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Biomedical subjects

J Seylaz

Publications and source records attributed to J Seylaz.

At least 127 records · Page 7Linked to original sources
PubMed1987

Systemically administered adenosine increases caudate blood flow in rabbits.

Adenosine has been proposed to be a chemical link between cerebral metabolism and blood flow. In the present study, we investigated whether the intravenous or intracarotid administration of adenosine could influence regional cerebral blood flow in anesthetized rabbits. The study was performed with the [14C]ethanol tissue sampling technique which enables quantitative, instantaneous, multiregional blood flow measurements. With either mode of adenosine administration, no change in cerebral blood flow was observed, except in the caudate nucleus in which a significant vasodilation took place. These data indicate that, in rabbits exogenous adenosine increases blood flow in highly specific brain areas, by mechanisms that are discussed.

Adenosine↗
PubMed1987

Continuous determination of the cerebrovascular changes induced by bicuculline and kainic acid in unanaesthetized spontaneously breathing rats.

Cerebral blood flow was sequentially determined (every 2-3 min) with helium clearance in two "vulnerable" structures: the hippocampus and the frontoparietal cortex during bicuculline (n = 11) and kainic acid (n = 9)-induced seizures in unanaesthetized, spontaneously breathing rats. Tissue partial pressures of oxygen and carbon dioxide were continuously and simultaneously evaluated in the same brain areas. All these variables were measured by mass spectrometry with a single gas sampling cannula previously implanted in each structure. The systemic variables, arterial blood pressure, arterial partial pressures of oxygen and carbon dioxide, pH, and bicarbonate concentration were also determined. Arterial and venous catheters were chronically implanted several days prior to the definitive experiments. Bicuculline induced short (about 15 min), recurrent, generalized seizures, with an abrupt rise in arterial blood pressure, an arterial metabolic acidosis and comparable blood flow increases (4-fold) in the hippocampus and the neocortex. A marked increase in tissue partial pressure of oxygen was always preceded by an increase in tissue partial pressure of carbon dioxide. After the seizures, in the 5 rats that survived, cerebral blood flow was significantly lowered; tissue partial pressure of oxygen and partial pressure of carbon dioxide also decreased, but to a lesser extent. Histological examination revealed two types of lesions: predominantly selective chromatolysis but also ischaemic cell change. Kainic acid first induced a decrease in arterial pressure and then hypertension during status epilepticus, with a return of arterial pressure towards basal levels during the recovery period (4 h after the injection). Respiratory alkalosis occurred throughout the experiment. Cerebral blood flow increased progressively to become maximal during status epilepticus. This vasodilatation was greater in the hippocampus (x 8) than in the neocortex (x 4). During recovery, cerebral blood flow tended to decrease but remained significantly elevated. In both structures, tissue partial pressure of oxygen was first lowered while tissue partial pressure of carbon dioxide was elevated; with the occurrence of the wet dog shakes, tissue partial pressure of O2 increased and tissue partial pressure of CO2 decreased. The changes in tissue gases were maximal during status epilepticus and tended to return to their basal levels thereafter, but no decrease in tissue partial pressure of O2 was observed, even 4 h after kainic acid administration. Histological analysis demonstrated ischaemic cell changes, particularly in the limbic system.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1987

Ultrastructural evidence for a functional unit between nerve fibers and type II cerebral mast cells in the cerebral vascular wall.

