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H H Vincent

Publications and source records attributed to H H Vincent.

At least 37 records · Page 2Linked to original sources
PubMed1990

Determinants of blood flow and ultrafiltration in continuous arteriovenous haemodiafiltration: theoretical predictions and laboratory and clinical observations.

In continuous arteriovenous haemofiltration (CAVH) or haemodiafiltration (CAVHD), it is important to obtain an adequate blood flow through the haemofilter to minimise the risk of excessive haemoconcentration and clotting. In this study we determined the resistance to blood flow of the extracorporeal device as well as the hydraulic permeability of the filter membrane is intensive care patients treated with CAVHD. Data were obtained for CAVH catheters and Scribner shunts and for a polyacrylonitrile (AN-69) plate filter, an AN-69 capillary filter and a polysulphone (PS) capillary filter. In accordance with recent literature we also predicted the resistance to flow by using Poiseuille's law and a formula for the estimation of blood viscosity. Although with all three filters an adequate blood flow was usually obtained, the resistance to blood flow was 2-3 times greater than the predicted value. With continued use of the filter, resistance to blood flow remained largely unchanged. When, in the laboratory, the AN-69 capillary filter was perfused with saline and with a viscous sucrose solution, the resistance to flow was only 1.4 time the predicted value, a difference that might result from small deviations of the capillary diameter. When perfused with blood, the resistance was 2.6 times greater than the predicted value. This was largely explained by gross underestimation of blood viscosity in these patients. By combining laboratory data on filter resistance during saline perfusion and a more accurate estimation of blood viscosity, a reasonably accurate prediction of blood flow rate would be feasible. In the clinic the hydraulic permeability of the filters decreased with time.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗
PubMed1990

Solute transport in continuous arteriovenous hemodiafiltration: a new mathematical model applied to clinical data.

A mathematical model of continuous arteriovenous hemodiafiltration is presented, by which the diffusive mass transfer coefficient (Kd) for a solute may be calculated from blood, filtrate and dialysate flow rates and solute concentrations. The model was applied to clinical data obtained with 0.6-m2 AN69 capillary dialyzers that had been used for up to 5 days. The diffusive mass transfer coefficient proved to depend on dialysate flow rate. Furthermore, it was related to the membrane index of ultrafiltration, as measured in the clinic, and to the filter resistance to blood flow. Measurement of these filter characteristics allowed a reasonable prediction of solute clearance.

Data Interpretation, Statistical↗
PubMed1988

Continuous arteriovenous haemofiltration and haemodiafiltration in acute renal failure.

Continuous arteriovenous haemofiltration (CAVH) was employed in ten patients with acute renal failure using an AN-69 plate filter. Special measures were taken to improve the efficiency of the technique, including the use of short, large-bore catheters for vascular access, predilution infusion of the substitution fluid, and moderate vacuum suction to the ultrafiltrate compartment. In five patients continuous arteriovenous haemodiafiltration was performed by the addition of slow dialysis at a dialysate flow of 1 litre per hour. This technically simple manoeuvre enhanced solute clearances up to 20 ml/min and obviated the need for standard intermittent dialysis sessions in all cases. Repeated measurements of transmembrane pressure and ultrafiltration rate permitted calculation of the in vivo membrane permeability index, which showed a reproducible decline with time. With relatively low heparin requirements an adequate filter performance could be maintained for over 48 h. The encouraging clinical results indicate that CAVHD, in spite of the invasive nature of this technique, may be considered a first-choice treatment for patients with acute renal failure in the intensive care unit.

Acute Kidney Injury↗
PubMed1987

Is beta 1-antagonism essential for the antihypertensive action of beta-blockers?

