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S Nitschkoff

Publications and source records attributed to S Nitschkoff.

At least 19 recordsLinked to original sources
PubMed1988

[Long-term hypotensive effects of substance P on the stress induced hypertension of primates].

The Substance P (SP) level in blood is lower in hypertensive individuals than in normotensive ones. Intravenous application of SP leaves the normotensive blood pressure largely unaffected, but decreases the enhanced blood pressure. Further studies on the effect of SP (i.v. application of 2.5 micrograms/kg b.w.) were performed on 26 primates; the results were as follows: With normotensive primates SP no effect on blood pressure. Upon repeated chasing and subsequent immobilization (load) the animals developed an arterial hypertension. Under the same load, the animals failed to develop hypertension if they were treated with SP 1 h before. A load-induced hypertension could be interrupted by injection of SP even after 3 weeks following initial load; the after-controls one year later revealed normotensive blood pressure values. Application of SP with two other animal groups with a manifest hypertonus lowered the blood pressure only transitorily. It is concluded that i.v. application of SP can prevent the development of stress-induced hypertension and, with existing manifest hypertension, leads to reduced blood pressure only transitorily. An indirect action with peripheral site of attack is assumed.

Animals↗
PubMed1983

[Hemodynamic changes after application of vasoactive substances in cats with unilateral renal artery constriction in addition to sinoaortal baroreceptor deafferentation].

The relationship between total peripheral resistance (TPR), cardiac output (CO) and venous return (VR) and their role in the response of mean arterial pressure (MAP) on intravenous adrenalin (10 micrograms/kg) and angiotensin II (0.5 micrograms/kg), resp., were investigated in normal cats (A), cats with unilateral renal artery stenosis (B) and cats with sinoaortal baroreceptor deafferentation (C). In the maximum MAP increase in group A there participated both TPR and VR through altered CO. In group B the MAP increased after angiotensin II only in consequence of an enhanced TPR, whereas the VR response was dampened; only after adrenalin the VR contributed a little to MAP increase through CO. In group C, the MAP increase after both substances was due exclusively to increased TPR; at a restricted ejection capacity of the heart the VR cannot act on the level of blood pressure.

Angiotensin II↗
PubMed1982

[Arterial hypertensive dysregulations on the basis of a cerebro-visceral stimulus constellation in baboons].

Basing on the hypothesis that disturbances of cerebral information processing on the basis of acute or chronic stress situations or profound neurotic alterations are being directed to the cardiovascular system only by predisposition to hyperreactivity, the influence of a psycho-nervous-humoral-hormonal stepped load schedule upon central nervous and vegetative functions was studied in baboons. Stochastic interventions into the natural day-night rhythm and application of NaCl and DOCA doses not per se causing a blood pressure rise, either single or in combination for altogether 3 years were used as disturbing factors. It has been revealed that experimental disturbance of the light-dark phases led to lasting deviations of the conditional-reflectory activity in the sense of a predominance of irritation processes. With motor response time, initially unchanged but from the second year of experiment significantly shortened by 35%, the failure rates at differentiation increased, on the average, from 6 to 45% and the intersignal responses by 100%. Even after exposure for several months, no disorders of the cardiovascular system occurred. It was only the coupling with an experimentally induced disturbance of electrolyte distribution that provoked a significant increase in mean arterial pressure, on the average, by 24% of the pre-control value with moderate increase of the circulating blood volume. The increases in free fatty acids and blood glucose concentrations by 14 and 23%, respectively, can be interpreted as additional hypertension-favouring factors. Despite an application of mineral corticoids for more than 1 year, it has been impossible to alter the contraction behaviour of the vascular smooth muscle cell in the sense of an experimentally induced predisposition to arteriolar hyperreactivity outlasting the discontinuation of disturbing factors. With higher nervous activity being clearly disturbed as before, the pressure got back to normal; testing the vascular reactivity to noradrenaline (1.0 microgram/kg b.w/min i.v., for 5 min) or angiotensin II (0.5 microgram/kg b.w. i.v.) at the end of the investigation period gave no enhanced pressure responses. By contrast, animals exposed exclusively to the described combination load for 18 weeks, showed a still normal system pressure and sensitivity to the applied noradrenaline and angiotensin II increased by 75-120% of the pre-control response. A liability of the cardiovascular system at acute stress situations (multiple partial immobilization) in long-term neurotically predamaged monkeys in the 24-h experiment was impressive by a cardiodepression during the nightly regeneration phase, reduced on the average by 35 beats/min against the control group. Thus, our results support the hypothesis of a cerebro-visceral pathoconstellation as the etiological principle of certain forms of the inhomogeneous clinical picture of primary hypertension.

