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Biomedical subjects

R G Pearl

Publications and source records attributed to R G Pearl.

85 records · Page 5Linked to original sources
PubMed1987

Pulmonary and systemic hemodynamic effects of central venous and left atrial sympathomimetic drug administration in the dog.

Systemic vasopressor or inotropic therapy may exacerbate existing pulmonary hypertension; the optimal agent and route of administration in this situation are unknown. The systemic and pulmonary hemodynamic effects of four sympathomimetic agents (dopamine, epinephrine, norepinephrine, and phenylephrine) during central venous and left atrial administration were investigated in the anesthetized dog. All four drugs increased both systemic and pulmonary artery pressures. Dopamine and epinephrine increased cardiac output and reduced systemic vascular resistance. Phenylephrine decreased cardiac output and increased systemic vascular resistance and left atrial pressure. Norepinephrine did not significantly affect cardiac output, systemic vascular resistance, or left atrial pressure. None of the four drugs affected pulmonary vascular resistance. The ratio of systemic to pulmonary vascular resistance decreased with epinephrine and increased with phenylephrine. There were no hemodynamic differences related to the route of infusion for any of the four drugs. However, pulmonary arterial concentrations of the three drugs measured (dopamine, epinephrine, and norepinephrine) were markedly lower during left atrial compared to central venous drug administration; systemic drug concentrations were similar or increased during left atrial compared to central venous drug administration. It is concluded that the relative effects on the systemic and pulmonary circulations differ for the four drugs; rational choice of a vasopressor will depend upon the hemodynamic situation and the desired effect. Left atrial catecholamine administration is effective in decreasing pulmonary arterial drug concentrations and may decrease adverse pulmonary effects in clinical practice.

Animals↗
PubMed1987

Care of the adult patient during transport.

Interhospital transport of the critically ill patient involves maintaining the same quality of care that was present before transport. This requires planning for equipment, space, and personnel needs during transport, and instituting adequate pathophysiologically based treatment and stabilization prior to transport. Under such conditions, transport can be safely accomplished and have a positive impact on patient care.

Adult↗
PubMed1986

Hemodynamic effects of positive end-expiratory pressure during continuous venous air embolism in the dog.

Positive end-expiratory pressure (PEEP) may decrease venous air embolism (VAE) by increasing venous pressure at the incision level. Because PEEP and VAE can both increase pulmonary vascular resistance, it is possible that the application of PEEP during VAE may increase right atrial pressure (RAP) relative to left atrial pressure (LAP) and thereby reverse the normal interatrial pressure gradient, allowing paradoxical air embolism in patients with a probe-patent foramen ovale. We studied atrial pressures during 0, 4, and 8 mmHg PEEP before and during continuous VAE in both supine and upright tilted dogs. Both PEEP and VAE increased pulmonary artery pressure and resistance. Prior to VAE, PEEP increased both RAP and LAP but did not affect the interatrial pressure gradient. VAE alone did not affect RAP, LAP, or the interatrial pressure gradient. Application of PEEP during VAE had similar effects as at baseline, namely an increase in RAP and LAP with no change in the interatrial pressure gradient. Although RAP exceeded LAP more frequently in the upright than in the supine dogs, the effects of PEEP and VAE on atrial pressures were similar in both groups. Our finding that PEEP and VAE did not disproportionately increase RAP compared with LAP is consistent with other studies demonstrating preservation of right ventricular function in situations of increased right ventricular afterload.

Animals↗
PubMed1986

Effect of injectate volume and temperature on thermodilution cardiac output determination.

Six combinations of injectate volume (10, 5, and 3 ml) and temperature (0 degree C and room temperature [RT]) are recommended by the manufacturers of thermodilution cardiac output catheters and computers. We prospectively studied the accuracy and variability associated with these six combinations in critically ill patients requiring intermittent mandatory ventilation. The six methods were similar in their average estimation of cardiac output but differed markedly in their reproducibility. The 10 ml 0 degree C and 10 ml RT combinations produced the least variability. The 5 ml 0 degree C and 5 ml RT combinations produced more variability. Variability was much greater with the remaining two combinations. The 3 ml RT combination resulted in an average range of 1.71 1/min within each set of three repeat measurements and an average absolute difference of 1.51 1/min from the values obtained with 10 ml 0 degree C (each the mean of three injections). We recommend the use of 10 ml 0 degree C or 10 ml RT for cardiac output determinations in critically ill patients. If it is important to minimize volume administration, the use of 5 ml injectate is acceptable for an estimation of cardiac output. The use of 3 ml injectate volumes is rarely, if ever, justified because the small reduction in volume administration results in a large increase in variability.