By histofluorescence microscopic examinations of pial arteries from rats and rabbits, we have observed that the routes of adrenergic fibers were apparently organized along successive sites of granular autofluorescent cells present in the adventitia. Subsequent electron microscopic studies showed that these cells were often situated in close apposition (80 to 200 nm) to the adventitial nerve bundles. The granular cells and nerve varicosities were frequently enclosed within the same basement membrane, with a membrane-to-membrane distance as small as 20 nm. However, no clear membrane differentiation was seen. These granular cells were identified histochemically by staining with Sudan Black, Oil Red O, Toluidine Blue, Alcian Blue, together with ultrastructural and pharmacological methods (48/80 compound and carbachol intracarotid infusions). The cells, many of which contained large amounts of lipids, showed morphological ultrastructural and pharmacological similarities to peripheral mast cells. Nerve bundles contained two types of varicosities: some of them degenerated after superior cervical ganglionectomy and were thus of sympathetic origin, whereas the others contained small clear vesicles (probably cholinergic) and/or large dense-cored vesicles (probably peptidergic). As we have shown that cholinomimetics induce exocytosis of these granular cells, the close relationship between these cells and the nerve fibers may indicate a neurogenic control of the cerebrovascular mast cell secretion. As these cells contain potent vasoactive substances, this relationship may be of importance in the genesis of physiological or pathological cerebrovascular events which are, as yet, poorly understood.

Animals↗
PubMed1987

Effect of the muscarinic agonist carbachol on pial arteries in vivo after endothelial damage by air embolism.

Reactions of pial arteries to the muscarinic agonist carbachol were tested in vivo in chloralose anesthetized cats before and after endothelial damage. Moderate endothelial damage was induced by arterial air embolism and verified by electron microscopy for the vessels tested. The experiments had three phases; First, the normal reactivity of pial arteries to carbachol (10(-7) to 10(-5) M) was tested using the microapplication technique, then, after air embolism, the reactivity was reinvestigated at the same vessel. Finally, pial arteries were taken out for scanning electron microscopy. The results show carbachol (10(-6) and 10(-5) M) induced significant dilations under control conditions, also after repetition at the same vessel. After air embolism, the reactions to carbachol were abolished. Morphologic data revealed that whereas control pial arteries showed intact endothelium, the embolized vessels revealed various degrees of endothelial alterations. All showed flattening of endothelial nuclei, to a greater or lesser degree, and in many cases, the endothelium had a wrinkled appearance; several arteries showed severe degradation of the intercellular junctions. It is concluded that (a) carbachol-induced muscarinic vasodilatation of pial arteries in vivo can be abolished after a morphologically verified endothelial lesion--thus confirming in vitro studies in larger arteries and (b) disturbed vascular function does not require rubbing of the endothelium, but occurs already with moderate endothelial damage.

Animals↗
PubMed1987

Nonuniformity of CBF response to NE- or ANG II-induced hypertension in rabbits.

The regional response of brain vasculature to moderate hypertension was investigated using two hypertensive drugs, norepinephrine (NE) and angiotensin II (ANG II), infused intravenously at low concentrations (increase in blood pressure 15-40 mm Hg). Regional cerebral blood flow (rCBF) was measured in unanesthetized and anesthetized rabbits using the [14C]ethanol saturation technique. In both groups of animals, NE and ANG II induced regional differences in the flow changes as compared with controls, confirming a regional (or segmental) heterogeneity in the regulatory mechanisms to hypertension. The responses to identical rises in blood pressure (BP) in most of the structures analyzed depended on the drug used. In the unanesthetized rabbits, the increase in vascular resistance induced by NE was greater than that induced by ANG II. With the two drugs, there was no correlation between the flow changes in any of the structures considered and either the BP increase or the BP level in unanesthetized animals. However, these flow changes were correlated with the BP increase in anesthetized animals, although differences between the effects of NE and ANG II were again observed. This study suggests that cerebrovascular regulatory mechanisms in hypertension are probably more complex than a simple myogenic reaction. Their heterogeneity and their dependence both on the cause of hypertension and on the presence of anesthetics suggest the intervention of an integrating pathway.

Anesthesia↗
PubMed1986

Cerebrovascular changes elicited by electrical stimulation of the centromedian-parafascicular complex in rat.