Animals↗
PubMed1980

[New viewpoints on the pathophysiology and pathogenesis of arterial hypertension].

The pathophysiology and pathogenesis of the arterial hypertension can be explained from disturbances in the meshed regulating circle. Newer knowledge concerns the noradrenergic transformation of the excitation at the synapse. Concerning the humoral pressor systems we refer to the tonin-angiotensin-system, it is furthermore emphasized the disturbance in the sodium-potassium-transport on the membrane. The depressor systems -- prostaglandins, kallikrein-kinin-system -- will in future certainly bring newer knowledge concerning their participation in the pathogenesis of arterial hypertension. The practical importance of such findings should be taken into consideration in the formation of the long-term therapy of arterial hypertension.

Angiotensin II↗
PubMed1980

[Lightmicroscopic studies of plasma permeability at the blood brain barrier in experimental neurogenic interoreceptive hypertension of the rat (author's transl)].

The plasma permeation with its consequences on the nervous system was studied by means of an experimental neurogenic interoreceptive hypertension model. Out of 30 experimental animals (5 controls) showed 7 cerebral extravasations with blood pressure value ranging from 160--170 mm Hg within 4 and 8 weeks, respectively, as proved by Evans Blue injection or subsequent staining of the plasma with Luxol Fast Blue. The permeation sites were found hood-shaped on arterioles with a diameter of 15--30 micrometers, in multifocal arrangement with a certain preference for the frontal cerebral structures. The cerebral damages proved to be microinfarctions, mostly incompletely anemic necroses and forms of neuronal degeneration. Topical coincidence with extravasations is not always present. Further causal factors of cerebral lesions are discussed.

Animals↗
PubMed1978

[Histological findings at the aorta ascendens after measurement of blood flow with ultrasonic doppler technique in chronic experiments with rabbits (author's transl)].

Following implantation of an ultrasonic transducer in the aortic wall of the rabbit, media destructions and pressure necrosis were ascertained when the transducer was fitted closley around the vessel. When the transducer however was fitted widley around the vessel few departures from the normal structure were registered. After ultrasound stress 0.2--0.5 Watt/cm2 5 Min. per die with a mean exposition at 86.6 days, necrosis of the media and proliferations of the intima were noted in the area of the ultrasound application. When the transducer were not protected this resulted in sharp incisures of the vessels giving undeniable proof of ultrasound damages in spite of the low efficiency. Alltogether the histological findings show, that provided correct methodology vasal measurement of blood is possible in chronic experiments.

Animals↗
PubMed1978

[Vasal flow measurements at the aorta ascendens using the ultrasonic doubler technique in chronic experiments on rabbits].

The conditions under which flow measurements using the ultrasonic doppler technique can be successfully carried out at the Aorta ascendens in chronical experiments were studied in 25 normal rabbits. Pressure necroses of the vascular wall at agar-agar-gel coupling arise only if the implanted pick-off with its inner diameter is less than the outer diameter of the aorta + about 10%. The ultrasonic intensity permissible in a chronic experiment is only about 0.3 W/cm2. With the 13 implantations the animals were maximally usable for 86.6 days; 70% of them were killed in good health. In a beat-to-beat analysis were determined: (1) heart rate, (2) discharge duration, (3) maximal rate of discharge, (4) acceleration of blood flow, (5) deceleration of blood flow, (6) beat volume, (7) contraction force of the left ventricle, and (8) discharge resistance. The control recordings obtained over several months are on the average within normal limits.

Animals↗
PubMed1978

[Changes in noradrenaline-induced vasoconstriction through ouabain blockade of the transmembranal electrolyte distribution].

