Search PubMed⌕ Search

Biomedical subjects

J F Liard

Publications and source records attributed to J F Liard.

At least 55 records · Page 3Linked to original sources
PubMed1984

Atropine potentiates the pressor response to arginine-vasopressin in conscious dogs.

The haemodynamic effects of bolus injections of increasing doses of arginine-vasopressin (AVP) were examined in conscious dogs chronically instrumented for the measurement of arterial pressure and cardiac output (aortic electromagnetic flowmeter), both before and after administration of the antimuscarinic agent atropine, 250 micrograms/kg. Haemodynamic variables were monitored and analysed using computerized techniques. The pressor response to AVP was markedly enhanced by atropine treatment, which decreased the relative fall of cardiac output but did not affect the relative increase in total peripheral resistance. It is therefore concluded that the fall in cardiac output which follows AVP administration is in part vagally mediated, and that preventing the vagal component of the cardiac output decrease contributes to the exaggerated pressor response induced by atropine.

Animals↗
PubMed1982

Cardiac output distribution during vasopressin infusion or dehydration in conscious dogs.

To better understand the role of arginine vasopressin in cardiovascular regulation, we measured in unanesthetized dogs regional blood flows with radioactive microspheres before and during 1-h vasopressin infusions that increased the vasopressin concentration of plasma by 11 +/- 0.6 pg/ml. Cardiac output measured by an electromagnetic flowmeter decreased by 13%. Blood flows to the skeletal muscle and skin, the areas most affected, decreased by 30.8 and 34.3%, respectively. In the same group of dogs a period of 48-h water restriction increased plasma vasopressin by 6.9 +/- 1.3 pg/ml and reduced cardiac output by 14.4%. Skeletal muscle blood flow decreased by 32.8%, a pattern strikingly similar to that following vasopressin infusion. Obvious differences between vasopressin infusion and dehydration were also noted, in particular in the skin and splanchnic areas. However, the possibility that vasopressin contributed to the cardiovascular adjustments to dehydration must be considered. The use of an antagonist of the vascular effects of vasopressin, [1-deaminopenicillamine, 2-(O-methyl)tyrosine]arginine-vasopressin ([dPTyr(Me)]AVP), did not permit us to clarify this issue, because this analogue given alone exerted pronounced systemic and regional cardiovascular effects that resembled those of vasopressin.

Animals↗
PubMed1981

Cardiovascular effects of vasopressin infused into the vertebral circulation of conscious dogs.

1. Seven conscious dogs received arginine-vasopressin infusions (100 and 1000 fmol min--1 kg--1) through catheters implanted in the left vertebral artery or the inferior vena cava while arterial pressure, cardiac output (electromagnetic flowmeter) and heart rate were measured. 2. Despite similar increases in plasma vasopressin concentrations, intravertebral administration induced a lesser increase in mean arterial pressure and a greater decrease in heart rate than the same infusion given intravenously. 3. These results suggest that vasopressin has an effect on structures of the central nervous system involved in cardiovascular control, possibly by affecting the baroreceptor reflex.

Animals↗
PubMed1981

Regional blood flows in salt loading hypertension in the dog.

An intravenous infusion of isotonic sodium chloride, 196 ml/kg per day, was administered for several days to eight dogs with their renal mass reduced. Mean arterial pressure, cardiac output (electromagnetic flowmeter), and regional blood flows (radioactive microspheres) were measured sequentially and the results compared with those obtained in six control dogs. The salt-loaded animals exhibited on the 1st day of the infusion a 25% increase of arterial pressure and cardiac output. Blood flows to the kidney, the splanchnic area, the skin, and the bone were not significantly changed, whereas skeletal muscle blood flow almost doubled. After several days, cardiac output returned toward control values but pressure remained elevated. Skeletal muscle blood flow, as most other regional flows, did not differ significantly from control values at that time. In four dogs studied 6 h after starting a faster saline infusion, most of the increase in cardiac output was also distributed to the skeletal muscle. Total peripheral resistance changes did not reflect the resistance of individual beds, because vasoconstriction appeared early in some areas but was masked by prominent, although transient, vasodilation in skeletal muscle.

Animals↗
PubMed1980

Parenteral nutrition and repeated hemodialysis of bilaterally nephrectomized conscious dogs. I. Experimental model.

The experimental model of the anephric, daily hemodialyzed conscious dog with exclusive nutrition was realized by means of a closed batch hemodialysis system (Rhodial 75) and a highly permeable polyacrylonitrile membrane (RP 6 dialyzer). Technical details, parenteral feeding, hemodialysis, and amino acid solutions preparations were described to realize a stable condition of the animals for further metabolic analyses during the early anephric period.