Both nonselective beta-blockers and beta 1-selective blockers are effective antihypertensive agents. beta 1-Blockade generally is considered to be responsible for their antihypertensive action, whereas beta 2-blockade is regarded as undesirable. These common assumptions notwithstanding, the mechanism by which beta-blockers lower blood pressure remains unknown. To examine the possibility that beta 2-blockade may contribute to the antihypertensive action of beta-blocker therapy, we studied the cardiovascular effects of compound ICI 118551, a beta 2-selective blocker. First, we showed that 50 mg t.i.d. orally is a beta 2-selective dose. In contrast to propranolol, 80 mg t.i.d., or atenolol, 100 mg once a day, 50 mg of ICI 118551 t.i.d. failed to block beta 1-mediated inotropic stimulation and stimulation of renin by isoproterenol. We then performed a double-blind, placebo-controlled trial in patients with mild essential hypertension to compare this compound with propranolol, 80 mg t.i.d., and showed that ICI 118551 significantly decreased systolic and diastolic blood pressure. This antihypertensive effect was demonstrated by direct as well as by indirect blood pressure measurements. Thus, contrary to prevailing thought, beta 2-blockade has an antihypertensive effect independent of, and distinct from, beta 1-blockade.

Adrenergic beta-Antagonists↗
PubMed1986

Stress levels of adrenaline amplify the blood pressure response to sympathetic stimulation.

The possibility that sympathetic pressor responses are modulated by adrenaline-mediated facilitation of neuronal noradrenaline release was explored in 17 subjects with borderline hypertension. Infusion of adrenaline, which raised plasma adrenaline by a factor of 8 to 9, augmented the rise in systolic and diastolic arterial pressure induced by standardized cold pressor and isometric exercise tests. The heart rate response to these tests was not affected. When a low dose of propranolol was given on top of the adrenaline infusion before the cold pressor test, the blood pressure response to cold exposure was not different from the response observed when the test was performed during saline infusion. Plasma noradrenaline was higher during adrenaline infusion then during saline infusion, both before and after the cold pressor and isometric exercise tests, and the effect of adrenaline on plasma noradrenaline was antagonized by propranolol. These observations are consistent with the hypothesis that stress levels of circulating adrenaline may amplify sympathetic pressor responses by facilitation of the release of transmitter noradrenaline.

Adolescent↗
PubMed1985

Prevention of epinephrine-induced hypokalemia by nonselective beta blockers.

Experimental evidence is presented that activation of beta 2 adrenoreceptors causes a dose-dependent decrease in plasma potassium, probably by shifting potassium into the cell. By this mechanism epinephrine may cause hypokalemia and predispose to cardiac arrhythmias. Prevention of these effects by nonselective beta blockers may contribute to the cardioprotective action of these drugs.

Adrenergic beta-Antagonists↗
PubMed1985

Compound ICI 118,551, a beta 2-adrenoceptor antagonist, lowers blood pressure.

Adrenaline may increase noradrenaline release and enhance sympathetic pressor effects through activation of pre-synaptic beta 2-adrenoceptors. Conversely, blockade of beta 2-receptors could lead to a fall in blood pressure. To test this hypothesis we performed a double-blind placebo controlled crossover study in nine patients with mild hypertension, comparing the effects of the beta 2-selective blocker ICI 118,551, 50 mg t.i.d. with those of propranolol, 80 mg t.i.d. Two hours after the first dose of ICI 118,551 or propranolol, plasma noradrenaline and blood pressure remained unchanged while heart rate and renin were reduced. After 1 week, blood pressure was significantly reduced by both drugs. The beta 2-selectivity of ICI 118,551 was confirmed by isoprenaline infusion studies. After 1 week of treatment ICI 118,551 had no effect on the beta 1-receptor mediated shortening of electromechanical systole (QS2I), the rise in systolic pressure and rise in renin, whereas these responses were blocked by a dose factor of eight after propranolol. ICI 118,551 and propranolol equally blocked the beta 2-receptor mediated fall in diastolic pressure and the rise in noradrenaline. We conclude that beta 2-selective blockade by ICI 118,551 lowers blood pressure. This finding is compatible with a role of pre-synaptic beta 2-receptors in blood pressure control.

Adrenergic beta-Antagonists↗
PubMed1983

Cardioprotection by blockade of beta 2-adrenoceptors.

