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Featured researches published by W. Wayne Lautt.


Progress in Neurobiology | 1983

Afferent and efferent neural roles in liver function.

W. Wayne Lautt

1. Overview 323 2. Ana t omy 324 2.1. Extrinsic nerves 324 2.2, Intrinsic nerves 326 3. Effects on hepatic vasculature 327 3. l, The hepatic artery 327 3.2, Portal vein 328 3.3. Capacitance vessels 329 3.4, Fluid exchange and diffusion 329 3.5. Cholinergic effects 330 3.6. Summary 330 4. Glucose metabol ism 331 4.1. Sympathetic nerves 331 4.1.1. Physiological role 332 4.2. Parasympathetic nerves 334 4.3. Central nervous stimulations 334 5. Lipi d metabolism 335 6. Norepinephrine overflow 335 7. Biliary system 336 8. Reflex st imulation of hepatic sympathet ic nerves 337 9. Afferent hepatic nerves 338 9.1. Pressure or volume receptors 338 9.2. Osmoreceptors 339 9.3. Ion receptors 340 9.4. Glucose and metabolic receptors 340 10. Miscellaneous effects 341 10.1. Circadian rhythms 341 10,2. Hepatic regeneration 342 10,3. Factors interfering with normal nerve functions 342 10,4 General precautionary notes 343 Acknowledgements 343 References 343


Comparative Biochemistry and Physiology B | 1985

The activity of hepatic γ-glutamyltranspeptidase in various animal species

Susan J. Sulakhe; W. Wayne Lautt

The activity of gamma-glutamyltranspeptidase was determined in liver homogenates derived from various animals belonging to different phylogenetic groups. Although gamma-glutamyltranspeptidase was present in all livers studied, the activity varied greatly, with the order of activity being: guinea pig much greater than frog much greater than rabbit greater than toad greater than dog congruent to cat = duck greater than hamster = budgerigar = goldfish congruent to rat = mouse. There was no trend with respect to enzyme activity, phylogeny, diet, or habitat.


General Pharmacology-the Vascular System | 1980

Hepatic parasympathetic neuropathy as cause of maturity-onset diabetes?

W. Wayne Lautt

Abstract 1. 1. Only when glucose is presented orally does the liver account for a major proportion of glucose uptake, indicating the presence of some factor in the gut that can augment the effects of insulin and/or hyperglycemia on the liver. 2. 2. It is proposed that glucose in the gut produces a reflex activation of hepatic parasympathetic nerves. These nerves produce a dramatic and rapid uptake of glucose and in the absence of cholinergic stimulation the liver is weakly affected by insulin, a state similar to that of the liver of the maturity-onset diabetic. 3. 3. Selective parasympathetic neuropathy is seen at the very early stages of diabetes. It is proposed that hepatic parasympathetic neuropathy results in a reduction of the livers ability to trap glucose. 4. 4. This would account for the postprandial hyperglycemia seen in the maturity-onset diabetic. This hyperglycemia leads, in turn, to hyperinsulinism and thence to peripheral insulin resistance.


Microvascular Research | 1978

Hepatic presinusoidal sphincters affected by altered arterial pressure and flow, venous pressure, and nerve stimulation.

W. Wayne Lautt

Abstract Alterations in hepatic circulation and oxygen uptake were monitored using an intact feline liver preparation with arterial and portal blood flows measured separately and hepatic venous pressure under experimental control. Oxygen extraction ratios, if interpreted cautiously, can be used to indicate sphincter-like control of diffusion parameters in the tissues. Presinusoidal (precapillary) sphincters do not alter fluid exchange parameters in the liver. The results shown here are interpreted as providing evidence that sphincters or sphincter-like segments of the hepatic vasculature do, however, affect diffusion parameters. Constriction of sphincters is associated with a reduced oxygen extraction ratio, dilation with increased extraction. The sphincters are initially constricted by hepatic nerve stimulation but show a secondary dilation due to maintained reduction in conductance of the hepatic artery (upstream). Sphincter dilation, indicated by increased oxygen extraction under selective experimental conditions, was suggested. Elevations in arterial blood pressure produced myogenic arterial constriction which resulted in secondary sphincter dilation. Similarly, graded occlusion of the hepatic artery resulted in sphincter dilation. Sphincters appear to be controlled by blood flow changes since oxygen extraction changes were correlated with changes in blood flow but not with changes in hepatic oxygen delivery. Myogenic stimuli do not appear to affect sphincters since elevated hepatic venous pressure did not cause sphincter constriction, nor did in impair oxygen uptake.


