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Biomedical subjects

D Kenny

Publications and source records attributed to D Kenny.

At least 19 recordsLinked to original sources
PubMed1992

Effect of omega-3 fatty acids on the vascular response to angiotensin in normotensive men.

There is a widespread interest in fish oil as a dietary supplement and possible nonpharmacologic adjunct in the treatment of hypertension. The effect of dietary fish oil on blood pressure is controversial and the effect on systemic hemodynamics and regional vascular reactivity in humans is unknown. To address these questions, a double-blind, placebo-controlled, crossover study on the effect of dietary fish oil substitution was performed during a carefully controlled diet in 8 normotensive men. Systemic hemodynamics and the forearm vascular response to intrabrachial artery infusions of norepinephrine, phentolamine and angiotensin II were obtained. Compared with a safflower oil placebo, dietary fish oil had no effect on cardiac output (6.42 +/- 0.38 vs 6.87 +/- 0.28 liters/min, p = not significant) or 24-hour blood pressure (122/68 +/- 3/3 vs 122/68 +/- 3/2 mm Hg, p = not significant). The vascular response to norepinephrine and phentolamine was unchanged. Fish oil, however, significantly (p < 0.05) reduced forearm vascular resistance responses to angiotensin II. These changes were associated with a reduction in plasma triglycerides (64 +/- 9 vs 39 +/- 4 mg/dl, p = 0.02) and an increase in plasma eicosapentaenoic acid levels (0.51 +/- 0.25 vs 1.72 +/- 0.35 microM, p < 0.05). Substitution of a moderate dose of fish oil for fat in a "Western diet" selectively attenuates the vascular response to angiotensin independently of changes in alpha-adrenergic vasoconstriction or systemic hemodynamics.

Adult↗
PubMed1992

Dietary fish oil and rheumatic diseases.

Dietary fish oil supplementation can induce several metabolic changes relevant to rheumatic diseases. Both experimental and clinical evidence show that dietary fish oil supplementation modulates inflammatory and immune responses. Many studies have shown beneficial, albeit modest, effects in the treatment of rheumatoid arthritis. Studies in murine models of systemic lupus erythematosus have been encouraging, but few studies have been performed to assess the effects of dietary fish oil in the human disease or in other systemic rheumatic diseases. Further study on the efficacy of dietary fish oil supplementation in the treatment of specific rheumatic diseases is warranted.

Arthritis, Rheumatoid↗
PubMed1992

The paradoxical effects of dietary fish oil on blood pressure.

Dietary fish oil supplementation has received considerable interest as a non-pharmacological adjuvant in the treatment of several diseases, especially hypertension. However, epidemiological, clinical, and experimental evidence conflict. A hypothesis is proposed that fish oil, may have a variable effect on vascular reactivity and consequently, blood pressure. A mechanism is proposed and reasons for the variation in the literature suggested. On the basis of this analysis a potentially adverse effect of dietary fish oil on blood pressure in some individuals is suggested.

Animals↗
PubMed1992

Reference values for urinary HMMA, HVA, noradrenaline, adrenaline, and dopamine excretion in children using random urine samples and HPLC with electrochemical detection.

Random urine samples were collected from 305 children aged from birth to 14 years and the values of hydroxymethoxymandelic acid, homovanillic acid, noradrenaline, adrenaline, and dopamine were measured by high-performance liquid chromatography with electrochemical detection. The results were reported relative to the urinary creatinine concentration and the values declined progressively with increasing age for each analyte with the exception of adrenaline. The results for each age group were not normally distributed and all values except outliers were retained in determining the upper reference limits.

Adolescent↗
PubMed1992

Differential relaxant effect of high concentrations of intravenous anesthetics on endothelin-constricted proximal and distal canine coronary arteries.

This study determined the direct effect of three intravenous anesthetics on isolated canine coronary arteries constricted with the potent endogenous vasoconstrictor endothelin. Arteries were divided into groups of large (1.3-2.5 mm) and small (250-500 microns) vessels, and arterial rings were suspended in tissue baths. The rings were stretched to an optimal resting tension and then preconstricted with an EC50 concentration of endothelin that was equivalent for both groups. Incremental concentrations (5 x 10(-6) M to 1.6 x 10(-2) M) of thiopental, ketamine, and propofol were added to the baths, and the relaxant responses were recorded. Small arteries demonstrated greater vasodilation at equivalent drug concentrations than did large arteries. These results demonstrate antagonism of the vasoconstrictor endothelin by intravenous anesthetics. Distal vessels are more sensitive than proximal vessels to the relaxant effects of the intravenous anesthetics studied. Direct effects on coronary vascular tone, however, are only apparent at concentrations above those seen clinically. Despite the potential for a differential effect on proximal and distal coronary arteries, we conclude that thiopental, ketamine, and propofol do not possess a direct effect on the tone of large or small canine coronary arteries at concentrations seen in routine clinical practice.

