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Biomedical subjects

L Vacek

Publications and source records attributed to L Vacek.

At least 19 recordsLinked to original sources
PubMed1994

[Protective effect of carvedilol on renal circulation and tissue injury in reperfusion of ischemic kidneys in rats].

In one-kidney rats the resting blood flow in the renal artery was recorded for 10 minutes then the artery was clipped for one hour and the following reperfusion blood flow was registered again for 10 minutes. The animals were divided into three groups: Series A, untreated control animals. Series B, two weeks before renal ischemia the rats were fed a diet containing 0.1% of BM-14.190, a derivate of carvedilol. Series C the rats received a diet with 0.1% of carvedilol. The resting renal blood flow was 4.58 +/- 0.13 ml/min (x +/- S.E.M.) in series A whereas 6.36 +/- 0.41 ml/min. in series B and 5.87 +/- 0.59 ml/min. in series C (p < 0.01), also the reperfusion blood flow in series B and C was significantly higher (p < 0.01) i.e. 3.65 +/- 0.25 ml/min. and 3.08 +/- 0.33 ml/min. respectively than in series A, 1.08 +/- 0.13 ml/min. The ischemia and the ensuing reperfusion elicited in series A serious injury, especially in renal proximal tubules and their reticulin skeleton whereas the renal injury in series B and C was of a markedly lesser degree. Carvedilol and its derivate BM-14.190 possess beside vasodilatory potency and alpha- and beta-adrenoceptor blocking activity a potent scavenger property. This may be the cause of the protective effect preventing the ischemia and reperfusion injury in the renal tissue.

Animals↗
PubMed1993

[Endothelial cells in tumors of the rectum and large intestine].

In 40 controls and 102 patients with tumours of the rectum and large intestine the number of circulating anuclear cell residues of endothelial cells was investigated. The number of these endothelia in the blood of patients was significantly higher (p < 0.001) than in healthy subjects. After successful surgery of the tumour and subsequent chemotherapy the number of endothelia in venous blood reached normal levels with in 1-2 months. Conversely in patients where despite surgery secondaries were detected in other organs, the number of endothelia remained elevated.

Colonic Neoplasms↗
PubMed1989

Regional differences of cardiovascular effects of diltiazem in the rat.

The dose-response relations of the central and peripheral effects of diltiazem were studied in 26 anaesthetized rats. Measured were the heart rate (HR), atrioventricular conduction time (PR), mean arterial blood pressure (BP), carotid and renal blood flow (Fc, Fr) and the corresponding relative regional resistance (RRc, RRr). The effects were evaluated by their maxima regularly reached 15-20 s after the i.v. bolus administration. The minimum dose which produced a significant HR decrease and PR prolongation were 0.4 and 2.0 mg/kg, respectively. In the mg/kg dose range a transient second degree AV block was regularly recorded. The lethal dose (cardiac arrest) was 20 mg/kg. BP significantly already decreased after 4 micrograms/kg. The dose-dependent decrease of Fr matched the hypotensive effect in the whole range due to unchanged RRr. In contrast Fc invariably increased at lower doses reflecting the RRc decay. Only in the mg/kg dose range Fc decreased in accord with BP since RRc dropped to a constant value (50% of control) with each administration. The peripheral reactions were significantly augmented in rats with renovascular hypertension. It is concluded that, in this model, the peripheral effects of diltiazem evidently surpass the central ones. The regional difference between the inert renal and responsive carotid vasculature might be due to a different mode of regulation of the respective vascular tone, hypothetically reflecting different density of membrane, potential-dependent Ca2+ channels.

Animals↗
PubMed1989

The effect of prostaglandins E2 and F2 alpha on carotid blood flow in rats with renovascular hypertension.