In continuation of their studies concerning changes in the reactivity of vascular segments under isolated perfusion in vivo with simultaneous experimental disturbance of transmembranous distribution of electrolytes, the authors investigated in ten rabbits the effect of noradrenaline in the ear with isolated circulation. After perfusion of an ouabain solution (total concentration: 0.4 X 10(-5) M), in dependence on the duration of the effect of glycoside the vasoconstrictor response to 0.1 and 0.5 micrograms noradrenaline was significantly strengthened, up to 40% of the initial value. After washing-out of the vascular segment under isolated perfusion with Krebs-Henseleit solution, and ensuing restoration of normal cation relationships, the vascular reactivity returned to its initial level. Potential analogous mechanisms of the etiology and pathogenesis of essential hypertension are discussed.

Animals↗
PubMed1977

[Changes of activity of alkaline phosphatase at the circulatory system in experimental hypertension of the rat (author's transl)].

Changes of activity of the alkaline phosphatase are investigated in the border of the outer media of vessels in two different models of hypertension (Goldblatt and Carotis-Sinus) in the rat. After onset of hypertension an increase of activity takes place in an area largely overlapping a necrosis of the outer medial region of the aorta. The formation of regenerated tissue leads to a thickening of the adventitia and to a decrease of the activities. Changes of the activities in the peripheral vessels presumably are due to participation of other factors. Indications to this effect are discussed.

Alkaline Phosphatase↗
PubMed1976

[Experimentally produced neurogenic-interoreceptive hypertension in the rat].

A hypertension characterized by systolic and diastolic blood pressure rises and increase in heart rate was produced in albino rats by excluding sino-aortal baroreceptors. Cardiac output and peripheral resistance, measured unter barbital narcosis, exhibited no significant changes in the development of hypertension. With the only exclusion of aortal baroreceptors there occurred almost the same blood pressure rises as with sino-aortal deafferentiation. It is concluded therefore that this kind of partial elimination of baroreceptors involving a simplified operational technique and lower risk will suffice for many problems being studied in hypertension research.

Animals↗
PubMed1976

[Reactivity of isolated arteries from hypertensive rabbits].

Isolated vessels (aorta thoracica, a pulmonalis, a. femoralis, a. renalis) of neurogenous-interoceptive and nephrogenous hypertensive rabbits showed a changed sensitivity to several vasoactive agents. An increased reactivity to noradrenaline, histamine, and serotonin in the aorta of neurogenous hypertensive rabbits, in the a. pulmonalis of neurogenous and renal hypertensive rabbits and in the a. femoralis of renal hypertensive animals in comparison with controls could be shown. Also registered was a hyperactivity to BaCl2 and KCl. All vessels of hypertensive rabbits were hyporeactive to angiotensin. They increased vascular reactivity was seen already in the 3rd week after removal of one kideny and pressoric receptors respectively. It is supposed that a "true supersensitivity" of the vascular smooth muscle cells of the hypertensive arteries does exist.

Angiotensin II↗
PubMed1975

[Biphasic effect of angiotensin II on conditioned reflectory reaction patterns in albino rats].

40 male albino rats were used to investigate the influence of one single i. v. dose of 10 ng/kg Angiotensin II upon established and stabilized conditional-reflectory response pattern (two-dimensional conditional-reflectory decision process and periodicities of conditional-reflectory processes). At normotonous blood-pressure values, Angiotensin II exerted a biphasic action on the conditional-reflectory response pattern. In the first phase of action (up to 30 min after injection) there prevailed centralnervous inhibition processes, while the second phase of action (30-70 min after injection) was marked by a general centralnervous excitation, which is reflected by extremely short times of response, and a pronounced sensitivity to optic, acoustic and tactile stimuli. The decision capacity of the animals was considerably reduced in both phases. The periodicities of conditional-reflectory processes (duration of periods in the minute range) are strongly disturbed in the first phase of action, and tend to normal in the second phase. Furthermore, Angiotensin II was found to have a selective, hierarchically ordered influence with regard to the duration and intensity of action. Thus, the information processing activity of the CNS underwent most pronounced changes. The centralnervous regulatory functions were less affected; the blood pressure regulation showed little and transient influence by Angiotensin II. In the discussion, the neurotropic and algogenic action of Angiotensin II, and the relation of the octapeptide effect with pathogenetic mechanisms of experimental neurotically induced hypertonia are dealt with.

Angiotensin II↗