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H Flohr

Publications and source records attributed to H Flohr.

At least 37 records · Page 2Linked to original sources
PubMed1992

The physiological and pathophysiological basis of glomerular permeability for plasma proteins and erythrocytes.

The barrier function of glomerular capillaries in vivo, which prevents the leakage of plasma proteins and cellular elements, depends on the basic morphological and electro-chemical fine structure of the glomerular capillary wall, and on a functional barrier maintained by components obtained from blood, which effect the definitive barrier against the leakage of plasma proteins and cellular elements. The functional component of the barrier may explain the variability and some of the phenomena known as functional proteinuria. A certain size and number of morphological "defects" are thought to represent the normal condition, but under pathological conditions they may increase in size and number, resulting in a shift to an increasing permeability for higher molecular mass proteins; also an increase of the size and number of larger defects may enable more red cells to pass the barrier compared with the normal condition. These defects are different from the minimal glomerular lesions which are due to charge defects in the glomerular capillary membrane, primarily the lamina rara interna and the lamina rara externa of the basement membrane.

Animals↗
PubMed1991

Role of the visual input in recovery of function following unilateral vestibular lesion in the goldfish. I. Short-term behavioural changes.

Vestibular compensation, i.e. the partial or complete recovery of function following lesion of a labyrinth, has been suggested to be based on a multisensory substitution process involving vestibular, visual and somatosensory information. Teleost fish would seem ideal subjects for testing this proposal, because equilibrium orientation in the intact animal is largely under the bimodal control of the vestibular and visual systems. The role of the visual input in the compensation of behavioural deficits elicited by hemilabyrinthectomy (HL) was studied in goldfish maintained over the first two postoperative hours under different lighting conditions. HL caused severe postural and locomotory symptoms, which were the same or similar under all lighting conditions. The rate at which the various deficits disappeared, however, was dependent not only on the presence of light but also on its direction of incidence. Animals maintained under overhead illumination reached the criterion of successful compensation (completion of 5-min continuous and unimpaired swimming) within 10 min, whilst under unilateral illumination (90 degrees to the vertical) the time to criterion was significantly increased; animals exposed to illumination from below or infra-red illumination showed little or no signs of compensation up to 2 h after HL. It is concluded (1) that the immediately postoperative stage of vestibular compensation in the goldfish represents an integral part of the recovery process, within which all observable deficits can be compensated with remarkable rapidity; and (2) that the visual input is both necessary and sufficient for the compensation of the immediately postoperative deficits. We term this early stage of recovery the 'acute' phase and consider it to be based on a visual substitution process, whereby the missing labyrinthine input to the (partially) deafferented vestibular neurons is functionally replaced by visual afferents.

Animals↗
PubMed1991

Role of the visual input in recovery of function following unilateral vestibular lesion in the goldfish. II. Long-term behavioural changes.

Previous behavioural studies in our laboratory have demonstrated that the visual input is both necessary and sufficient for the acquisition of the acutely compensated state following hemilabyrinthectomy (HL) in the goldfish. Here we examine the role of the visual input in the maintenance of the compensated state. Exposure of acutely compensated animals to illumination from below (IFB) or infra-red illumination (IRI) elicited a decompensation: whereas IRI was no longer effective 4 days after HL, the susceptibility to IFB disappeared slowly over a number of weeks. Exposure of acutely compensated animals to unilateral illumination (UI) induced a highly asymmetrical dorsal light response 1 day after HL: tilt towards the ipsilateral side was extreme, whilst tilt towards the contralateral side was similar to preoperative values. This pronounced side difference decreased rapidly over the next 3 days and then more slowly over the following weeks and months. The findings show (1) that the maintenance of the acutely compensated state is temporarily dependent not only on the presence of light but also on its direction of incidence; and (2) that the visual-vestibular integration governing posture and locomotion is strongly biased in favour of the visual input to the lesioned side during the early postoperative period and subsequently returns to near preoperative values. The present results are compatible with the hypothesis that acute vestibular compensation in the goldfish is based on a visual substitution process. The latter is not permanent, however, the chronic course of compensation being characterized by a progressive decrease in reliance on visual cues. The observed changes in visual-vestibular integration with time are assumed to reflect modifications in inter- and/or extra-vestibular commissural systems by which the intact labyrinth gradually strengthens its control over the deafferented nuclear complex.

Animals↗
PubMed1991

Molecular mechanisms of brainstem plasticity. The vestibular compensation model.

