PubMed HealthSearch

Biomedical subjects

W Kuschinsky

Publications and source records attributed to W Kuschinsky.

14 recordsLinked to original sources

Unimportance of perivascular H+ AND K+ activities for the adjustment of pial arterial diameter during changes of arterial blood pressure in cats.

The role of perivascular H+ and K+ in the adjustment of pial arterial diameter during changes in arterial blood pressure was investigated in chloralose anesthetized cats. Blood pressure was reduced by i.v. mecamylamine or pentolinium and was increased by i.v. hypertensin. Pial arterioles and arteries with a control diameter ranging from 37--218 microns at a spontaneous mean arterial blood pressure of 128 +/- 16 (SD) mm Hg were studied. Vascular diameter as measured by TV image splitting showed the typical reactions, i.e. constriction during increase (up to 200 mm Hg) and dilation during decrease in blood pressure (down to 60 mm Hg). Perivascular H+ and K+ activities were measured using pH microelectrodes (Hinke type) and K+ ion exchanger microelectrodes, respectively. Under control conditions perivascular pH was 7.25 +/- 0.11 (SD) and K+ activity was 2.46 +/- 0.65 (SD) mM, respectively. During changes in blood pressure the vascular reactions of pial arteries were not accompanied by significant alterations in perivascular H+ or K+ activity. From these data it can be concluded that mechanisms other than those which are mediated by H+ or K+ are involved in the adjustment of pial arterial diameter during changes in arterial blood pressure.

Angiotensin II

Measurements of the perivascular PO2 in the vicinity of the pial vessels of the cat.

PO2's in the environment of the pial micro-vessels of the cat were measured using recessed tip oxygen microelectrodes. Measurements were made on the surface of vessels with internal diameters ranging from 200 micrometers to 22 micrometers. Blood oxygen partial pressures were also measured inside these vessels by penetrating the vessels with sharpened electrodes. Both intravascular and extravascular PO2 values decreased progressively from the large arterial vessels down to the small arterioles. The observed values of intravascular PO2 showed a systematic longitudinal decrease from 98.5 +/- 10.7 (SEM) mm Hg in the largest vessels down to 72.6 +/- 3.6 mm Hg in the smallest vessels. In addition to the longitudinal gradient, a transmural gradient was observed across the walls of the microvessels. The difference between blood PO2 and vessel surface PO2 was 27.0 +/- 2.5 mm Hg in the largest vessels and 6.0 +/- 2.2 in the smallest. The mean wall thickness in these groups of vessels were 27.0 +/- 1.5 and 7.5 +/- 0.8 micrometers respectively. Measurements of the minimum tissue PO2 on the exposed surface of the cortex yielded a value of 25.4 +/- 6.6 mm Hg. Systemic arterial partial pressure of oxygen averaged 94.7 +/- 4.7 mm Hg. The data indicate that significant gradients for oxygen exist both longitudinally and radially in association with the pial vessels. The longitudinal gradients represent losses of oxygen from the precapillary vessels. The transmural gradients are apparently the result of both consumption by the microvessel wall and diffusional gradients due to oxygen flux into the extravascular space.

Animals

Perivascular pH and pial arterial diameter during bicuculline induced seizures in cats.

The aim of the present study was to correlate locally at the same pial artery the vascular reaction with the perivascular pH during the initial phase of functional hyperemia. As a model of functional hyperemia, bicuculline (3 mg/kg i.v.) induced seizure was taken. Normally, a strong increase of blood pressure occurs together with the start of seizure. Since a discrimination between metabolically induced and pressure dependent vascular reactions is not possible under such conditions, the cats (anesthetized with 40--50 mg/kg chloralose) received in addition 3 mg/kg phentolamine and 10 mg/kg pentobarbital. Under these conditions a significant increase of blood pressure started only 50 s after the onset of seizure. Perivascular pH was recorded using spear type pH microelectrodes in the subarachnoid space surrounding a pial artery. The diameter of the respective artery was measured continuously. After onset of seizure an immediate, increasing perivascular acidosis developed which was accompanied by an increase in pial arterial diameter. The maximal decrease of pH was 0.29 units and occurred 30 s after the start of seizure. These data show that a decrease in perivascular pH can be one factor mediating functional hyperemia in the brain.

Acid-Base Equilibrium

The dilating effect of histamine on pial arteries of cats and its mediation by H2 receptors.