Electrical stimulation of the centromedian-parafascicular complex (CM-Pf) in anesthetized (chloralose) and paralyzed (tubocurarine) rats elicits a widespread cerebrovascular dilatation. Regional cerebral blood flow (rCBF) was measured in dissected tissue samples of 10 brain regions (medulla, pons, cerebellum, inferior colliculus, superior colliculus, frontal parietal and occipital cortices, caudate-putamen and corpus callosum) by [14C]iodoantipyrine method. In unstimulated and sham-operated rats rCBF ranged from 40 +/- 3 (ml/100 g/min) in corpus callosum to 86 +/- 6 (ml/100 g/min) in inferior colliculus. During CM-Pf stimulation, rCBF increased significantly (P less than 0.05, analysis of variance and Scheffe's test) in all cerebral regions bilaterally ranging from +118% in parietal cortex to +38% in cerebellum. Although cerebral vasodilation elicited by CM-Pf stimulation persisted after unilateral transection of the cervical sympathetic trunk, the cortical CBF was significantly reduced (P less than 0.05) on the denervated side. Acute adrenalectomy significantly (P less than 0.05) decreased elevated rCBF during CM-Pf stimulation in all cortical regions (frontal-36%, parietal -34%, and occipital -27%) and in caudate nucleus (-37%). Thus, excitation of neurons originating in, or fibers passing through the CM-Pf can elicit a powerful cerebral vasodilation. The cerebral vasodilation is modulated by cervical sympathectomy and circulating adrenal hormones. We conclude that CM-Pf elicited vasodilation is at least partly mediated by intrinsic neural pathways.

Adrenalectomy↗
PubMed1986

Stress and local cerebral blood flow: studies on restrained and unrestrained rats.

The degree of stress has been compared between two protocols used for the measurement of local cerebral blood flow (LCBF) in conscious rats. The first method involved acute surgical procedures (cannulation of both femoral veins and arteries) under halothane anesthesia. It was followed by a recovery period (2-3 h) during which the rat was before LCBF measurement. The second method employed chronic cannulation of the abdominal aorta and vena cava, allowing the LCBF assays to be performed on freely moving rats. Plasma corticosterone and a glucose tolerance tests showed that the freely moving rats were less stressed than the gently restrained ones. The LCBF of the two groups were not significantly different except in the frontal and parietal cortex, where it was more elevated in the freely moving rats. LCBF may be sensitive to the environmental conditions in freely moving rats whereas these vascular effects may be reduced after 2-3 h of gentle restraint. The two protocols tested in this study could be considered as good methods for studying LCBF in conscious rats, although some stress remained in gently restrained rats. Freely moving rats can be used for behavioural studies providing that the time lag of the arterial samples is taken into account. Since the basal LCBF values of gently restrained rats are minimally affected by the stress inherent in the preparation, this convenient protocol could be considered as useful for numerous investigations.

Animals↗
PubMed1986

Local cerebral blood flow in gently restrained rats: effects of propranolol and diazepam.

The cerebrovascular consequences of the gentle restraint commonly used for the measurement of local cerebral blood flow (LCBF) in conscious rats has been tested by using two drugs, propranolol and diazepam. Propranolol induced small LCBF decreases in 7 structures suggesting that the cerebral circulation was partially controlled by the activation of intra or extracerebral aminergic pathways in this protocol. Sedative doses of diazepam reduced LCBF in most of the structures but anxiolytic doses increased it in 4 structures. This effect may be due to a regionally differentiated modification of activity in the brain due to the selective inhibition of limbic structures by diazepam. Since propranolol and diazepam induced only small changes, the LCBF of gently restrained rats appeared to be minimally affected by the stressful situation imposed by the protocol.

Animals↗
PubMed1986

Transmural gradient of tissue gas tensions in the canine left ventricular myocardium during coronary clamping and reactive hyperemia.

