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L H Smaje

Publications and source records attributed to L H Smaje.

At least 37 records · Page 2Linked to original sources

Microvascular pressures and filtration coefficients in the cat mesentery.

1. Filtration coefficient and hydrostatic pressure have been measured in single capillaries and venules in the cat mesentery using a modification of the Landis (1927) single vessel occlusion technique. 2. Venules were found to be filtering fluid, not absorbing it as is often supposed. 3. The mean filtration coefficient in capillaries was 0.018 micrometers . s-1 . mmHg-1 (1.35 X 10(-10)m . s-1 . Pa-1) while that in venules, was 0.027 micrometers . s-1 . mmHg-1 (2.02 X 10(-10)m . s-1 . Pa-1). 4. In both capillaries and venules, filtration coefficient increased with decreasing pressure. 5. The difference between directly measured venular pressure and that calculated from the occlusion data was used to determine the contribution of the interstitium to fluid exchange. In the mesentery superfused with Krebs solution the tissue pressure so determined was found to be zero or subatmospheric initially but became increasingly positive with lengthening exposure of the mesentery.

Animals↗

Simultaneous measurement of pressure in the interstitium and the terminal lymphatics of the cat mesentery.

1. Simultaneous measurements of the pressure in terminal lymphatics and interstitial tissue have been made in the exteriorized cat mesentery superfused with either physiological salt solution (Krebs solution) or a water-immiscible fluorocarbon, FC-80. 2. The pressures within individual terminal lymphatics were measured using glass micropipettes attached to a servo pressure-measuring system. Tissue pressures were recorded using saline-filled cotton-wool wicks. 3. Mean pressure recorded in the terminal lymphatics of the Krebs-superfused mesentery were slightly above atmospheric (+0.2 mmHg, n = 45), while those recorded in the FC-80-superfused mesentery were slightly below atmospheric (-0.2 mmHg, n = 46). 4. Tissue pressures were also slightly subatmospheric in the in situ mesentery, and the recently exposed tissue. Continuous superfusion with Krebs solution caused the tissue pressure to rise to atmospheric pressure or above; with FC-80-superfusion the tissue pressure also rose, but never to above atmospheric pressure. 5. Isolated strips of mesentery immersed in Krebs solutions of different concentrations gained weight, but when immersed in FC-80 no change in weight was detected. 6. It was concluded that the interstitial gel of the mesentery is normally unsaturated and that superfusion with Krebs solution leads to tissue oedema. This tendency is less marked in FC-80-superfused preparations. Possible mechanisms for lymph formation and propulsion are discussed.

Animals↗

The organization of the salivary gland microcirculation.

1. The microvasculature of the rabbit submandibular salivary gland has been investigated employing in vivo microscopy, blood flow measurements, latex casts, microsphere injections and examination of fixed sections of the gland.2. Two principal microcirculations were distinguished in the living gland, one supplying the acini and the other the intralobular ducts. Parasympathetic nerve stimulation (2, 5 or 10 sec(-1)) elicited different responses in each of the two microcirculations. Flow in the capillaries around the acini slowed initially before increasing. In contrast, flow in the intralobular duct capillaries increased soon after beginning stimulation.3. In some experiments both whole gland flow and microvascular flow were monitored simultaneously. Whole gland flow increased at the same time as flow in the acinar capillaries was decreasing and as flow in the intralobular duct capillaries increased. Flow in acinar capillaries increased about 5 sec after glandular flow started to increase.4. These observations could be explained if either the vascular beds of the acini and the intralobular ducts were arranged in parallel or if arteriovenous anastomoses were to shunt the acinar circulation. No such anastomoses were found in latex casts made of the gland vasculature, and microspheres injected into the artery supplying the gland were not found in the venous effluent.5. The intraglandular distribution of microspheres was measured in histological sections of the injected glands to give an estimate of the distribution of blood flow between the duct and acinar microcirculations. At rest and during maintained stimulation about 55% of the blood flow passed through the intralobular duct microcirculations, whilst during this initial 15 sec of stimulation this proportion was increased to over 70%. This finding is consistent with a parallel arrangement of the two microcirculations.6. The conclusions drawn from these observations are that the duct and acinar microcirculations are arranged in parallel, that there are differences in the way the vasodilatation is mediated in these circulations, and that arterio-venous anastomoses play no significant role in this gland.

Animals↗

The effect of drugs on mass transport across capillaries and venules.

1. The single vessel occlusion technique has been applied to venules to investigate the effect of drugs on mass transfer. 2. The filtration coefficient in venules is greater than that in capillaries and in both types of vessel the filtration coefficient is negatively correlated with hydrostatic pressure. 3. Vasoactive drugs have no effect on capillary filtration coefficient. 4. Acetylcholine and isoprenaline do not increase vanular filtration coefficient but histamine, bradykinin, 5-Ht and SPF do and may do so independently of protein leakage.

Acetylcholine↗

Bradykinin and functional vasodilatation in the salivary gland.

Blood flow through the submandibular gland of the dog was measured and the venous effluent monitored for potential mediators of the functional vasodilatation by passing it over a series of assay tissues. On chorda lingual nerve stimulation there was salivation, an increased blood flow and the release of a bradykinin-like substance (kinin) into the venous effluent. In about half of the preparations, increasing the frequency of stimulation from 2 to 10 Hz led to an increased output of kinin, whereas in the others successive stimulations led to a decreasing output of kinin in the face of normal secretory and vascular responses. Following the administration of atropine, the vasodilatation persisted, salivation was abolished and after several stimulations kinin release could no longer be detected. Release of prostaglandin did not appear to be responsible for the vasodilatation. It is concluded that neither kallikrein nor kinin is the main mediator of parasympathetic vasodilatation in the salivary gland.

Animals↗