Medical Hypotheses | 1979

Autonomic neural control of liver glycogen metabolism.

W. Wayne Lautt

Neural and humoral induction of hepatic glycogenolysis occurs via different pathways. Sympathetic nerve stimulation activates alpha adrenergic receptors to produce what is probably a cyclic AMP independent, Ca++ dependent activation of glycogen phosphorylase. Evidence suggests that phosphorylase a is activated by inhibition of phosphorylase phosphatase and perhaps by activation of phosphorylase kinase. Blood borne catecholamines act via beta adrenergic receptors to produce a cyclic AMP dependent activation of phosphorylase kinase. Additionally, hepatic parasympathetic nerves can produce a dramatic shut-down of hepatic glucose output by activation of glycogen synthetase and inhibition of glycogen phosphorylase. The observed minor effect of insulin or intravenous glucose on hepatic glucose uptake compared to the effect of oral doses of glucose suggests that an additional factor other than insulin can produce hepatic glucose uptake: this factor could be, and probably is, the hepatic parasympathetic nerves. The present hypotheses result from a combination and extrapolation of whole animal physiological and in vitro biochemical data.


Life Sciences | 1976

Effect of hepatic nerve stimulation on hepatic uptake of lidocaine in the cat

W. Wayne Lautt; F. Steve Skelton

Abstract Hepatic blood flow and lidocaine uptake were measured using a hepatic venous long-circuit preparation in cats anesthetized with pentobarbital-Na. The processes involved with hepatic elimination of lidocaine were not affected by stimulation of the hepatic nerves. The lack of neural influence on hepatic extraction ratios of lidocaine supports the contention that nerve stimulation does not result in shunting or redistribution of blood to non-nutritive sites. In species which do not show complete vascular escape from neurogenic vasoconstriction, a reduced lidocaine elimination would be anticipated since it was shown that reduced hepatic blood flow results in reduced lidocaine elimination. In the intact rat one third of the lidocaine in the blood was extracted on each passage through the liver. This extraction ratio is not affected by arterial levels of lidocaine, by changes in blood flow or by activation of the hepatic nerves.


Journal of The Autonomic Nervous System | 1984

The effect of intraportal and intravenous glucose infusion and an intravenous glucose tolerance test on insulin and glucagon levels in conscious cats with normal and chronically phenol-denervated livers.

W. Wayne Lautt

Cats were prepared with chronically implanted catheters in the portal and femoral vein for administration of glucose. A femoral arterial catheter was used for blood sampling. After at least 5 days following the implantations, cats received an infusion of 3 mg/kg/min into the portal vein and the insulin and glucagon responses were compared with a similar infusion into the femoral vein. The hypothesis predicted that glucose receptors in the liver would result in greater pancreatic hormonal responses than would be seen with the femoral infusions of glucose. This did not occur. There was no statistically significant difference between the rise in insulin and the decrease in glucagon elicited by the glucose infusion into the two alternate infusion sites. A sham-denervated series showed similar responses. A group of cats that underwent hepatic denervation using topical phenol application to the hepatic plexus near the hilum of the liver was tested. The responses of the denervated group were similar to those for the control and sham-operated groups, confirming that hepatic glucose receptors do not serve as an afferent limb of a hepato-pancreatic reflex controlling insulin and glucagon release in conscious cats. In all experiments, a bolus of glucose (500 mg) was injected i.v. to represent a tolerance test. The responses of blood glucose levels, pancreatic insulin and glucagon and recovery from the stimulus were similar in all groups which suggests that hepatic nerves are not essential for a normal hepatic response to intravenously infused glucose. It is suggested, however, that hepatic nerves may be important in producing normal hepatic responses to oral glucose loads.


Canadian Journal of Physiology and Pharmacology | 1980

Hepatic nerves: a review of their functions and effects

W. Wayne Lautt


Canadian Journal of Physiology and Pharmacology | 1978

Hepatic parasympathetic neural effect on glucose balance in the intact liver.

W. Wayne Lautt; Chong Wong


Canadian Journal of Physiology and Pharmacology | 1978

Hepatic glucose balance in response to direct stimulation of sympathetic nerves in the intact liver of cats.

W. Wayne Lautt; Chong Wong

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F. Steve Skelton

University of Saskatchewan

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Susan J. Sulakhe

University of Saskatchewan

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