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.
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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