Amino Acids↗
PubMed1980

Regional blood flows in high-cardiac-output hypertension.

1. Mean arterial pressure, cardiac output (electromagnetic flow-meter) and regional blood flows (15 micrometer radioactive microspheres) were measured repeatedly in eight dogs receiving a salt and water load after renal mass reduction as well as in six control animals. 2. As previously observed, hypertension developed in the salt-loaded dogs with an initial increase in cardiac output followed by a secondary rise in total peripheral resistance. 3. Much of the early increase in cardiac output was distributed to the skeletal muscle vascular bed. 4. Total peripheral resistance changes did not reflect the resistance of individual vascular beds in the early stages of salt and water load hypertension; indeed, resistance in the muscle vascular bed was decreased and that in the splanchnic area and the bone increased on the first day of salt and water load when total peripheral resistance was unchanged.

Animals↗
PubMed1980

Hemodynamic effects of exogenous and endogenous vasopressin at low plasma concentrations in conscious dogs.

The possibility that vasopressin plays a role in cardiovascular control arouses increasing interest. We studied in unanesthetized dogs the hemodynamic consequences of 1-hour vasopressin infusions that modified plasma concentrations over a range similar to that found in physiological situations. We also examined the cardiovascular events following the stimulation of endogenous vasopressin release by an increase in plasma osmolality. In dogs with baroreceptor reflexes intact, vasopressin infusions which increased plasma vasopressin concentration by 2-20 fmol/ml did not affect mean arterial pressure. However, they significantly decreased cardiac ouput (measured by an electromagnetic flowmeter) and increased total peripheral resistance. After baroreceptor denervation, vasopressin infusion rates as low as 40 fmol/kg per min (0.017 microU/kg per min) led to an increase in mean arterial pressure. Cardiac output was unaffected until much higher infusion rates were used. Changes in total peripheral resistance were very similar to those calculated in dogs with intact baroreceptors. The release of vasopressin following infusions of hypertonic solutions either intravenously or into a carotid artery induced detectable hemodynamic changes which appeared in many respects similar to those following low infusion rates of vasopressin. We conclude that physiological plasma concentrations of vasopressin have hemodynamic effects even though they do not normally modify arterial pressure, presumably because of some particular interaction of vasopressin with the baroreceptor reflex.

Animals↗
PubMed1980

The baroreceptor reflexes in experimental hypertension.

Experimental hypertensions following sino-aortic deafferentation or manoeuvres not involving initially the baroreceptor reflexes are discussed in relation with a simple graphical analysis of these reflexes. Blood pressure increases only slightly as a result of interruption of the sino-aortic afferences, but its variability is markedly enhanced. On the other hand, the final level of arterial pressure in various forms and non-neurogenic hypertension appears independent from the presence of the baroreceptor reflexes ("resetting"). Thus, the baroreceptor reflexes are of primary importance in limiting variations around a given level of arterial pressure, but they do not really set this level since it can be modified easily by other blood pressure control systems. In order to emphasize the role of the baroreflex in the short-term regulation of blood pressure and other haemodynamic variables, its significance in "whole-body autoregulation" and in the cardiovascular effects of vasopressin is discussed.

Animals↗
PubMed1979

Effects of propranolol in chronic two-kidney Goldblatt hypertension in rats.

Propranolol administered subcutaneously in a dise of 30 mg/kg twice a day for 3 weeks did not significantly lower systolic tail blood pressure (STBP) in chronic two-kidney Goldblatt hypertension in rats. Plasma renin activity (PRA) measured at the end of the treatment was not significantly different in propranolol treated and dextrose treated rats, although there was marked bradycardia in propranolol treated rats. However, 3 out of 10 propranolol treated hypertensive rats had pressures in the normotensive range during the last week of therapy. PRA values in these three rats were significantly lower than those in dextrose treated hypertensive rats. STBP on day 20 showed a positive correlation with PRA in both propranolol (r = 0.90, p less than 0.01) and dextrose (r = 0.85, p less than 0.01) treated hypertensive rats. Hypertension was associated with an increase in heart weight, which was significantly blunted but not abolished by propranolol treatment. Thus, propranolol did not decrease blood pressure in most rats with chronic two-kidney Goldblatt hypertension; when it did lower blood pressure, its antihypertensive effect appeared related to its renin suppression effect. Furthermore, propranolol mitigated hypertension induced cardiac hypertrophy, independently of its antihypertensive effect.

Animals↗