When neurones are active there is an entry of Na+, which must subsequently be pumped out, and an increase in their oxygen consumption rate (Qo2). The Na+ pump derives its energy from ATP, splitting it into ADP and Pi, and it has reasonably been proposed that the changes in concentrations of ATP, ADP and Pi lead to a stimulation of the O2 consumption by the mitochondria and hence to a restoration of the stock of ATP. Here we present evidence suggesting that Qo2 must be controlled differently in the retinal photoreceptor cells of the honeybee drone. Stimulation of drone photoreceptors with a flash of light causes an entry of Na+ (ref. 4) and a transient increase in Qo2 that indicates respiration of the right order of magnitude to provide ATP to pump the Na+ out. We report intracellular recordings of changes in intracellular sodium (Nai+) and potassium (Ki+) in response to single light flashes and have compared the time course of extra oxygen consumption (delta Qo2) with these ion changes and other indices of Na+ pumping. We found that the time course of pumping seems to lag behind the time course of delta Qo2. It follows that the mitochondrial respiration must be stimulated by some signal which is generated earlier than the rise in ADP produced by the Na+ pump.

Adenosine Triphosphate↗

PubMedDate not supplied

[Transmission of the anterior chamber pressure to the center of the vitreous body and to the posterior pole of the eye of the miniature swine. Measurement of isovolumetric and direct pressure].

Experimental variations of the anterior chamber pressure (P.I.C.) are transmitted at about 300 ms to the middle of the vitreous. The response time to a sudden experimental increase in P.I.C. to the centre of the vitreous is variable and depends essentially on the control intra-ocular pressure: the more it is raised the shorter the response time. The pressure in the centre of the vitreous (P.I.V.) has a pulsatile character probably due to transmission of arterial pulsation. The higher the intra-ocular pressure the greater the amplitude of these pulsations. Recording of P.I.V. close to the surface of the retina show abrupt falls despite the fact that the P.I.C. and systemic arterial pressure remain stable. These results are discussed in relationship to autoregulation of the retinal circulation and the physiopathology of glaucoma.

Animals↗

PubMedDate not supplied

[Diffusion of O2 in the normal and the ischemic retina of miniature pigs].

Transretinal PO2 profiles were recorded during normoxia and hyperoxia in normal and ischemic retinal territories in anesthetized miniature pigs using double barrelled recess type microelectrodes. In normoxia and hyperoxia the PO2 in the normal territory decreased from the inner retina and the choroid towards the mid-retina, indicating that the choroid cannot supply O2 to the whole normal retina. Preretinal and transretinal PO2 measurements in ischemic territories following a laser occlusion of a retinal branch vein demonstrated that in normoxia the direction of PO2 gradients prevents O2 diffusing from the choroid to reach the inner retina. This explains why the ischemic territories are hypoxic. In the contrary, during hyperoxia the intraretinal PO2 gradient indicates an O2 flux from the choroid to the inner retina resulting to marked preretinal PO2 increase at the affected territories. We proposed the hypothesis that in the ischemic retinas the hyperoxia does not induce a rise of the O2 consumption of the outer retina. Hence hyperoxia could be a useful tool to restore the oxygenation of the inner hypoxic retinal layers.

Animals↗

PubMedDate not supplied

[The role of prostaglandins in the regulation of retinal blood flow].

Hypercapnia causes vasodilatation of retinal arterioles. Prostaglandin E1, injected close to retinal arterioles from the vitreal side cause vasodilatation apparently similar to that caused by hypercapnia. An inhibitor of prostaglandin synthase (indomethacin) was injected into the ocular circulation. There was a reversible inhibition of the retinal vasodilatation normally induced by hypercapnia. Indomethacin injected close to retinal arterioles from the vitreal side causes reversible vasoconstriction and inhibits the vasodilatory effect of hypercapnia. It is concluded that prostaglandin E1 satisfies three criteria for a candidate for a mediator of hypercapnia-induced arteriolar dilatation.

Animals↗

PubMedDate not supplied

[Panphotocoagulation. Mechanism of action and early indications].

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Animals↗