The effect of intraventricular histamine on blood flow in the caudate nucleus of the cat was studied by means of the hydrogen clearance technique. Bilateral ventriculo-cisternal perfusion was installed. After a control period during which both lateral ventricles were perfused with mock CSF with the same composition, the drug under study was added to one side (experimental side) while the other side was perfused further with the control mock SCF (control side). At each point in time, blood flow at the experimental side was compared to that at the control side. Histamine (10(-3) M) caused a severe vasodilatation and this effect was completely antagonised by the H2-receptor blocker cimetidine (10(-2) M). Cimetidine had no vasoactive effects of itself in the concentration used. The H2-receptor agonist Dimaprit (10(-3) M) had a vasodilator effect although less important than histamine. Indirect evidence was gained that H1-receptors are not active in the vascular bed under study.

Animals↗

PubMedDate not supplied

Response of local blood flow in the caudate nucleus of the cat to intraventricular administration of carbachol.

The effect of perfusion of the cerebral ventricles with artificial cerebrospinal fluid containing carbachol on the blood flow in the caudate nucleus of the cat and the possibility to inhibit this effect by anticholinergic drugs was studied by means of the hydrogen clearance technique. After a control period during which both lateral ventricles were perfused with artificial CSF of identical composition, the drug under study was added on one side (experimental side) while the other side continued to be perfused with the control artificial CSF (control side). The blood flow on the experimental side and on the control side were compared. A dose dependent response to carbachol was observed. Lower concentrations of carbachol (10(-6) up to 10(-4)M) caused vasodilatation whereas high concentrations (10(-3)M) caused local vasoconstriction. The increase in the local blood flow caused by the low carbachol concentrations was reduced by both atropine (10(-5)M) and hexamethonium (10(-3)M). The fall in CBF observed with the high carbachol concentration was prevented by atropine (10(-5)M). It may be concluded that low, physiologically more meaningful, carbachol concentrations cause a local vasodilatation due to interaction with both muscarinic and nicotinic receptors.

Animals↗

PubMedDate not supplied

Hemispheric blood flow in the rat after unilateral common carotid occlusion: evolution with time.

Acute occlusion of one common carotid artery in the anesthetized normocapnic rat results in a moderate cerebral blood flow (CBF) decrease in both cerebral hemispheres. No asymmetrical perfusion is observed when the overall flow in each hemisphere is considered. The increase in blood flow which normally occurs in hypercapnia is strongly impaired in the cerebral hemisphere on the occluded side resulting in an important asymmetrical hemispheric perfusion. The days (1, 5, 15, 30) following unilateral carotid occlusion normal control CBF values are found in both hemispheres in normocapnic conditions. Hemispheric perfusion asymmetry in hypercapnia also becomes progressively less pronounced with time but a slight asymmetry still persists one month after unilateral carotid occlusion.

Animals↗

PubMedDate not supplied

The influence of nonrespiratory alkalosis on cerebral blood flow in cats.

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Acute Disease↗

PubMedDate not supplied

Cerebral blood flow in cats after an acute hypertensive insult with damage to the blood-brain barrier.

Cerebral blood flow was measured with the 133Xenon clearance method in anesthetized cats under controlled ventilation. An acute pressure increase in the carotid system increases the cerebrovascular permeability to Evans blue, indicating damage to the blood-brain barrier. In these conditions the reactivity or cerebral blood vessels toward changes in the acid-base balance is altered: the CO2 reactivity is less pronounced, while the effect of increasing the plasma (HCO-3) is more pronounced than in normal cats. Autoregulatory capacity toward moderate alterations in arterial blood pressure or in intracranial pressure is well maintained in these conditions.

Acid-Base Equilibrium↗

PubMedDate not supplied

Effect of non-respiratory alkalosis on brain tissue and cerebral blood flow in rats with damaged blood-brain barrier.

Acute alterations in plasma bicarbonate concentration have minimal effects on intracerebral pH and cerebral blood flow, perhaps due to blood-brain barrier mechanisms. To test this hypothesis, the consequences of an acute rise in the plasma bicarbonate concentration were studied in anesthetized rats previously subjected to an acute pressure pulse in the carotid system with unilateral damage to the blood-brain barrier. In rats subjected to a "heavy" hypertensive insult, the hemisphere on the side of the lesion showed a lactic acidosis, edema, and a depression of cerebral blood flow. An increase in the plasma bicarbonate concentrations of 15--20 mEq/1 during 35 minutes provoked a marked rise in the total CO2 content of this hemisphere, and a further increase in the lactate concentration, but did not later the brain edema nor affect further the already very low cerebral blood flow. An increase in the lactate concentration and a decrease of cerebral blood flow in the "reference" hemisphere indicated that the lesion was not completely unilateral. In rats subjected to a "moderate" hypertensive insult the changes were less pronounced and statistically not significant for all the parameters. There results illustrate the importance of an intact blood-brain barrier for the maintenance of intracerebral pH in the face of acute alterations in plasma [HCO3]. The impaired cerebral blood flow after an acute hypertensive insult did not appear to be influenced by the intracerebral [HCO3].

Alkalosis↗