Mass spectrometry was used for the continuous, simultaneous and quantitative measurement of oxygen (PO2) and carbon dioxide (PCO2) partial pressures in the subendocardial and subepicardial layers of the left ventricle in 11 anaesthetized ventilated dogs. Under control conditions, PO2 was significantly lower in the subendocardium (13.5 +/- 4.5 mm Hg) than in the subepicardium (20.7 +/- 2.3 mm Hg), whereas PCO2 did not differ significantly (43 +/- 8.8 and 51 +/- 9.2 mm Hg respectively). These variables were not correlated with blood pressure or coronary blood flow. Subendocardial and subepicardial PO2 decreased less than 5 s after coronary occlusion. These changes were more rapid and severe in the subendocardium. After occlusion for 90 s: subendocardial PO2 was 4.1 +/- 6.3 mm Hg while subepicardial PO2 was 6.7 +/- 15.0 mm Hg (P less than 0.05). PCO2 reached peak values of 56 +/- 25 mm Hg subendocardial and 82 +/- 22 mm Hg subepicardial at 2.67 +/- 0.71 min and 3.43 +/- 0.93 min after coronary clamping. A reactive hyperemia occurred after coronary unclamping with different time courses and amplitudes for systolic and diastolic stroke flows while PO2 recovered with different kinetics. Subendocardial PO2 increased with a lower initial slope, probably in relation with the delay in the diastolic hyperemia. The observed delayed subendocardial hyperoxia, unrelated to the hyperemia, may indicate a delay in the recovery of normal work and metabolism in the inner layers of the myocardium.

Animals↗
PubMed1986

Two neural mechanisms in rat fastigial nucleus regulating systemic and cerebral circulation.

We have studied in anesthetized (alpha-chloralose) and paralyzed (d tubocurarine) rats the effects of electrical stimulation of the fastigial nucleus (FN) on local cerebral blood flow (lCBF) and its relationship to intracerebral PO2, and PCO2 and to the systemic arterial pressure (Pa). Mass spectrometry was used to measure quantitatively lCBF (repetitively) and cerebral PO2 and PCO2 (continuously). A systematic exploration of the FN for an increase in Pa and/or lCBF revealed that the most active sites for the rise in Pa were localized within the rostral FN, while those that elicited an increase in lCBF were found throughout the rostrocaudal extent of the FN. The increase in lCBF elicited from the caudal FN was not associated with changes in Pa. The increase in lCBF was concomitant with an increase in intracerebral PO2 and a slight decrease in PCO2. Although the increases in Pa and lCBF were dependent on stimulus frequency, their frequency-response curves were different. We conclude that 1) in contrast to the neurons or fibers of passage of the rostral FN, which mediate an increase in Pa, the neurons or fibers of passage that elicit changes in lCBF are localized along the rostrocaudal axis of the FN; 2) changes in the local gas partial pressures are not responsible for the vasodilation observed; and 3) the cerebral vasodilation and systemic vasoconstriction evoked by FN stimulation are probably mediated by two different neural mechanisms.

Animals↗
PubMed1986

Histamine-induced constriction and dilatation of rabbit middle cerebral arteries in vitro: role of the endothelium.

We studied the effects of histamine on perfused rabbit middle cerebral arteries in vitro. Intact and endothelium-denuded preparations were compared. Histamine caused concentration-dependent constrictions in intact vessels which were competitively inhibited by an H1 receptor antagonist. This constriction was potentiated by either H2-receptor blockade or endothelium denudation. The greatest potentiation was observed with intraluminal as opposed to extraluminal administration. The H1 receptor agonist pyridylethylamine induced similar concentration-dependent constriction in intact and denuded preparations. After preconstriction, histamine, in the presence of an H1 receptor antagonist, dilated intact vessels to a maximum of 45.1%, and endothelium-denuded vessels to a maximum of 22% (p less than 0.02). We conclude that rabbit middle cerebral arteries possess H1 constrictory and H2 dilatory receptors, and that many of the H2 dilatory receptors are situated on the endothelial cells.

Acetylcholine↗