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Biomedical subjects

I Leusen

Publications and source records attributed to I Leusen.

At least 73 records · Page 4Linked to original sources
PubMed1979

Restoration of CSF [HCO3-] after its experimental lowering in normocapnic conditions.

It is accepted that in hypercapnia the rise in cerebrospinal fluid bicarbonate concentration (CSF [HCO3-]) occurs because of local HCO3--generating mechanisms, dependent on carbonic anhydrase, as well as on diffusion of HCO3- from plasma. To investigate further the regulation of CSF [HCO3-], CSF HCO3- formation was studied under conditions of pure isocapnic CSF "metabolic" acidosis. In anesthetized normocapnic dogs CSF [HCO3-] was lowered to approximately 15 mmol/l by perfusing the brain ventricles with a low HCO3- solution for 45 min. In dogs with normal plasma [HCO3-], CSF [HCO3-] rose by approximately 7 mmol/l in 2 h after the end of the perfusion. Lowering plasma [HCO3-] to 10 mmol/l by infusing HCl, limited the CSF [HCO3-] rise to 2 mmol/l, indicating the importance of plasma HCO3- for the restoration of CSF [HCO3-]. The small and persistent rise of CSF [HCO3-] at low plasma [HCO3-] occurred against a concentration gradient with blood. Intraventricular injection of acetazolamide had no further effect on this small rise. It is concluded that under the conditions of our experiments the CSF [HCO3-] rise is significantly dependent on plasma [HCO3-] and the caronic anhydrase-dependent HCO3- generation in the CNS is less important.

Acetazolamide↗
PubMed1978

Depression of regional blood flow and wall thickening after brief coronary occlusions.

The effects of a 15-min coronary occlusion and subsequent reperfusion were investigated in conscious dogs previously instrumented for measurement of left ventricular pressure, dP/dt, regional wall thickening, electrograms, and myocardial blood flow. Coronary occlussion reduced overall left ventricular function only slightly but eliminated systolic wall thickening in the ischemic zone and reduced regional myocardial blood flow in the ischemic zone from 1.04 +/- 0.04 to 0.27 +/- 0.02 ml/min per g and the endo/epi flow ratio from 1.23 +/- 0.04 to 0.44 +/- 0.04, while S-T segment elevation increased from 1.1 +/- 0.3 to 8.2 +/- 0.9 mV. After release of the occlusion, S-T segment elevation disappeared within 1 min while reactive hyperemia in the previously occluded artery and a transient increase in cardiac diastolic wall thickness occurred and then subsided by 15 min. In contrast, systolic wall thickening and the endo/epi flow ratio remained significantly depressed for more than 3 h. Thus reperfusion after a 15 minute coronary occlusion results in a prolonged period of reduced regional myocardial blood flow, particularly in the endocardial layers, which correlates with the prolonged depression of regional myocardial shortening and wall thickening.

Animals↗
PubMed1978

Selected brain amino acids and ammonium during chronic hypercapnia in conscious rats.

Glutamic, aspartic, and gamma-aminobutyric acid (GABA), glutamine, and ammonium were measured in the brains of unanesthetized normocapnic and hypercapnic (10% CO2; 5 min to 3 wk) rats. Hypercapnia increased glutamine and GABA and decreased glutamic and aspartic acids. Changes occurred within 1 h and were maintained during the observation period of 3 wk. On return to normocapnia amino acid concentrations were almost normal after 1 h. Based on the time course it is concluded that intracerebral hypercapnia is more likely the stimulus for change than acidosis. Ammonium content was unchanged for at least 1 h after the onset of hypercapnia but increased thereafter. Experiments in which glutamine synthesis by brain was impeded by inhibiting the enzyme glutamine synthetase favor the hypothesis that the rise of ammonium content in hypercapnia is initially not seen because of increased glutamine synthesis. The changes observed may have a role in metabolic pH homeostasis of brain tissue and may also be relevant to the modified brain excitability in hypercapnia.

Acid-Base Equilibrium↗
PubMed1977

Regional blood flow in response to exercise in conscious dogs.

Regional blood flow was measured with the microsphere method in conscious dogs under resting conditions and during moderate exercise on the treadmill. With respect to total organ blood flow, exercise induced a marked increase in blood flow to the calf muscles and to the myocardium, and a significant decrease in the arterial blood supply to the liver. Slight changes in blood flow to the other organs under study (various skeletal muscles, skin, brain, kidneys, intestine) were not significant. Study of the blood flow distribution within the myocardium showed a slight decrease of the ratio of subendocardial to subepicardial blood flow in the left ventricular free wall in response to exercise, and within the brain there was a relative increase in the blood flow to the cerebellum.

Animals↗
PubMed1977

Brain amino acids in conscious rats in chronic normocapnic and hypocapnic hypoxemia.

