Intraocular pressure (IOP) and arterial blood pressure (BP) were recorded manometrically in normotensive Wistar Kyoto rats (NR) and stroke-prone spontaneously hypertensive rats (SHR). IOP was significantly lower in SHR (7.8 +/- 0.2 mm Hg) compared to NR (15.9 +/- 0.4 mm Hg). In NR, administration of vasoactive substances (kallikrein, bradykinin, angiotensin I and II) or bloodletting resulted in significant IOP reactions, which ran nearly parallel to the acute BP changes. In SHR, however, IOP showed little reaction after comparable changes in BP. The cause of the low IOP in SHR is unknown. It is assumed that in SHR rarefaction of arterioles and capillaries and a decrease in the compliance of eye vessels, in combination with an increase in the distensibility of the bulbus at this low IOP level, contribute to the lack of IOP response after administration of vasoactive drugs.

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SUMMARY Cerebral blood flow (CBF) was measured in anaesthetised cats with 133Xe clearance method under normal conditions and with hyperammonaemia. Elevation of blood ammonia concentration by an intravenous infusion of ammonium acetate caused an increase in CBF and a parallel decrease in cerebrovascular resistance (CVR). These parameters reached, however, plateau at an arterial blood ammonia level exceeding 500 Mmol/l. Cerebrovascular reactivity to CO2 diminished following elevation of blood ammonia concentration and at arterial blood ammonia level exceeding 500 umol/l it was virtually abolished. In contrast, hyperammonaemia influenced neither cerebrovascular responsiveness to papaverine nor autoregulatory properties of the cerebral circulation. It is concluded, therefore, that hyperammonaemia exerts some dilatatory effect on cerebral vessels and severely impairs chemical regulation of CBF but does not elicit cerebral vasomotor paralysis.A pathogenic role of ammonia in hepatic encephalopathy and coma had already been recognised at the end of the last century.' However, the mechanisms by which hyperammonaemia affects the central nervous system are not clear. Especially, the effect of ammonia on regulation of the cerebral blood flow (CBF) still remains to be elucidated.In 1976 Chandler and Kindt2 demonstrated significant elevation of intracranial pressure (ICP) in patients suffering from hepatic encephalopathy of different aetiologies. An increase in ICP by 200-300% of control values has also been found in rhesus monkeys during hyperammonaemia elicited by intravenous infusion of ammonium acetate.3 Altenau and Kindt4 using the same experimental model have found that ammonia intoxication causes an increase in CBF and impairs cerebrovascular reactivity to CO2 and autoregulatory properties of cerebral circulation. Basing on these results, these authors have postulated that ammonia intoxication brings about the cerebral vasomotor paralysis leading to an increase in intra- cranial blood volume, which in turn would produce an elevation of ICP.The present study was undertaken to evaluate the effect of elevation of blood ammonia concentration on CBF and its responsiveness to CO2. Furthermore, cerebrovascular reactivity to papaverine, the agent known to affect cerebral vessels in a manner different from carbon dioxide, as well as autoregulatory properties of cerebral circulation were examined under normal conditions and with hyperammonaemia in order to elucidate whether an elevation of blood ammonia concentration may result in the vasomotor paralysis of the cerebral vessels. Materials and methodsThe experiments were carried out on 82 cats of either sex weighing between 2 4 and 3 8 kg. Anaesthesia was induced with pentobarbital sodium (Nembutal-Abbott) injected intraperitoneally in a dose of 20 mg/kg and maintained with intravenous alpha-chloralose (60 mg/kg). A tracheostomy was performed and catheters inserted into the left femoral artery and vein for measurement of mean arterial blood pressure (MABP), collection of arterial...

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The effect of stimulation of the medial and lateral reticulo-hypothalamic-hippocampal (RHH) systems on cerebral blood flow (CBF) and electrical activity of the hippocampus and neocortex was examined in 19 encéphale isolé cats. ECoG was recorded from posterior sigmoid gyri and marginal gyri and hippocampal activity from dorsal hippocampus. Changes in hippocampal activity were evoked by electrical stimulation of RHH systems. CBF was measured by external monitoring of the clearance of 133Xe given as a single bolus in the carotid artery. Stimulation of the lateral system resulted in desynchronisation of ECoG and hippocampal activity without changes in CBF. Stimulation of the medial system elicited desynchronisation in ECoG modulated by theta-like synchrony, theta activity in the hippocampus and a 45% CBF increase. After atropine administration, low frequency, high voltage waves appeared in both ECoG and hippocampal activity, but no change in CBF was observed. During stimulation of the medial system there were no changes in the type of electrical activity but the CBF response was still preserved (increase by 50%). Stimulation of the lateral system did not change either the type of electrical activity or the CBF. The results indicate that the two systems of neuronal pathways, which mediate two different patterns of electrical response in the dorsal hippocampus but similar ECoG activity in the neocortex, elicit different CBF responses. It is argued that the alterations of electrical activity of the neocortex and hippocampus mediated by these two pathways depend on the cholinergic system, whereas the CBF changes depend on a different mechanism.

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Using the 133Xe clearance method it is shown that NH4Cl infusion into the anterior mesenteric vein decreased capillary blood flow in the liver. Phentolamine completely and propranolol partially prevented the depressive action of NH4Cl on hepatic blood flow. NH4Cl infused into the jugular vein provoked a slight increase in the hepatic blood flow. The adrenaline-like action of ammonium ion on the blood circulation in the liver region is discussed.Blood flow in the vessels of the portal system in ruminants has been the topic of only a few reports [reviewed by Webster, 1974] despite the peculiarity of the digestive processes in these animals. Sellers, Stevens and McLeod [1964] and Sellers [1965] showed that the increased concentration of volatile fatty acids as well as CO2 in the rumen fluid caused a con)siderable rise of blood flow iln the rumen wall. The portal blood flow increased proportionally to the amount of metabolizable energy intake in the feed [Webster and White, 1973]. Weekes and Webster [1975] also confirmed the stimulating influence of volatile fatty acids on blood flow through the liver.Since ammonium ion has been recognized as an adrenaline-like agent in the regulation of tissue metabolism [Prior, Cliford, Gibson and Visek, 1971, Wiechetek, Garwacki andBarej, 1975] one could expect its depressive influence on the blood circulation in the liver. However, the influence of dietary protein level on the blood flow in the portal vein could not be assessed [Webster, 1974]. It seems that in normal conditions of digestion the influence of rumen volatile fatty acids dominates the regulation of physiological processes in this region.Therefore in the present paper we attempted to evaluate changes in the blood flow through the liver of sheep loaded with ammonium chloride through the portal vein and jugular vein. Simultaneously the pharmacological blockade of alpha and beta adrenergic receptors has been used for estimation of the adrenaline-like action of ammonia on the hepatic circulation.99