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Biomedical subjects

H Geiger

Publications and source records attributed to H Geiger.

At least 73 records · Page 4Linked to original sources
PubMed1994

Posterior fossa neurovascular anomalies in essential hypertension.

Intraoperative observations, necropsy, and angiographic studies support the presumption that neurovascular compression of the left ventrolateral medulla may cause neurogenic hypertension. Pulsatile irritation of the ventrolateral medulla at the root-entry zone of cranial nerves IX and X increases blood pressure in animals. To identify and assess the distribution of neurovascular compression at the ventrolateral medulla in human beings, we did a prospective single-blind study in 24 patients with essential hypertension, in 14 patients with renal hypertension, and in 14 normal subjects. To detect neurovascular compression, we used axial and coronal double-echo and magnetic-resonance angiography sequences. Blood pressure control and duration of hypertension were not different in the two groups of patients. 20 patients with essential hypertension had magnetic tomographic evidence of left-sided neurovascular compression at the ventrolateral medulla; 2 patients with renal hypertension and 1 of the normal subjects had a positive finding on the left. On the right side, we found signs of neurovascular compression in 4 patients with essential hypertension, in 4 with renal hypertension, and in 2 of the normal subjects. With magnetic resonance tomography, it is possible to evaluate the neurovascular relations in the posterior fossa and detect neurovascular compression at the ventrolateral medulla. These data in living subjects give further evidence of an association between neurovascular compression at the left ventrolateral medulla and essential hypertension.

Adult↗
PubMed1994

Vascular angiotensin and the sympathetic nervous system: do they interact?

We tested the hypothesis that local vascular formation of angiotensin (ANG) II and the sympathetic nervous system potentiate each other. Isolated rat hindquarters were perfused with an artificial medium, and ANG I and II release was measured by high-performance liquid chromatography and radioimmunoassay. Electrical stimulation of the lumbar sympathetic chain (0.5, 2, and 8 Hz) did not affect vascular ANG release in Sprague-Dawley (SD) rats. Hypertensive, ren-2 transgenic (TG+) rat hindquarters released significantly more ANG I (110 +/- 19 vs. 65 +/- 21 fmol/30 min in SD rats) and ANG II (235 +/- 22 vs. 140 +/- 30 fmol/30 min); however, nerve stimulation did not alter ANG release in TG+ rats. Captopril inhibited vascular ANG II release by 90%, but neither captopril nor ANG II receptor blockade by losartan affected the pressor response to nerve stimulation in SD and TG+ rats. Isoproterenol failed to increase either vascular ANG release or pressor response to nerve stimulation in SD or spontaneously hypertensive rat hindquarters. Exogenous renin, which increased vascular ANG release approximately 100-fold, prolonged the pressor responses to nerve stimulation. We conclude that the vascular renin-ANG system does not interact with the sympathetic nervous system locally. However, high concentrations of ANG II, which can be induced by circulation-derived renin, may prolong the duration of sympathetic nerve-induced vasoconstriction.

Adrenergic beta-Agonists↗
PubMed1994

Impaired cardiovascular reflexes precede deoxycorticosterone acetate-salt hypertension.

We hypothesized that impaired cardiopulmonary reflexes but not altered baroreceptor reflexes precede deoxycorticosterone acetate (DOCA)-salt hypertension. Uninephrectomized rats were given either DOCA and 0.9% NaCl as drinking water, 0.9% NaCl alone, or tap water. We measured mean blood pressure, heart rate, and renal sympathetic nerve activity. After 8 days, mean blood pressure was not different in DOCA-salt and control rats. Volume-sensitive cardiopulmonary reflexes were tested by intravenous volume loading with saline (10% body weight in 15 minutes), which decreased renal sympathetic nerve activity without changing mean blood pressure or heart rate. This response was blunted in DOCA-salt rats. Chemosensitive cardiopulmonary reflexes were tested by 15-minute infusions of the serotonin 5-HT3 agonist phenylbiguanide, which decreased renal sympathetic nerve activity without changing mean blood pressure or heart rate. Sustained decreases in renal sympathetic nerve activity occurred during phenylbiguanide infusion in controls but were blunted over time in DOCA-salt rats. The arterial baroreflex responses to graded infusions of methoxamine and nitroprusside were analyzed by sigmoidal curve fitting. There were no differences in gain of renal sympathetic nerve activity or heart rate between the groups. Thus, DOCA-salt rats exhibit impaired cardiopulmonary reflexes before the onset of hypertension; the volume-sensitive reflexes are more severely affected than chemosensitive reflexes. The arterial baroreceptor reflex is unaltered. The decreased sensitivity of cardiopulmonary reflexes may contribute to DOCA-salt hypertension.