Anesthetics↗
PubMed1992

Cocaine depresses myocardial contractility and prolongs isovolumetric relaxation in conscious dogs with partial autonomic nervous system blockade.

The direct effects of cocaine on myocardial contractility and isovolumetric relaxation were investigated in conscious dogs (n = 8) chronically instrumented for measurement of hemodynamics, including left ventricular pressure (LVP) and subendocardial segment length. Experiments were performed in the presence of pharmacologic blockade of beta-adrenergic, cholinergic, and ganglionic receptors because cocaine indirectly produces significant alterations in systemic hemodynamics through central and peripheral sympathomimetic actions. Myocardial contractility was quantitated using the preload recruitable stroke work (PRSW) versus end-diastolic segment length (EDL) relationship. LVP-segment length loops were generated in the unsedated control state and after cocaine administration with use of preload reduction by abrupt inferior vena caval constriction, and PRSW versus EDL slope (Mw) and length intercept (Lw) were calculated. In addition, regional preload recruitable work area (PRWA) and stroke work at constant EDL (SWEDL) were also determined. Ventricular relaxation was assessed using a time constant of isovolumetric relaxation assuming a nonzero asymptote of LVP decay. Systemic hemodynamics, myocardial contractility, and isovolumetric relaxation were recorded and calculated before and 1, 3, 5, and 10 min after cocaine administration (2 mg/kg intravenously, i.v.). Mw was significantly (p less than 0.05) reduced by cocaine (63 +/- 8 during control to 45 +/- 8 mm Hg at 1 min after drug administration). PRWA also reflected significant decreases in myocardial contractility after cocaine administration (1,800 +/- 260 during control to 1,200 +/- 220 mm Hg.mm2 at 1 min after drug administration). Similar results were observed with SWEDL (469 +/- 60 during control to 317 +/- 52 mm Hg.mm at 1 min after cocaine administration). All three indexes of contractile state demonstrated complete recovery of contractile function by 10 min after cocaine administration. The time constant of isovolumetric relaxation was prolonged by cocaine (35 +/- 2 during control to 46 +/- 3 ms at 3 min after drug administration), indicating impairment of diastolic function. Ventricular relaxation returned to control levels within 5 min after cocaine administration. No cocaine-induced alterations in coronary blood flow (CBF) or changes in calculated pressure work index (PWI, an indicator of myocardial O2 consumption) were observed. The present results suggest that cocaine produces direct negative inotropic and lusitropic effects independent of changes in myocardial O2 supply and demand and autonomic nervous system activity in conscious chronically instrumented dogs.

Animals↗
PubMed1991

Regional myocardial function after repetitive brief episodes of ischemia: effect of altering the duration of the reperfusion period.

How recovery of regional contractile function in myocardium is influenced by alterations in the duration of reperfusion after repetitive brief coronary artery occlusions was investigated in chronically instrumented, conscious dogs. All animals underwent five 5 minute left anterior descending coronary artery occlusions with a final 5-hour reperfusion period. Dogs were randomly assigned to one of three groups determined by the duration of reperfusion (5, 10, or 15 minutes) between successive 5-minute occlusion periods. A shortening of the duration of the reperfusion period between occlusions led to reduced recovery and progressive deterioration in systolic shortening after multiple occlusion-reperfusion sequences. With 15-minute reperfusion periods, the percentage of segment shortening (%SS) during the first through fourth reperfusion periods ranged from 17.1 +/- 2.6% to 18.2 +/- 1.8% and did not differ from the preocclusion control value (18.8 +/- 1.7%) by the end of the final reperfusion period. In contrast, in those dogs with 5-minute reperfusion periods, %SS was significantly reduced from the preocclusion control value (20.2 +/- 2.2%) at the completion of the final 5-hour reperfusion period (11.4 +/- 1.5%). Results of the present study indicate that after only a few brief periods of coronary artery occlusion, rapid and cumulative deterioration in regional contractile function can occur when the duration of intermittent reperfusion is sufficiently brief.

Animals↗
PubMed1991

Dipyridamole-induced decrement of functional recovery of postischemic reperfused myocardium in conscious dogs with well-developed coronary collateral circulation.