Adult↗
PubMed1986

Nitroglycerin-responsive pulmonary hypertension in idiopathic pulmonary hemosiderosis.

Idiopathic pulmonary hemosiderosis (IPH) is an uncommon disease found predominantly in pediatric patients. It can produce severe chronic pulmonary injury that results in chronic hypoxemia, pulmonary insufficiency, and progressive pulmonary fibrosis, leading to irreversible pulmonary hypertension and death. We studied the pulmonary hemodynamics in an 9-yr-old boy with IPH to determine if pulmonary hypertension contributed to exacerbations of this disease. Our results showed that this patient demonstrated pulmonary hypertension during acute exacerbations. Initially, the elevated pulmonary artery pressure responded both to oxygen and to a pulmonary vasodilator in the form of nitroglycerin. However, this improvement was not sustained. We conclude that pulmonary hypertension is probably a result of chronic hypoxemia experienced by patients with pulmonary hemosiderosis. Further investigation is warranted to assess whether or not intervention aimed at reducing pulmonary artery pressure in IPH improves outcome.

Child↗
PubMed1985

Metabolic alkalosis due to plasmapheresis.

Progressive metabolic alkalosis developed in two patients undergoing daily plasmapheresis for diffuse intrapulmonary hemorrhage associated with glomerulonephritis (Goodpasture's-like syndrome). The metabolic alkalosis promptly resolved when the plasmapheresis procedure was altered so that 3 percent albumin and cryoprecipitate rather than fresh frozen plasma were used as replacement for the removed patient plasma. The development of metabolic alkalosis during plasmapheresis can be explained by the large sodium citrate load given during the procedure. Severe metabolic alkalosis may develop in patients with decreased renal function when they are treated with plasmapheresis. The metabolic alkalosis can be prevented by appropriate modifications in the plasmapheresis protocol.

Aged↗
PubMed1984

Aminophylline potentiates sodium nitroprusside-induced hypotension in the dog.

The biochemical mechanisms by which nitroso-vasodilators cause smooth muscle relaxation remain controversial. One theory states that the effects of nitroso-vasodilators are mediated by increased intracellular levels of cyclic GMP due to activation of guanylate cyclase. To test this hypothesis, the authors examined the effects of sodium nitroprusside (SNP) in anesthetized dogs with an without pretreatment with the phosphodiesterase inhibitor aminophylline. Aminophylline pretreatment resulted in a 2.8-fold potentiation of the hypotensive effects of a continuous infusion of SNP. Potentiation also was seen for the effects of SNP on stroke volume, heart rate, and plasma cyclic GMP levels. These results support the hypothesis that nitroso-vasodilators exert their effects via guanylate cyclase activation. The authors advise caution when vasodilator therapy with agents such as SNP, nitroglycerin, or hydralazine is instituted in patients receiving aminophylline and when aminophylline is either instituted or discontinued in patients on vasodilator therapy.

Aminophylline↗
PubMed1983

Pulmonary vasodilator effects of nitroglycerin and sodium nitroprusside in canine oleic acid-induced pulmonary hypertension.

The hemodynamic effects of nitroglycerin (TNG) and sodium nitroprusside (SNP) were studied in a canine model of pulmonary hypertension. Oleic acid administration resulted in pulmonary hypertension with a 133% increase in pulmonary vascular resistance (PVR), a 40% increase in mean pulmonary artery pressure (MPAP), and a 28% decrease in cardiac output (CO). In this model, subsequent TNG administration increased CO 40%, decreased PVR 43%, and decreased MPAP 12%; pulmonary hemodynamics during TNG administration were not significantly different from those prior to oleic acid administration. SNP produced systemic hypotension but did not alter either PVR or MPAP and increased CO only 14%. The efficacy of TNG in this model may relate to its ability to dilate preferentially the pulmonary vascular bed.

Animals↗
PubMed1983

Niacin reduces oxygen toxicity in mouse alveolar macrophages.

Niacin at concentrations of 0.1-10 mM resulted in a dose-dependent reduction of oxygen toxicity in a mouse alveolar macrophage model. These concentrations of niacin did not affect alveolar macrophage function under normoxic conditions. Our results are consistent with observations from other groups that niacin reduces oxygen toxicity in bacteria and paraquat toxicity in bacteria and rats. The mechanism by which niacin reduces oxygen toxicity may involve the ability of niacin to function as an alternate substrate for NAD synthesis. Niacin may have clinical value in the prevention of oxygen toxicity.