The effects of different beta-adrenoceptor agonists and antagonists on plasma noradrenaline and potassium concentrations were studied in patients with borderline hypertension. Heart rate, arterial pressure and the heart rate corrected duration of total electromechanical systole (QS2I) were also measured. Infusion of the beta-adrenoceptor agonists isoprenaline (non-selective) and salbutamol (beta 2-selective), but not prenalterol (beta 1-selective) caused dose-dependent increments in plasma noradrenaline. Isoprenaline and salbutamol decreased plasma potassium dose-dependently. For a given effect on heart rate and QS2I the fall in potassium was less pronounced after prenalterol. The effects of isoprenaline were also studied after the beta-adrenoceptor antagonists propranolol, 320 mg day-1 for 1 week (non-selective) and atenolol, 100 mg day-1 for 1 week (beta1-selective). The effects of isoprenaline, when infused in equipotent chronotropic doses, on noradrenaline and potassium were not affected by atenolol, whereas they were completely abolished by propranolol. The rise in noradrenaline during beta-adrenoceptor stimulation could be explained by presynaptic facilitation of noradrenaline release. The fall in potassium probably reflects stimulation of Na-K-ATPase dependent transport of potassium into the cell. Both effects were seen after beta 2- but not after beta 1-adrenoceptor stimulation. Hypokalaemia and raised levels of noradrenaline are also known to occur under such stressful conditions as acute myocardial infarction, when circulating levels of the endogenous beta 2-adrenoceptor agonist adrenaline are high. Blockade of these effects by beta-adrenoceptor antagonists may contribute to the cardioprotective effect of these drugs. This warrants further consideration of the clinical significance of beta-blocker selectivity.

Adrenergic beta-Agonists↗
PubMed1976

Postoperative impairment of mucous transport in the lung.

Impairment of mucous transport is considered significant to the postoperative development of atelectasis, but the association has never beed demonstrated in humans. Tantalum powder, which adheres to airway mucus, can be used to study mucociliary transport. The postoperative clearance of insufflated tantalum powder (mean diameter, 2.5 mum) was investigated in 25 patients. Eighteen patients underwent intra-abdominal vascular surgery and 7 undersent lower-extremity orthopedic procedures. At the completion of surgery, tantalum was insufflated into both lungs of each patient to outline a representative sample of airways from the trachea to the small bronchi. Tantalum clearance was evaluated from serial radiographs obtained immediately after insufflation, at approximately 6, 18, 26, and 48 hours later, and thereafter whenever appropriate. In the 7 orthopedic patients, clearance of tantalum was progressive and usually complete within 48 hours. Atelectasis did not occur in this group. In 14 of the 18 patients who had abdominal surgery, mucociliary clearance was markedly abnormal in that tantalum was retained for up to 6 days. Pooling of tantalum-labeled mucus occurred in dependent bronchi in 16 of these 18 patients. Pooling preceded and always accompanied radiographically visible atelectasis. Lobar atelectasis occurred in 6 patients and segmental atelectasis in 8. Tantalum-labeled mucus moved peripherally in atelectatic lobes or segments and was retained in these bronchi until re-expansion took place. Thus, impaired ciliary function and mucous transport are associated with and implicated in postoperative pulmonary atelectasis.

Aged↗
PubMedDate not supplied

A mathematical model of continuous arterio-venous hemodiafiltration (CAVHD).

Continuous arterio-venous hemodiafiltration (CAVHD) differs from conventional hemofiltration and dialysis by the interaction of convection and diffusion, the use of very low dialysate flow rates and by the deterioration of membrane conditions during the treatment. In order to study the impact of these phenomena on diffusive transport, we developed a mathematical model of the kinetics of CAVHD solute transport from plasma water to dialysate. The model yields an expression of the diffusive mass transfer coefficient, Kd, as a function of blood, filtrate and dialysate flow rates and solute concentrations, which can be measured in the clinical setting. This paper gives a description of the model derivation. Kd is demonstrated to vary depending on dialysate flow and duration of treatment.

Blood Flow Velocity↗