Vestibular compensation is the process of behavioral recovery that occurs following unilateral deafferentation of the vestibular nerve fibers (unilateral labyrinthectomy, UL). Since UL results in a permanent loss of vestibular input from the ipsilateral vestibular (VIIIth) nerve, vestibular compensation is attributed to CNS plasticity and has been used as a general model of lesion-induced CNS plasticity. Behavioral recovery from the ocular motor and postural symptoms of UL is correlated with a partial return of resting activity to neurons in the vestibular nucleus (VN) on the deafferented side (the "deafferented VN"), and lesions to the deafferented VN prevent compensation; therefore, the regeneration of resting activity within the deafferented VN is believed to have a causal role in vestibular compensation. The biochemical mechanisms responsible for the adaptive neuronal changes within the deafferented VN are poorly understood. Neuropeptide hormone fragments, such as adrenocorticotrophic hormone (ACTH)-4-10, have been shown to accelerate vestibular compensation and can act directly on some VN neurons in vitro. Antagonists for the N-methyl-D-aspartate (NMDA) receptor have been shown to inhibit vestibular compensation if administered early in the compensation process. Biochemical studies in frog indicate marked alterations in the phosphorylation patterns of several proteins during compensation, and the in vitro phosphorylation of some of these proteins is modulated by ACTH-(1-24), calcium (Ca2+), and calmodulin or protein kinase C. It is therefore possible that ACTH fragments and NMDA antagonists (via their effects on NMDA receptor-mediated Ca2+ channels) modulate vestibular compensation through their action on Ca(2+)-dependent pathways within VN neurons. Recent studies have shown that some Ca2+ channel antagonists and the Ca(2+)-dependent enzyme inhibitor calmidazolium chloride facilitate vestibular compensation. How the regulation of Ca2+ may be related to the neuronal changes responsible for vestibular compensation is unclear at present.

Adrenocorticotropic Hormone↗
PubMed1985

[Not Available].

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Biology↗
PubMed1984

A reevaluation of intervestibular nuclear coupling: its role in vestibular compensation.

Recent experimental observations indicate that pathways interconnecting the bilateral vestibular nuclei (VN) may provide positive-feedback loops for signals across the midline. The implications of such positive feedback are considered in the context of vestibular compensation. A simple conceptual model of the interconnected VN is studied analytically, based on the hypothesis that the restoration of central symmetry is achieved via changes of neural gain in closed commissural loops. A wide variety of experimental conditions related to vestibular compensation are investigated. Analytic model predictions are compared to behavioral and neurophysiological findings in the literature. The results show that organized control over commissural gains in closed loops coupling the bilateral VN is fully compatible with all phenomena cited in the article. In particular, such a mechanism for vestibular compensation can reconcile observations such as the fact that Bechterew phenomena and decompensation can both be elicited from the compensated state. Placing the site of vestibular compensation in pathways linking the VN has many implications. Other forms of central neural plasticity (e.g., vestibuloocular reflex (VOR) gain plasticity) may rely on a similar principle, since modulation of transmidline coupling can be a very powerful means of altering responses in a bilateral nervous system.

Animals↗
PubMed1982

Effects of ACTH4-10 on vestibular compensation.

ACTH4-10, a fragment of the adrenocorticotropic hormone (ACTH) molecule, has marked effects on the compensation process following unilateral labyrinthectomy. In Rana temporaria ACTH4-10-treatment (5-250 micrograms/kg) influences both the acquisition and the maintenance of the compensated state. The compensation process is slowed down by hypophysectomy but can then be restored by the administration of ACTH4-10. It is concluded that ACTH-like neuropeptides might physiologically be involved in the plastic processes underlying functional recovery from CNS lesions.

Adrenocorticotropic Hormone↗
PubMed1982

[Aprotinin-ACD-blood. II. The effect of aprotinin on the release of cellular mediators and enzymes in banked blood (author's transl)].

The concentration of the toxic mediators histamine and serotonin as well as the activity of lactate-dehydrogenase and alkaline phosphatase in banked blood increase significantly during storage. After initial addition of Aprotinin to ACD-Blood the level of these substances remained almost in normal range. The influence of these toxic mediators on the development of shock lung is discussed.

Alkaline Phosphatase↗
PubMed1981

Influence of cholinomimetics and cholinolytics on vestibular compensation.

The influence of cholinomimetics and cholinolytics on vestibular compensation was investigated in Rana temporaria. In compensated animals cholinomimetics induced a complete decompensation with reappearance of all symptoms characteristic of the precompensated state. Cholinolytic exerted antagonistic effects. They induced postural and locomotor symptoms which were a mirror-image of those observed in the precompensated state. The findings support the assumption that the compensatory reorganization of the vestibular system involves the modification of cholinergic brain stem synapses.

Animals↗
PubMed1976

Regional distribution of vascular resistance in two models of experimental renovascular hypertension.

The regional distribution of the peripheral vascular resistance was studied in normotensive and hypertensive Wistar rats. Two models of experimental hypertension were investigated: (I) in 32 animals the right renal artery was constricted by a silver clip (two-kidney Goldblatt hypertension); (II) in 46 animals the left kidney was removed and the right renal artery was clipped as in the first group (one-kidney Goldblatt hypertension). The normotensive control group comprised 61 untreated animals of the same strain and age. The distribution of cardiac output to 14 tissues was determined by means of the particle distribution technique. The resistance was increased in all regions investigated, a decreased or unchanged resistance was not observed. For most of the investigated tissues the regional resistance was increased exactly in proportion to the total peripheral resistance (TPR). Exceptions to this were found in 2 regions where the change of local resistance deviated from that of TPR: the splanchnic area and the skeletal muscle. In both cases the 2 models differed from each other. In the two-kidney model the increase of resistance in the splanchnic circulation was more intense than in other organs. In contrast, in the one-kidney model the local change of resistance was less than that of TPR. The change of skeletal muscle resistance was not significantly different from the change of TPR in the two-kidney model, while in the one-kidney model the increase of local resistance was significantly higher than that of TPR. It is concluded that the etiology of the abnormal resistance is different in the 2 models investigated and that known extrinsinc pressor factors may play a role in the two-kidney, but not in the one-kidney Goldblatt hypertension.

Abdomen↗