No abstract

The hepatic microcirculation was observed microscopically in the transilluminated liver of the rat. The portal and hepatic venous microvessels were classified into four orders according to their branching hierarchy, and the hepatic sinusoids into branching, direct and interconnecting types according to their topographic arrangements. The diameters of the various orders of microvessels and types of sinusoids were measured by serial photomicrography, and the velocity of the erythrocytes in these various microvessels and sinusoids by the dual-slit photometric technique. The microvascular volume flows were calculated from these data. In both portal and hepatic venous systems, the erythrocyte velocity and the volume flow significantly decreased in successive orders of the microvessels in apparent relation to the cross-sectional areas. The diameters of the three types of sinusoids did not significantly differ, but the velocity of the erythrocytes in the direct sinusoid was significantly faster than that in the branching sinusoid while that in the inter-connecting sinusoid fluctuated widely.Although the terminal ramification of the hepatic microvasculature was studied many years ago by Mall [1906], it was Elias [1949] who first classified the various types of terminal portal aborization, but he did not extend the study to the entire hepatic microvasculature. Also, a systematic quantitative study of the microvascular flow in the intact liver has not been done. The present paper reports studies on the topographic classification and distribution of the hepatic microvessels and sinusoids in vivo, and on the quantitative measurements of their diameters and the velocity of the erythrocytes in these vessels. METHODSFifty male Wistar rats of about 175 g body-weight were anaesthetized with sodium pentobarbital (40 mg/kg ip). The animal breathed spontaneously through a tracheotomy tube and the body temperature was maintained by a heating bed. As described by Cheng, Ho and Ma [1973], the anterior margin of the liver was transilluminated for direct microscopic observation through a cover-glass, using an Olympus Vanox microscope with an Oel+W 22 x /0.65 (Leitz) or an FL 40 x /0 75 (Olympus) objective, and the centre-line velocity of the erythrocytes in a hepatic microvessel or sinusoid projected on a screen was measured by a two-slit photometric method [Wayland and Johnson, 1967] with processing of the photometric signals by an on-line cross-correlation computer technique [Intaglietta, Tompkins and Richardson, 1970;Ma, Koo, Kwan and Cheng, 1974]. The diameter of the hepatic microvessels and sinusoids was measured with a caliper from enlarged photomicrographs taken serially with a camera fitted on top of the microscope and connected to an automatic exposuremeter system (Model PM-10-A, Olympus), using Kodak Plus-X film (ASA-125) and a Kodak Wratten green filter (No. 58). The microvascular volume flow (Q) in the hepatic microvessel was calculated from Wayland's [1973]

No abstract

After intravenous injection of tetrodotoxin in a dose which led to respiratory failure in the rat, the phrenic nerve continued to convey massive bursts of nerve impulses from the medullary centre for some time after cessation of respiratory movement, contraction of diaphragm and diaphragmatic muscle action potentials. In artificially ventilated intact rats the contractile response of a hemidiaphragm to indirect and direct stimulation diminished and disappeared together when tetrodotoxin was injected intravenously. In curarized rats, the response to direct stimulation disappeared when tetrodotoxin was given. In artificially ventilated rats which had one phrenic nerve cut 2 months previously, the contractile response of the denervated hemidiaphragm to direct stimulation and that of the intact opposite hemidiaphragm to indirect stimulation both diminished and stopped after the administration of tetrodotoxin. Action potentials were elicited from the biceps brachii muscle and its motor nerve following stimulation of the motor cortex; after injection of tetrodotoxin, both nerve and muscle action potentials diminished and disappeared together. It appears from the evidence presented that the failure of respiration in tetrodotoxin poisoning is due to paralysis of the respiratory muscles which were apparently more susceptible to the action of tetrodotoxin than the respiratory and other motor nerves or the non‐respiratory striated muscles.

The in vivo hepatic microvascular bed of the rat was observed microscopically in the transilluminated liver and the diameter of the hepatic sinusoids was measured by serial photomicrography. Intraportal infusion of tyramine induced concentration-dependent constriction of the hepatic sinusoids, but also dilatation of the sinusoids when the dose was small. These effects were attributed to the release of endogenous noradrenaline which activated either alpha-or beta-adrenergic receptors and caused constriction, or dilatation, of the sinusoids respectively. Adrenaline and noradrenaline induced similar changes in the hepatic sinusoids as tyramine, while phenoxybenzamine induced dilatation, and propranolol constriction, of the sinusoids. All the above responses were abolished by pretreatment with reserpine. A possible noradrenaline-mediated basal vasomotor tone in the hepatic sinusoids for autonomic control of the blood flow in the sinusoids was postulated.The regulation of hepatic blood flow is still unsettled [Greenway and Stark, 1971], while the regulation of blood flow in the hepatic sinusoids is even more obscure. Studies of the effect of catecholamines on the hepatic circulation in various species of experimental animals provided evidence for the presence in the liver vascular bed of alpha-adrenergic receptors [Green, Hall, Sexton and Deal, 1959;Bender and Horvath, 1965;Nardi, 1966;Greenway, Lawson and Mellander, 1967] and beta-receptors [Scholtholt, Lochner, Renn and Shiraishi, 1967;Geumei and Mahfouz, 1968;Greenway and Lawson, 1969;Ross and Kurrasch, 1969;Fischer, Takacs, Bencsath and Vaslaki, 1970]. We have recently demonstrated the presence in the hepatic sinusoids of the rat of both alpha-and beta-receptors which could provide antagonistic constrictor-dilator components in the sinusoids.The purpose of the present study is, therefore, to determine whether the above receptors respond to the released endogenous neuro-transmitter noradrenaline, and to elucidate the role of such adrenergic constrictor-dilator mechanism in the hepatic sinusoids in the control of blood flow in the terminal hepatic microcirculation. Some of the findings have been reported in an abstract . METHODS