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]
SUMMARY1. The terminal microcirculation in the transilluminated ventral margin of the rat liver was observed and recorded by a video-microscope system. The volumetric flow rate in a liver sinusoid was calculated from the observed diameter of the sinusoid and the intra-sinusoid erythrocyte flow velocity.2. The topographic distribution of liver sinusoids within an arbitrary boundary of a microscopic field of terminal liver microcirculation was observed and the total inflow and outflow in the field were determined.3. Both vagus nerves at the lower end of the oesophagus were stimulated at supramaximal voltage. Vagal stimulation dilated the calibre of liver sinusoids and paradoxically diminished the erythrocyte flow velocity in each individual liver sinusoid, but the total volumetric flows in a microscopic field remained unchanged.4. Vagal stimulation also increased the number of liver sinusoids in a microscopic field by opening previously closed liver sinusoids. This recruitment contributed two-thirds of the total increase of the sinusoidal capacity while the other one third was the result of distension of existing liver sinusoids.
This study was designed to establish the existence of cholinergic vascular receptors in the terminal portion of the rat liver microcirculation. The liver microcirculation was observed in vivo by a transillumination technique through a television microscope. The changes in the caliber of the liver sinusoids were measured directly on the television screen. Infusion of the parasympathetic neurotransmitter acetylcholine into the portal venous circulation caused a concentration-dependent dilation of liver sinusoids. Similar dilatation effects were observed for other cholinergic receptor agonists. Atropine, the specific cholinergic receptor blocker, inhibited this dilator effect, displacing the acetylcholine concentration-effect curve to the right. In contrast, physostigmine, the cholinesterase inhibitor, caused displacement of the curve to the left. In conclusion, cholinergic receptors are present in the terminal portion of the liver microcirculation, subserving the functional role of vasodilatation.
Coronary hypoperfusion was elicited in alpha-chloralose-anesthetized open-chest dogs by reducing left coronary perfusion pressure to 50 mmHg. Left coronary blood flow, as well as left ventricular oxygen extraction, oxygen consumption, and contractile force were measured. The reduction in perfusion pressure caused significant reductions in coronary flow, oxygen consumption, and peak reactive hyperemic flow. During hypoperfusion in 11 dogs, intracoronary infusion of the specific alpha 1-adrenergic antagonist prazosin (0.1 mg/min) increased coronary flow and oxygen consumption by 22 and 16%, respectively. Peak increases were observed after 6-8 min of prazosin infusion (0.6-0.8 mg prazosin), and both increases were statistically significant (P less than 0.05). In seven additional dogs, beta-adrenergic blockade with propranolol (1.0 mg ic) did not significantly affect the actions of prazosin. In five additional dogs, the specific alpha 2-adrenergic antagonist yohimbine (1.3 mg ic) in the presence of propranolol (1.0 mg ic) did not affect coronary flow or oxygen consumption during coronary hypoperfusion. Those results suggest that an alpha 1- but not an alpha 2-adrenergic constrictor tone was operative in the left coronary circulation under the conditions of these experiments.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.