Animals↗
PubMed1983

Acute hemodynamic effects of nitroglycerin in pulmonary hypertension.

Therapy of pulmonary hypertension is limited by the low potency and adverse effects of current pulmonary vasodilators. The hemodynamic effects of nitroglycerin in human pulmonary hypertension are not known. We administered nitroglycerin to nine patients with chronic pulmonary hypertension. Nitroglycerin increased cardiac index 40% (p less than 0.01), increased stroke volume 40% (p less than 0.01), decreased pulmonary vascular resistance 40% (p less than 0.01), and decreased mean pulmonary artery pressure 15% (p less than 0.01). Pulmonary vascular resistance decreased more than 25% in eight of the nine patients. In four patients the effects of intravenous nitroglycerin were reproduced by topical nitroglycerin preparations; cardiac index increased 50%, stroke volume increased 48%, pulmonary vascular resistance decreased 43%, and mean pulmonary artery pressure decreased 19%. Five of six patients treated with long-acting nitrates had substantial improvement of their symptoms. We conclude that therapy with nitroglycerin can be effective in patients with severe pulmonary hypertension.

Adult↗
PubMed1979

d-Amphetamine-induced increase in catecholamine synthesis in the corpus striatum of the rat: persistence of the effect after tolerance.

The effect of d-amphetamine on in vivo catecholamine synthesis in four regions of rat brain was determined by measuring the accumulation of dopa after inhibiton of dopa decarboxylase. In doses up to 2.5 mg/kg, d-amphetamine caused dose-dependent increases in striatal dopa accumulation to a maximum of 280% of control; further increases in dose resulted in smaller effects until 10 mg/kg d-amphetamine was not significantly different from control. d-Amphetamine did not alter dopa accumulation in telencephalon, in diencephalon-mesencephalon, or in pons-medulla oblongata. d-Amphetamine did not affect either dopamine levels in striatum or NE levels in pons-medulla oblongata; at high doses, d-amphetamine did reduce norepinephrine levels in telencephalon and in diencephalon-mesencephalon. Daily administration of pre-session but not of post-session d-amphetamine produced tolerance to the effects of d-amphetamine on milk consumption in rats. The ability of d-amphetamine to increase striatal catecholamine synthesis was not altered by the development of tolerance to d-amphetamine. These results suggest that tolerance to d-amphetamine is not related to its effect on catecholamine synthesis but instead occurs via changes in aspects of catecholamine metabolism other than synthesis via change in catecholamine release, reuptake, or receptor sensitivity, or via changes in non-catecholaminergic mechanisms.

Animals↗
PubMed1976

The existence of tolerance to and cross-tolerance between d-amphetamine and methylphenidate for their effects on milk consumption and on differential-reinforcement-of-low-rate performance in the rat.

Administration of d-amphetamine (2.5 mg/kg) or methylphenidate (20 mg/kg) decreased milk consumption in rats. When these drugs were administered daily, tolerance developed to this effect over the course of 20 days. Cross-tolerance to the effects on milk consumption occurred between d-amphetamine and methylphenidate over a 4-fold range of dose of both drugs. Administration of d-amphetamine (1.5 mg/kg) or methylphenidate (10 mg/kg) disrupted responding under differential-reinforcement-or-low-rate (DRL) contingencies. Both drugs increased response rate, decreased frequency of reinforcement and shifted the mode of the inter-response time distribution to the left. When the drugs were administered daily, tolerance developed to all these effects over the course of 20 days. Cross-tolerance to the effects on DRL behavior occurred between d-amphetamine and methylphenidate over a 4-fold range of dose of both drugs. Daily administration of d-amphetamine (2.5 mg/kg) but not of methylphenidate (20 mg/kg) resulted in decreased norepinephrine (NE) levels in brain; the decreased norepinephrine levels, which occur with repeated d-amphetamine administration, are believed to result from the storage in noradrenergic neurons of p-hydroxynorephedrine, a metabolite of d-amphetamine. Radioactivity was not detectable in brain 24 hours after the last of 15 daily doses of radiolabeled methylphenidate. These results suggest that d-amphetamine, but not methylphenidate, is metabolized to a compound which is stored in noradrenergic neurons. The existence of behavioral cross-tolerance between d-amphetamine and methylphenidate is therefore inconsistent with the hypothesis that tolerance to the behavioral effects of d-amphetamine is due to the metabolism of d-amphetamine to p-hydroxynorephedrine, a false transmitter in noradrenergic neurons.

Animals↗