The effect of i.v. bolus administration of PGE2 and PGF2 alpha on carotid blood flow (Q) and mean arterial blood pressure (MAP) was recorded in 21 anaesthetized normotensive control (N) and 12 rats with 1K1C renovascular hypertension (RH). From the measured parameters the regional vascular impedance (PVI) and the change in blood volume were calculated. In normotensive animals both PGs elicited a dose-dependent initial fast increase of Q (threshold dose 0.4 ng/kg) and a decrease of MAP and PVI (threshold dose 0.4 micrograms/kg). Subsequently, Q decreased below the initial level. MAP and PVI remained depressed after E2 but increased after F2 alpha. The time course of the Q and MAP responses was analyzed in more detail at a standard dose 4 micrograms/kg. The average time to peak of the first phase was 12 s and of the second approximately 80 s. The initial levels of Q and MAP were reestablished within 3 to 4 minutes. The total volume of carotid blood flow obtained by planimetric integration was unaltered after F2 alpha but depressed after E2. In hypertensive animals both phases of the response to E2 were significantly retarded and the Q response was nearly abolished. On the other hand, the time course of the reaction to F2 alpha was unchanged but the magnitude of the second pressoric phase was reduced. Thus, the capacity of the carotid vascular bed to dilate remains the same in RH while the ability to constrict is limited. It is concluded that the response of MAP and Q to both PGs are relatively independent.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[The occurrence of endothelial cells in the blood in deep venous inflammation].

The number of anuclear residues of endothelial cells in the blood stream was investigated in 22 patients suffering from deep phlebitis and no other disease. The level of endothelaemia in these patients was in all instances higher than in 24 healthy subjects. Assessment of the endothelaemia in patients with deep phlebitis makes more accurate assessment of the diagnosis and the follow-up of regression of the disease possible.

Endothelium, Vascular↗
PubMed1984

Distribution of microspheres in the brain of hypertensive rats.

The blood perfusion of different parts of the brain tissue was examined by means of microspheres 15 and 50 micron in diameter, in normotensive control rats and in animals with experimental renovascular hypertension. The microspheres were labelled with fluorescein isothiocyanate and their numbers in the tissue were determined in consecutive histological sections by UV microscopy. In the control rats, the incidence of wedged microspheres per 1 mm3 tissue was high in the cerebellum, cerebral cortex, subcortical tissue and pons Varolii, but low in the thalamic and hypothalamic regions, indicating that these parts were relatively poorly perfused with blood. The significantly greater accumulation of microspheres in the cortex and subcortical tissue of hypertensive rats seems to have been due to hypertensive narrowing of the arterioles. Conversely, the diminished incidence of microspheres in the thalamus and hypothalamus may have been due partly to microsphere trapping in the narrowed upstream blood vessels and partly to thinning of the capillary network. Total microsphere recovery in the brains of the control and the hypertensive rats was almost identical, implying that only the distribution of brain blood perfusion is altered in experimental hypertension.

Animals↗
PubMed1979

Early stages of experimental atheromatosis.

In female Wistar rats, fed an atherogenic diet, the early changes of serum lipids and the deviation of the vasomotor response to adrenaline and acetylcholine were compared with morphological manifestations. It has been found that the first sign may be detected as the shift in serum lipoproteins and lipids just in a few days. Merging and decrease of alpha-lipoproteins and an increase of the beta-lipoprotein fraction proved as the most sensitive indicator. In the course of several weeks, an alteration of hemodynamic response to adrenaline and acetylcholine occured. The animals revealed a diminished depressoric response to acetylcholie, whereas their blood pressure response to adrenaline in the pressoric phase was decreased but the depressoric phase was markedly expressed. The morphological impairment of the vascular system followed with a delay of several months, although a lipoid infiltration of the liver appeared after 6 weeks of the atherogenic dietary regimen.

Acetylcholine↗
PubMed1978

Blood pressure response to bolus administration of vasoactive drugs in the rat.

The time course of systemic blood pressure response in normotensive anaesthetized rats was studied after a bolus administration of standard doses (0.4 microgram/kg) of noradrenaline, adrenaline, isoprenaline, acetylcholine, serotonin, bradykinin, and histamine. The single stimulus of a vasoactive agent elicits a blood pressure deviation with typical phasing. The time dimension of the individual wave is less variable and less dose dependent than their amplitude. Under the given experimental conditions the blood pressure response is predominantly determined by the peripheral vasomotor reactions; the cardiac component is of minor importance. Though the overall responses to the individual drugs are quite characteristic, they seem to comprise several common components. Thus the peripheral vascular system is supposed to consist of different regulatory subsystems which take part in the systemic blood pressure control by typically timed responses. The pattern of the reaction is then given by their unequal combination and various intensity.

Animals↗