We studied the effect of histamine and H1 or H2 blockers on the diameter of pial arteries (39-227 micron) using microapplication into the perivascular space. Concentration-response curves for histamine showed dilations which started at 10(-7) M and were maximal at 10(-5) and 10(-4) M. The H2 blocker, cimetidine, induced no vascular reaction over the whole concentration range tested (10(-7) to 10(-3) M). The H1 blocker, mepyramine, was not vasoactive in the concentration range from 10(-7) to 5 X 10(-5) M and evoked dilations at higher concentrations. The concentration-response curve for histamine was only slightly displaced by 10(-5) M mepyramine but was significantly shifted to the right by 10(-5) M cimetidine. The dilating effect of histamine could be reduced in a stepwise manner by increasing concentrations of cimetidine. These findings are in accordance with a selective antagonism between histamine and cimetidine at the H2 receptors of smooth muscle cells of pial arteries. The insignificant role of H1 receptors in histamine-induced dilations is supported by the finding that a combination of H1 and H2 blockers resulted in the same reduction of histamine-induced dilation as did the application of the H2 blocker.

Animals

The use of microelectrodes for measurement of local H+ activity in the cortical subarachnoidal space of cats.

pH microelectrodes with pointed tip (Hinke-type) were constructed for the continuous measurement of the local pH in the perivascular space of pial arteries in the feline cerebral cortex. The sensitive tip had a length of 20-60 mu and a base diameter of 10-25 mu. As reference electrode, a micropipette (tip diameter 2 mu), filled with 150 mM KCl was used. Calibration curves were linear and showed a sensitivity of 54.5-57.5 mV/pH unit at 38 degrees C. Advantages of such electrodes are the easy penetration of the subarachnoid membrane, the long life span, the quick response, and a minimal drift. The electrodes were tested in vivo during hyper- and hypoventilation and during local perivascular injection of mock spinal fluid at varying pH. A close correlation was observed between the change in perivascular pH and the corresponding change in pial arterial diameter.

Animals

Influence of H+ on K+ on adenosine-induced dilatation at pial arteries of cats.

The influence of changes in the perivascular K+ and H+ concentrations upon adenosine-induced dilatations of pial arteries was investigated by localized perivascular application using micropuncture technique. Adenosine (10(-9)-10(-3) M) was dissolved in mock spinal fluids with varying bicarbonate and potassium concentrations (5 and 22 mM HCO3-, and 6 and 10 mM K+). Concentration response curves revealed that adenosine induced the same change in pial arterial diameter when dissolved either in an inert (11 mM HCO3-) or in a constrictory (22 mM HCO3-) mock spinal fluid. However, adenosine, when dissolved in a more acidic or higher potassium-containing solution (5 mM HCO3-, or 6 or 10 mM K+) produced a diminished dilatatory effect. It is concluded that, for a quantification of the individual contributions of several metabolic factors in the regulation of vascular resistance, it is necessary to consider their interactions.

Adenosine

The dilatatory action of adenosine on pial arteries of cats and its inhibition by theophylline.

The effect of adenosine upon pial resistance vessels was studied using local microapplication from the perivascular side and measurement of vascular diameter. Concentration-response curves revealed a concentration-dependent dilatatory effect of adenosine between 10(-7) and 10(-3) M. The degree of dilatation was independent of initial vessel size (47-260 mu). The dilatations due to adenosine could be reduced by theophylline in a reversible competitive antagonism. Concentration-response curves for theophylline yielded no vascular reaction at concentrations of up to 10(-5) M theophylline. From these data is is concluded that the pial arterial resting tone is not influenced under our experimental conditions by adenosine formed and released by brain tissue. The dilatations measured at high theophylline concentrations are apparently due to a mechanism different from the adenosine antagonism.

Adenosine

Alpha-receptor stimulation by endogenous and exogenous norepinephrine and blockade by phentolamine in pial arteries of cats.

The question regarding the existence of an alpha-adrenergic component of pial arterial tone was investigated using a microapplication technique combined with the measurement of vascular diameter. Concentration-response curves for the alpha-receptor blocker, phentolamine, revealed no vascular reaction for a concentration range from 2.5 x 10(-11) to 2.5 x 10(-7) M. At higher concentrations (up to 1.3 x 10(-3) M) concentration-dependent dilations were observed. Constrictions of pial arteries induced by perivascular injection of 2.5 x 10(-6) M norepinephrine could be reduced by 38% and 73% when phentolamine was applied simultaneously in concentrations of 2.5 x 10(-7) and 2.5 x 10(-6) M, respectively, whereas constrictions due to 2.5 x 10(-4) M norepinephrine were not reduced by 2.5 x 10(-6) M phentolamine, indicating a competitive antagonism between norepinephrine and phentolamine for pial arteries. Stimulation of the cervical sympathetic chain (90 seconds, 10 v, 1.4 msec, 20 Hz) induced constrictions of pial arteries (mean 12%) which could be reduced by two-thirds during the simultaneous application of 2.5 x 10(-7) M phentolamine. Since the constriction induced by norepinephrine applied exogenously or released endogenously could be reduced by a concentration of phentolamine which had no vascular effect per se, we conclude that the resting tone of the pial arteries is not influenced by an alpha-adrenergic component under our experimental conditions. The dilations induced by high concentrations of phentolamine are believed to be nonspecific.

Animals