Analysis of Variance↗
PubMed1993

Effect of ACE inhibitors on atrial natriuretic factor in the brains of rats with reduced renal mass.

We tested the effect of renal insufficiency, with and without angiotensin (Ang) converting enzyme (ACE) inhibition, on blood and brain atrial natriuretic factor (ANF) in rats. Two ACEs, one which penetrates into the CNS and one which does not, were used to distinguish between peripheral and central ACE effects. Rats underwent 5/6 nephrectomy (5/6-NPX) by ligation of renal arterial branches. After seven days, 28 5/6-NPX rats received lisinopril 20 mg/kg/day and 28 5/6-NPX rats received quinapril 30 mg/kg/day orally for five days, while 28 5/6-NPX control rats and 28 sham rats did not. Body weight, blood pressure, drinking and urine volume were monitored. At sacrifice, urine, plasma, and brain tissue was collected. ANF in 16 brain areas was measured by radioimmunoassay. 5/6-NPX resulted in increased blood pressure, increased urine volume, proteinuria, and increased drinking. Both ACEs lowered blood pressure to sham values and decreased proteinuria. Both ACEs increased plasma renin activity and decreased plasma ANF. However, only lisinopril decreased drinking and urine volume. 5/6-NPX increased ANF values in six brain areas, namely the periventricular preoptic nucleus, the arcuate nucleus, the perifornical nucleus, the periventricular hypothalamic nucleus, the paraventricular nucleus, and the dorsal raphe nucleus compared to sham rats. These same increases in brain ANF were also observed in 5/6-NPX rats given quinapril, compared to shams. However, lisinopril lowered ANF to sham levels in the periventricular preoptic nucleus, the arcuate nucleus, and the perifornical nucleus. In the three additional brain areas, namely the periventricular hypothalamic nucleus, the paraventricular nucleus, and the dorsal raphe nucleus, lisinopril did not effect the elevated ANF concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Early interstitial changes in hypertension-induced renal injury.

To elucidate the mechanisms of hypertensive renal injury, we investigated the time course and extent of changes in matrix composition, as well as cell proliferation and infiltration in two-kidney, one clip rats. The nonclipped kidneys from hypertensive and sham-operated control rats (n = 5 to 10 in each group) were studied at 7, 14, 21, and 28 days after clipping. Systolic blood pressure was elevated by day 7 (154 +/- 3 versus 111 +/- 4 mm Hg in sham group, P < .001, n = 10 each). Hypertension resulted in an early expansion of the interstitial volume by 37%, whereas hypertensive vascular changes and glomerular injury did not become evident until day 21. Immunofluorescence studies revealed an early interstitial accumulation of collagens I, III, IV, V, VI, and fibronectin by day 7. In contrast, the glomeruli showed a mild to moderate increase in collagens I, III, IV, V, laminin, and fibronectin but not collagen VI later in the established phase of hypertension. Staining for proliferating cell nuclear antigen as a marker of cell replication was increased in tubular epithelial but not interstitial or glomerular cells. A progressive infiltration of macrophages (16 +/- 2 versus 9 +/- 1 ED1+ cells/mm2, P < .05, n = 6) and T lymphocytes (93 +/- 15 versus 74 +/- 7 CD4+ cells/mm2, n = 8) in the cortical interstitium had already occurred by day 7. On the other hand, only macrophages increased in number within the glomeruli. Thus, renovascular hypertension leads to an early tubular cell proliferation, mononuclear cell recruitment, and deposition of matrix proteins primarily within the interstitium. We conclude that the injury producing nephrosclerosis in this model extends far beyond the glomeruli. Both the tubules and the interstitium are actively involved and may be the more important initial sites of injury.

