodium reabsoption reaches a maximum at high GFR because NaCl reabsorption varies in proportion to bicarbonate reabsorption.

Acetazolamide↗
PubMed1978

Cardiac performance: independence of adrenergic inotropic and chronotropic effects.

During right atrial pacing in open-chest anesthetized dogs, the relationships between reduction in stroke volume and rise in heart rate were identical in control experiments, during intravenous infusion of isoproterenol, and after blockade of adrenergic beta-receptors by propranolol. To examine the mechanism of this constant relationship, left ventricular volume was estimated by continuous recordings of myocardial chord length (MCL) between ultrasonic elements inserted into the anterior ventricular wall. Diastolic filling curves were curtailed by raising heart rate and end-diastolic MCL was reduced. At constant heart rate, end-diastolic MCL was not altered by isoproterenol infusion, except for a slight rise at heart rates exceeding 220 beats/min. End-systolic MCL, however, was reduced, accounting for larger stroke volume during isoproterenol than during propranolol infusion. The reduction in end-systolic MCL was constant at all heart rates examined. Hence, chronotropic changes influence end-diastolic volume and inotropic changes influence end-systolic volume; their effects on stroke volume regulation are, therefore, virtually independent.

Animals↗
PubMed1978

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.

Acetazolamide↗
PubMed1977

Oxygen requirement of renal Na-K-ATPase-dependent sodium reabsorption.

The oxygen requirement of the Na-K-ATPase-dependent sodium transport system was examined in anesthetized dogs infused with 15% mannitol-Ringer solutions at a rate of 35 ml/min. Because of renal vasodilatation and abolished autoregulation, filtered sodium (FNa) could be varied over a wide range by progressive aortic constriction. Sodium reabsorption (RNa) and renal oxygen consumption (RVO2) varied in proportion to FNa (r greater than 0.9). Ouabain, which inhibits Na-K-ATPases, reduced RVO2 by 45 +/- 6%. During subsequent aortic constriction, the ratio delta RNa/delta FNa averaged 0.45 (glomerulotubular balance) (r less than 0.9), whereas RVO2 was not significantly altered. Comparisons of deltaRNa/deltaFNa before and after ouabain administration, indicate that about half of an increase in sodium delivery to the distal nephron is reabsorbed by the Na-K-ATPase-dependent sodium transport system and that deltaRNa/deltaRVO2 (Na/O2 ratio) of this system averages 14.5 +/- 1.3. This Na/O2 ratio corresponds to 2.4 sodium ions transported per ATP dephosphorylated as found in other tissues.

Adenosine Triphosphatases↗
PubMed1977

Effect of glycine and glucagon on glomerular filtration and renal metabolic rates.

A rise in glomerular filtration rate (GFR) during saline infusion increases outer medullary more than cortical metabolic rate. To determine whether other GFR-increasing agents have a similar effect, renal metabolic rates were estimated by the heat-production technique during infusion of glycine or glucagon. Glycine and glucagon increased GFR by 17 +/- 2 and 32 +/- 2%, renal blood flow (RBF) by 34 and 21%, and outer medullary metabolic rate by 42 +/- 3 and 59 +/- 4%, respectively. Cortical metabolic rate rose by 7 +/- 1% during glucagon, and it increased by 29 +/- 2% during glycine infusion, suggesting a stimulation unrelated to sodium reabsorption. To determine whether glucagon influenced renal metabolism independent of its GFR-increasing effects, vasodilation was achieved by ureteral or suprarenal aortic constriction. Glucagon was without effect on RBF, GFR, and metabolic rate, but infusion of acetylcholine still raised RBF. We conclude that glucagon increases GFR by dilating vascular segments participating in autoregulation, and that energy-requiring NaCl reabsorption in the outer medulla is increased secondary to increased delivery of NaCl.

Acetylcholine↗