Search PubMed⌕ Search

Biomedical subjects

J F Liard

Publications and source records attributed to J F Liard.

71 records · Page 4Linked to original sources
PubMed1976

Haemodynamics and body fluid volumes in response to fluid loading in conscious dogs: non-excretory renal influences.

1. Twelve conscious, chronically instrumented dogs were subjected to rapid loading with sodium chloride solution (150 mmol/1; saline) before and 1 day after bilateral nephrectomy (six dogs) or ureterocaval anastomosis (six dogs). Measurements were performed up to 3 h after the fluid load and included cardiac output with an electromagnetic flowmeter, mean arterial pressure and right atrial pressure with chronically implanted catheters, interstitial fluid pressure with a plastic capsule, heart rate, extracellular fluid volume, erythrocyte volume, plasma volume, plasma protein concentration and other variables. 2. The increase in cardiac output in response to saline load was significantly prolonged in the anephric dogs compared with those with uretero-caval anastomosis; mean arterial pressure, right atrial pressure and heart-rate changes were similar in both groups. 3. Plasma volume appeared to increase more in the anephric dogs than in those with uretero-caval anastomosis during the first hour after the infusion, although conflicting results were obtained with different estimates of plasma volume changes. Interstitial fluid pressure increased significantly less in the anephric dogs in the early stages of the fluid load. 4. Effective vascular compliance (the ratio of the change in blood volume to the change in right atrial pressure) appeared increased in the anephric dogs. On the other hand, the change in cardiac output for a given change in right atrial pressure was found to increase after bilateral nephrectomy. 5. It is suggested that the prolonged increase in cardiac output observed in anephric dogs was not the consequence of preferential plasma volume expansion nor of decreased venous compliance, but may reflect an alteration in the cardiac function curve.

Animals↗
PubMed1976

Lack of hypotensive effect on central injection of angiotensin inhibitors in spontaneously hypertensive (SH) and normotensive rats.

1. Injections of antagonists of angiotensin II into the cerebral ventricles of normotensive and spontaneously hypertensive rats were performed in order to assess the role of the isorenin-angiotensin system in the brain. 2. No hypotensive effect was obtained in either normotensive or hypertensive rats, suggesting that intracranial isoangiotensin has little role in the pathogenesis of spontaneous hypertension in the rat.

Angiotensin II↗
PubMed1975

Hemodynamic and humoral characteristics of hypertension induced by prolonged stellate ganglion stimulation in conscious dogs.

Recent evidence has suggested that cardiac factors may play a role in the evolution of arterial hypertension. To test the possibility that an increase in cardiac-performance can lead to a sustained increase in systemic blood pressure, we electrically stimulated the left stellate ganglion of six conscious dogs continuously for a 7-day period and monitored cardiac output and arterial blood pressure. In all six dogs, stimulation elicited an abrupt rise in systemic blood pre-sure that was entirely due to rise in cardiac output that lasted at least 6 hours. After 1 day of continuous stimulation, cardiac output retured to control values, but blood pressure remained elevated. After 7 days of stimulation, blood pressure was increased by an average of 25 mm Hg and peripheral resistance by 35 plus and minus 4%. Measurements of blood volume, plasma renin activity, circulating catecholamines (three of the six dogs), and sodium balance showed that none of these factors could explain the development pf this sustained hypertension. Pharmacologic blockade with phenoxybenzamine prevented in large part the rise in blood pressure in short-term stellate ganglion stimulations, whereas propranolol had very little effect on the pressor response, although it nearly abolished the increase in cardiac output. The data indicate that continuous stimulation of the stellate ganglion in conscious dogs leads to substained rises in both blood pressure and peripheral resistance; these changes are apparently mediated by increased activity of the sympathetic nervous system.

Animals↗
PubMedDate not supplied

Hemodynamic effects of antagonists of the vasoconstrictor action of vasopressin in conscious dogs.