The effects of dipyridamole (20 and 40 micrograms/kg/min intravenously) on the time course of functional recovery of myocardium after five 5-minute coronary artery occlusions and four 5-minute reperfusions and a subsequent 5-hour reperfusion period were studied in chronically instrumented, conscious dogs with well-developed coronary collateral circulation. In comparison with vehicle-treated control dogs, those given dipyridamole (20 and 40 micrograms/kg/min, respectively) 15 minutes before and during coronary occlusion had a greater depression of regional segment shortening (38 +/- 7% and 19 +/- 4%, respectively, vs control levels of 69 +/- 10% of preocclusion values) during acute coronary artery occlusion. After a 5-hour reperfusion period, segment shortening returned to preocclusion values in the control group but remained decreased in the dipyridamole groups (87 +/- 4% and 75%, respectively). These results suggest that dipyridamole in a dose-dependent manner exacerbates recovery of contractility of postischemic reperfused myocardium in dogs with well-developed coronary collateral circulation.

Animals↗
PubMed1991

Isoflurane causes only minimal increases in coronary blood flow independent of oxygen demand.

Studies on the coronary circulation during halothane or isoflurane anesthesia are conflicting. Also, little attention has been paid to the time course of the effect of these agents on the coronary circulation. Therefore, we investigated the direct and temporal effects of halothane and isoflurane on coronary hemodynamics in chronically instrumented dogs, in the presence and absence of autonomic nervous system blockade. On different days anesthesia was induced via inhalation with 5% halothane or isoflurane in 100% oxygen. After tracheal intubation, anesthesia was maintained at 1.0 MAC for 30 min. Hemodynamics were recorded continuously. Myocardial oxygen consumption was estimated from the pressure-work index. A total of 36 experiments (four sets of experiments) were completed using nine chronically instrumented dogs. Induction of anesthesia with halothane caused a significant (P less than 0.05) increase in coronary blood flow (from 40 +/- 6 to 68 +/- 11 ml/min), which reached a peak at 1.4 +/- 0.3 min. These changes were secondary to increases in heart rate, arterial pressure, and pressure-work index (10.2 +/- 1.4 to 15.9 +/- 0.8 ml O2.min-1.100g-1). With autonomic nervous reflexes eliminated, halothane caused no change in coronary blood flow. Inhalation of isoflurane caused a greater (P less than 0.05) increase in coronary blood flow (from 39 +/- 6 to 85 +/- 14 ml/min) than did halothane; flow reached a peak at 1.8 +/- 0.6 min. With autonomic reflexes eliminated, isoflurane continued to produce an increase (P less than 0.05) in coronary blood flow (from 39 +/- 4 to 53 +/- 5 ml/min), which reached a peak at 2.1 +/- 0.4 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1991

Endothelium-dependent vasodilation of canine coronary collateral vessels.

The objective of this study was to determine whether endothelium-mediated relaxation occurs in canine coronary collateral vessels. Responses to endothelium-dependent vasodilators in coronary collateral vessels (250-350 microns) were compared with those obtained in normal native coronary arteries of similar size. Rings of small arteries and collateral vessels were suspended in baths, and tension was recorded. All rings were constricted with prostaglandin F2 alpha (3 microM) and subsequently exposed to cumulative concentrations of acetylcholine or bradykinin. In separate experiments, the procedure was repeated in the presence of 300 microM NG-monomethyl-L-arginine (L-NMMA) to inhibit endothelium-mediated vasodilation. Endothelium-dependent relaxation was further studied in the presence of indomethacin, and endothelium-independent relaxation was examined with sodium nitroprusside. Acetylcholine and bradykinin relaxed both normal native and collateral rings. In preconstricted small arteries and collateral vessels the concentration at 50% of maximal response of acetylcholine was 85.5 +/- 19.5 and 61.0 +/- 14.0 microns, and bradykinin was 11.9 +/- 7.4 and 10.7 +/- 2.1 microns, respectively. L-NMMA attenuated the response to acetylcholine and bradykinin in both groups. The results indicate that endothelium is present and functional in canine coronary collateral vessels. Both small coronary arteries and collateral vessels are equally responsive to endothelium-dependent vasodilators and inhibition of endothelium-dependent relaxing factor.

Acetylcholine↗
PubMed1991

Clinical issues related to discontinuing digoxin therapy in elderly nursing home patients.