The influence of hypoxemia on the brain content of several organic acids and NH+4, AND ITS RELATIONship to the accompanying hypocapnia was studied in unanesthetized rats subjected to hypoxemia for periods ranging between 2 hours and 7 days. Under acute conditions, 'mild' hypoxemia (FO2 = 6--7%), these increases were greater and accompanied by increased gamma-aminobutyric acid (GABA) and decreased glutamic and aspartic acid levels; glutamine and NH+4 remained normal. When hypocapnia was prevented, 'severe' hypoxemia induced only a rise in GABA and slight elevations in lactic and alpha-ketoglutaric acid. During prolonged severe hypoxemia, the effects on the brain amino acids were maintained throughout, indicating that they are independent from the intracerebral pH which should progressively normalize. The effect on lactic acid gradually disappeared. The results show that during hypocapnic hypoxemia the rise in brain GABA is hypoxemia dependent, the decrease in glutamic and aspartic acid is hypocapnia dependent and the increase in lactic acid is in a large way alkalosis dependent.

Amino Acids↗
PubMed1977

Glutamate and glutamine in the brain of the neonatal rat during hypercapnia.

In order to study the influence of hypercapnia on the content of glutamate and glutamine in the developing brain, pregnant rats and their offspring were kept in CO2 rich (6-10%) atmosphere and the litters were killed at different ages between 4 and 28 days. In the hypercapnic rats the content of both amino acids in the brain increases with age with almost the same time course as in normocapnic rats. At any age the glutamate content is lower in the hypercapnic animals than in control rats, whereas the glutamine content, beyond the first 8 days of life is increased. Both effects are rapidly reversible on return to air breathing. Although the glutamate-glutamine system is in full development, the influence of hypercapnia can be compared to that observed in adult rats. Hypercapnia did not change the glutaminase and the glutamine synthetase activity of the brain.

Aging↗
PubMed1976

The CSF HCO3 increase in hypercapnia relationshp to HCO3, glutamate, glutamine and NH3 in brain.

To study the role of carbonic anhydrase in the CSF [HCO3] increase in respiratory acidosis and its effect on brain ammonia, anesthetized rats were subjected to hypercapnia (7% CO2) for 2 hours. The animals received periodic intraventricular injections of either 'mock' CSF or 'mock' CSF and acetazolamide for 45 minutes prior and during hypercapnia when: (a) plasma [HCO3-] was allowed to increase normally and (2) plasma [HCO3] increase was prevented by i.v. HC1 infusion, CSF [HCO3] increased 8.5 mM/L after 2 hours of hypercapnia (delta PCO2 40) in the rats with intraventricular 'mock' CSF injections, and only 6 mM/L in the animals with acetazolamide injections. CSF [HCO3-] increased 7 mM/L during hypercapnia and HCl infusion with intraventricular 'mock' CSF injections, but only 2 mM/L with acetazolamide injections. Changes in total brain CO2 (increase) and brain glutamic acid (decrease) in hypercapnia were not affected by intraventricular acetazolamide and i.v. HCl. The increase of brain NH4+ and glutamine in hypercapnia was reduced in these conditions. It is concluded that there are at least two sources for the CSF [HCO3-] increase in hypercapnia; one formed in the CNS and dependent on carbonic anhydrase, and the other derived from plasma [HCO3-] increase.

Acetazolamide↗
PubMed1976

Effect of variation in dietary NaCl intake on total and fractional renal blood flow in the normal and mercury-intoxicated rat.

We studied the effect of different chronic (3-4 weeks) dietary salt intakes on intrarenal hemodynamics of normal and mercury-intoxicated rats. Cardiac output (CO), total renal blood flow (RBF), and the zonal perfusion rate in the outer cortex (OC) and inner cortex (IC) were measured by the radioactive microsphere method. The distribution of cortical blood flow was calculated as the distribution index (DI), which reflects the ratio OC/IC. Rats were placed on a high salt diet (group I), intermediate salt diet (group II), or low salt diet (group III). For each group control rats (subgroup A) and mercury-intoxicated rats (subgroup B) were studied. No effect of the different salt intakes on the DI could be detected. The DI in group IA was 2.35 +/- 0.14; in IIA, 2.40 +/- 0.16; and in IIIA, 2.38 +/- 0.09 (P greater than 0.05). After mercury injection RBF changed from 5.32 +/- 0.36 ml/g.min(-1) (IIA) to 3.31 +/- 0.20 ml/g.min(-1), IIB and from 4.32 +/- 0.11ml/g.min(-1) (IIIA) to 1.98 +/- 0.10 ml/g.min(-1) (IIIB) P less than 0.01). The DI was lowered to 1.53 +/- 0.06 (IIB) (P less than 0.05) and to 1.16 +/- 0.10 (IIIB) (P less than 0.01). In both IIB and IIIB a marked elevation of the blood urea was noted (IIB = 97 +/- 9 MG/100 ML AND IIIB = 182 +/- 25 mg/100 ml). In group IB no effect on RBF, OC, IC, or DI could be observed (for all values, P greater than 0.05) despite similar histological renal lesions. Group IB rats also had normal blood urea levels (31 +/- 6 mg/100 ml;P greater than 0.05). We conclude (1) that variations in dietary salt intake appear to have no detectable effect on the intracortical blood flow distribution; and furthermore (2) that the mercury-induced acute renal failure (ARF) is characterized hemodynamically by a total renal and preferential outer cortical ischemia and that chronic salt loading prevents the ARF while preserving normal renal perfusion.

Acute Kidney Injury↗