Two antagonists of the pressor action of arginine-vasopressin (AVP) were studied in conscious, normally hydrated dogs: 1-deaminopenicillamine-4-valine-8-D-arginine-vasopressin, or dPVDAVP, and 1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid)2-(O-methyl)tyrosine arginine-vasopressin, or d(CH2)5Tyr(Me)AVP. We first examined the hemodynamic effects of these antagonists when given alone. The infusion of dPVDAVP, 200 ng/kg/min, increased cardiac output (measured with an aortic electromagnetic flowmeter) by 23% and heart rate by 27%, leaving arterial pressure unchanged. Most of the change in cardiac output reflected a large increase in skeletal muscle blood flow, as determined by radioactive microspheres. The injection of d(CH2)5Tyr(Me)AVP, 10 micrograms/kg, had little effect on cardiac output, arterial pressure, and heart rate. We then examined the ability of the two antagonists to block the hemodynamic responses to injections of AVP. In the absence of the antagonists, AVP induced dose-related increases in mean arterial pressure and total peripheral resistance, as well as decreases in heart rate and cardiac output. The antagonist dPVDAVP shifted the dose-response curves to the right without changing their slope. On the contrary, the hemodynamic response to AVP was strikingly modified following blockade with d(CH2)5Tyr(Me)AVP. Cardiac output and heart rate increased, whereas total peripheral resistance decreased, for doses of AVP between 25 and 400 ng/kg. It is concluded that some antagonists of the pressor action of vasopressin may influence hemodynamics of conscious dogs by effects other than competitive antagonism at the level of vascular receptors.

Animals↗
PubMedDate not supplied

Atropine potentiates the pressor effect of arginine-vasopressin in conscious dogs.

The hemodynamic effects of injections of arginine-vasopressin (AVP) at different doses were measured before and after administration of atropine (250 micrograms/kg), propranolol (2 mg/kg), or phenoxybenzamine (5 mg/kg) in conscious dogs. Measurements of arterial pressure derived from a chronic indwelling catheter, and aortic flow derived from an aortic electromagnetic flow probe, were digitized and analyzed by computer to assess mean and pulsatile arterial pressure, cardiac output, total peripheral resistance, heart rate, and other hemodynamic variables. AVP alone moderately increased arterial pressure and decreased cardiac output and heart rate. For doses between 20 and 40 ng/kg, mean arterial pressure increased by 17.4 +/- 1.5 mm Hg. After atropine, the same dose of AVP increased pressure by 51.6 +/- 3.2 mm Hg. The bradycardiac response to AVP was blunted by atropine as was the decrease in cardiac output. The effect of AVP on total peripheral resistance was not affected by atropine. Neither alpha- nor beta-adrenergic blockade enhanced the pressor effect of arginine-vasopressin. Our results indicate that the potentiation of the pressor response to AVP previously reported with total autonomic blockade is largely due to preventing a vagallymediated decrease in cardiac output in conscious dogs.

Animals↗
PubMedDate not supplied

Baroreceptor reflex influence on peripheral circulations in salt-loading hypertension in dogs.

To determine the importance of cardiovascular reflexes in the vasodilation found in skeletal muscle in the early stages of salt-loading hypertension in dogs, we gave for several days an intravenous infusion of isotonic sodium chloride, 190 ml/kg/day, to seven dogs with their renal mass reduced following extensive destruction of their arterial baroreceptor afferents. Mean arterial pressure, cardiac output (electromagnetic flowmeter), and regional blood flows (radioactive microspheres) were measured sequentially and the results compared with those obtained in five control dogs. The salt-loaded animals exhibited an increase in cardiac output and in arterial pressure on the first day of infusion. Blood flow to the splanchnic area, the skin, the bone, the skeletal muscle, the heart, the lungs and the brain increased significantly, but vascular conductance was unchanged in most territories, including skeletal muscle. After 5 to 7 days, cardiac output returned toward control values, but pressure remained elevated. Apart from the myocardium, the regional blood flows were normalized and the conductances were decreased. These results indicate that cardiovascular reflexes are responsible for the transient early vasodilation in skeletal muscle which characterizes salt-loading hypertension in intact animals.

Animals↗