Digoxin is commonly used to treat congestive heart failure. Digoxin augments ventricular systolic performance, but does not benefit patients whose congestive heart failure is caused by poor diastolic function. We studied 47 elderly nursing home patients who were receiving long-term digoxin therapy. The left ventricular ejection fractions were measured using both a standard and a highly portable echocardiography machine. Thirty-five of 47 patients had normal ejection fractions (50% or greater). In this subgroup, 23 patients were in normal sinus rhythm. Digoxin was discontinued in 14 patients with good systolic function and normal sinus rhythm, but in nine cases physicians refused to stop the digoxin. Follow-up evaluations showed no deterioration off digoxin. Excellent correlations existed between estimated left ventricular ejection fractions from the two echocardiography machines. Many nursing home patients taking digoxin do not need it. Physician reluctance to discontinue digoxin may change with the availability of highly portable echocardiography.

Aged↗
PubMed1990

Calcium channel modulation of alpha 1- and alpha 2-adrenergic pressor responses in conscious and anesthetized dogs.

The influence of halothane and isoflurane on alpha-adrenergic-mediated vasoconstriction before and following calcium channel modulation was investigated in chronically instrumented dogs. After ganglionic, cholinergic, and beta-adrenergic blockade, systemic hemodynamic responses following equieffective pressor doses of phenylephrine (0.6 micrograms/kg iv), a selective alpha 1 agonist, and azepexole [B-HT 933] (20 micrograms/kg iv), a selective alpha 2 agonist, were obtained. The calcium channel stimulator Bay k 8644 (0.5 and 1 micrograms.kg-1.min-1) was infused intravenously for 10 min and phenylephrine and azepexole administered at the end of each infusion. On different days, each dog was subsequently anesthetized with equihypotensive concentrations of halothane (1.7%) or isoflurane (2%) in oxygen and the same pharmacologic interventions were repeated in the presence of halothane or isoflurane. Twenty-one experiments (three groups) using seven chronically instrumented dogs were completed. Halothane and isoflurane produced significant (P less than 0.05) attenuation of the increase in arterial pressure after bolus administration of phenylephrine and azepexole. Bay k 8644 augmented the pressor responses mediated by both phenylephrine and azepexole in all three groups. Thus, halothane and isoflurane nonselectively reduced the pressor response to both alpha 1- and alpha 2-adrenergic receptor stimulation and this was probably not mediated by inhibition of transmembrane calcium flux through dihydropyridine sensitive channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1990

Enhanced alpha-adrenergic vasoconstriction by n-3 fatty acids in conscious dogs.

The effect of dietary fish oil supplementation on cardiac function and the pressor response to selective agonists of postjunctional alpha 1- and alpha 2-adrenoceptors was investigated in chronically instrumented dogs (n = 12). Following ganglionic, cholinergic, and beta-adrenergic blockade, dose responses to phenylephrine (0.3-1.2 micrograms/kg iv), a selective alpha 1-adrenoceptor agonist, and azepexole (B-HT 933, 5-20 micrograms/kg iv), a selective alpha 2-adrenoreceptor agonist, were obtained in conscious dogs. Fish oil capsules containing eicosapentaenoic acid (1.12 g) and docosahexaenoic acid (480 mg) were administered orally twice daily for 1 wk, and dose-response curves were repeated. Dose-response curves were again obtained 1 wk after fish oil was discontinued. Fish oil supplementation resulted in significantly (P less than 0.05) increased arterial pressure at rest, and after autonomic nervous system blockade there was an increase in peripheral vascular resistance. Cardiac output was reduced in fish oil-treated dogs during autonomic nervous system blockade. The pressor response to selective alpha 1- and alpha 2-adrenoceptor stimulation was increased secondary to elevated peripheral vascular resistance. Hemodynamics and exaggerated vascular reactivity returned to control 1 wk after dietary fish oil was discontinued. The results of this study demonstrate that dietary fish oil supplementation produces an increase in arterial pressure via peripheral vasoconstriction and that the vascular response to alpha-adrenergic stimulation is exaggerated.

Adrenergic alpha-Agonists↗
PubMed1990

Cardiovascular ochronosis: a case report and review of the medical literature.

Ochronosis is a rare disorder of tyrosine metabolism due to a deficiency of the enzyme homogentisic acid oxidase. The most common clinical manifestations include alkaptonuria, spondyloarthropathy, large joint arthritides and pigmentation of cartilage. Cardiac involvement may occur due to the deposition of polymerized homogentisic acid in the aortic, mitral and pulmonic valves. Usually, this leads to increasing rigidity and calcification. The only functionally significant valve lesion reported appears to be aortic stenosis. A possible link between ochronosis and coronary artery disease has been postulated. Further, a link between peripheral vascular disease and ochronosis may be present. We describe a case of ochronotic cardiovascular disease and review the literature on the subject.

Aged↗