Animals↗
PubMed1993

[Is hyperlipidemia a factor in the progression of renal failure?].

Many experimental results support the hypothesis that increased plasma lipid concentrations may have a deleterious effect on the course of chronic renal diseases. Until now a clear causal relationship has not been proved. Because reliable results of prospective controlled trials are not available that would demonstrate a beneficial effect of lipid-lowering interventions on the course of chronic renal diseases, it is not possible at this time to provide a general recommendation for a lipid-lowering drug therapy. Nevertheless, I would support the prescription of HMG CoA reductase inhibitors for patients with extremely increased total cholesterol and LDL cholesterol concentrations despite the restricted data of already existing experimental and clinical studies. It should be stressed that every patient with glomerular disease and concomitant hyperlipidemia constrains us to weigh advantages and side-effects of a lipid-lowering regimen. We have to wait for the results of prospective and controlled multicenter studies to give a final recommendation for therapeutic consequences in patients with chronic renal disease and hyperlipidemia.

Animals↗
PubMed1992

Kaempferol-3-O-glucosyl(1-2)rhamnoside from Ginkgo biloba and a reappraisal of other gluco(1-2, 1-3 and 1-4)rhamnoside structures.

A kaempferol-3-O-glucorhamnoside from Ginkgo biloba is defined as the 3-O-alpha-L-[ beta-D-glucopyranosyl(1-2)rhamnopyranoside] on the basis of 2D NMR evidence. Complete assignments of the 1H and 13C NMR spectra of this compound and of its known p-coumaroyl derivative are presented for the first time. The NMR distinctions of 1-2, 1-3 and 1-4 linked glucopyranosylrhamnopyranosides are discussed and indicate (i) that the 13C NMR assignments for one published gluco(1-3)rhamnoside are in need of modification, (ii) that the published structure of hordenine-O-[6-O-t-cinnamoyl-beta-glucosyl(1-4)-alpha-rhamnoside] from Selaginella doederleinii is not distinguished from the 1-3 linked glucorhamnoside structure, and (iii) that the 8-prenylkaempferol-3-O-[glucosyl(1-4)rhamnoside]-7-O-glucoside and the equivalent 4'-O-methylated xylosyl(1-4)rhamnoside from Epimedium pubescens and E. washanense, respectively, are (1-2)-linked.

Carbohydrate Sequence↗
PubMed1992

Alterations in brain atrial natriuretic polypeptide levels in hypophysectomized rats.

Twelve days after hypophysectomy depleted atrial natriuretic polypeptide (ANP) concentrations were measured in the plasma and in 8 of 18 microdissected brain nuclei of rats. Reduced ANP levels were found in brain structures (subfornical organ, organum vasculosum laminae terminalis, preoptic and hypothalamic periventricular nuclei, paraventricular nucleus, lateral hypothalamic area), which are directly involved in the central regulations of salt and fluid homeostasis, as well as in the medial amygdaloid nucleus and the locus ceruleus. ANP concentrations in the median eminence, medial preoptic and arcuate nuclei did not alter by hypophysectomy. Elevated ANP concentrations were measured only in the supraoptic nucleus of hypophysectomized rats.

Amygdala↗
PubMed1992

Parathyroid hormone modulates the release of atrial natriuretic peptide during acute volume expansion.

In this study we investigated the effect of volume expansion on plasma and atrial concentrations of atrial natriuretic peptide (ANP) in the presence and absence of the parathyroid gland and under normocalcemic and hypocalcemic conditions. After volume expansion ANP concentration in plasma was significantly (p < 0.001) higher in intact (702 +/- 86 pg/ml) than in hypocalcemic parathyroidectomized (PTX) (271 +/- 38 pg/ml) rats. Plasma ANP of PTX rats rendered normocalcemic with oral calcium supplementation increased to 402 +/- 85 pg/ml after volume expansion. Results from this study suggest that parathyroid hormone (PTH) is required for augmented ANP secretion in response to acute volume loading and alterations of extracellular calcium may modulate volume-induced ANP release in PTX rats. We would discuss that a parathyroid gland-cardiac atria interaction exists and that changes in serum level of PTH may play a role in the regulation of fluid homeostasis via ANP secretion.

Animals↗
PubMed1992

Effect of antihypertensive therapy on the progression of non-diabetic renal disease.

There is a clear, inverse association between the level of blood pressure and the progression of renal disease. This association appears to extend well within the "normotensive" blood pressure range. Currently, there are no absolutely incontrovertible data from prospective, randomized trials in humans documenting that high blood pressure is the cause of an accelerated loss of GFR, or that the loss in renal function can be prevented by lowering blood pressure below 140/90 mmHg. Nevertheless, an aggressive lowering of blood pressure in patients with hypertension and renal disease seems reasonable and desirable. First, the control of blood pressure lowers the "all causes" risk of cardiovascular morbidity and mortality in all patients with elevated blood pressure. Second, any detrimental effects on GFR are uncommon or transient in these patients. Third, the beneficial effects on GFR are firmly supported in animal studies and in humans with malignant hypertension. Fourth, a growing body of evidence from human trials supports the inverse correlation between blood pressure and decrease in GFR, even below a level of 140/90 mmHg. The evidence for these conclusions is reviewed.

Antihypertensive Agents↗
PubMed1992

Effects of angiotensin-converting enzyme inhibition in diabetic rats with reduced renal function.

To test the effect of converting enzyme inhibition (CEI) on diabetes, with or without renal insufficiency, we studied streptozotocin-induced diabetic rats, with or without reduced renal mass, which were treated with insulin in sufficient amounts to maintain glucose values in the mild to moderately hyperglycemic range. We found that diabetes increased glomerular filtration rate (GFR) (inulin clearance, 2.3 +/- 0.5 ml/min vs 1.9 +/- 0.1 ml/min; p < 0.05) and blood pressure (137 +/- 15 mm Hg vs 116 +/- 6 mm Hg; p < 0.05) but did not increase plasma atrial natriuretic peptide (ANP) values, when compared with control rats (72 +/- 38 vs 68 +/- 24 pg/ml). CEI decreased GFR and blood pressure to control values. In rats with diabetes and concomitantly reduced renal mass, hypertension, elevated ANP values, proteinuria, and glomerulosclerosis were prominent features. CEI was associated with reduced blood pressure (172 +/- 17 mm Hg vs 138 +/- 15 mm Hg; p < 0.05), without a concomitant decrease in GFR (1.1 +/- 0.1 ml/min vs 1.1 +/- 0.1 ml/min). Further, CEI reduced the elevated ANP values (140 +/- 34 pg/ml vs 66 +/- 19 pg/ml; p < 0.05) to those of control rats. CEI reduced proteinuria by 50% and ameliorated the histopathologic changes. In separate experiments, rats with 5/6th nephrectomy and hypertension but without diabetes were also found to have elevated ANP levels that decreased to control values with CEI. The data speak for a renal protective effect of angiotensin I-converting enzyme inhibition in this model but do not support a specific role for ANP in the model of diabetes with concomitantly reduced renal mass.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

Biochemical assessment and clinical evaluation of a bilirubin adsorbent column (BR-350) in critically ill patients with intractable jaundice.

We investigated the efficacy of an anion-exchange adsorbent column (ASAHI BR-350, DIAMED) for removal of bilirubin and bile acids in five patients with intractable jaundice of various origin. Four litres of plasma were separated by membrane plasma separation (Plasmaflow OP-05) at a rate of 22.5 ml/min. The plasma was then perfused through an anion exchange adsorbent and returned to the venous blood line of the plasma separation. In some of the patients this procedure was combined with regular hemodialysis treatment. The concentration of total bilirubin was cut by 31 to 60%; total bile acids were reduced by 20 to 74%. Three patients recovered and had a favourable outcome. Two patients died despite the bilirubin adsorption treatment. The effects of the adsorbent column on specific blood parameters, including the coagulation system, were measured. Our data suggest that bilirubin adsorption should be examined further as a treatment for critically ill patients with intractable jaundice.

Adsorption↗