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Biomedical subjects

D Kenny

Publications and source records attributed to D Kenny.

At least 91 records · Page 5Linked to original sources
PubMed1989

Alterations of alpha 1 and alpha 2 adrenoceptor-mediated pressor responses by halothane and isoflurane anesthesia.

The mechanism by which halothane and isoflurane interfere with catecholamine-mediated vasoconstriction was investigated, utilizing selective agonists of postjunctional alpha1 and alpha2 adrenoceptors in chronically instrumented dogs. After ganglionic, cholinergic, and beta adrenergic blockade, dose responses to phenylephrine (0.3-1.2 micrograms/kg, iv), a selective alpha1 adrenoceptor agonist, and azepexole [B-HT 933] (5-20 micrograms/kg, iv), a selective alpha2 adrenoceptor agonist, were obtained in conscious dogs. Each dog was subsequently anesthetized with either halothane (1.7%) or isoflurane (2%) in oxygen in equihypotensive concentrations. After a 1 h equilibration period, the dose response curves were repeated. Twenty experiments in ten chronically instrumented dogs were completed. Halothane and isoflurane produced significant (P less than 0.05) attenuation of both the increase in systolic and diastolic arterial pressure after bolus administration of all doses of phenylephrine and azepexole. No specific selectivity of either volatile anesthetic for alpha1 or alpha2 mediated pressor responses was found. Therefore, in chronically instrumented dogs, alpha1- and alpha2-mediated pressor responses were similarly influenced by halothane and isoflurane. The present results suggest that both halothane and isoflurane act as functional antagonists to alpha adrenergic mediated vasoconstriction.

Adrenergic alpha-Agonists↗
PubMed1989

Paracetamol suppositories: a comparative study.

Paracetamol suppositories in two different bases were given to children who had fever after operations. Plasma concentrations and the effect on temperature were compared. There was a significant correlation between peak plasma concentrations and maximum drop in temperature. A lipophilic base produced better results than a hydrophilic base.

Acetaminophen↗
PubMed1989

Effects of nisoldipine on coronary collateral perfusion and hemodynamics in chronically instrumented dogs.

The effect of a new dihydropyridine slow-channel calcium blocking agent, nisoldipine, on hemodynamics and myocardial blood flow in normal and collateral-dependent areas distal to a chronic coronary artery occlusion were studied in chronically instrumented, conscious dogs. Nisoldipine produced significant and dose-related decreases in arterial blood pressure, an elevation of heart rate and large increases in coronary blood flow velocity. In dogs with an Ameroid constrictor previously implanted to enhance coronary collateral development, this agent produced large increases in perfusion distal to a chronic coronary artery occlusion. In addition, despite a reduction in arterial pressure, nisoldipine preserved renal cortical, intestinal and skeletal muscle blood flow while increasing tissue flow within liver and cerebral cortex. Thus, nisoldipine increases oxygen supply to collateral-dependent myocardium in the presence of reduced driving pressure for collateral perfusion.

Animals↗
PubMed1978

Activity of serum alpha-amylases in cystic fibrosis.

A new method which uses a differential inhibitor to measure pancreatic and salivary type alpha-amylases (EC 3.2.1.1) was applied to serum samples from 46 cystic fibrosis (CF) patients (age range 4-14 years) and 50 controls of the same age group. The levels of pancreatic type amylase were lower in the CF patients (median 26.5 I.U./1) than the controls (median 81.5) (P less than 0.001). The results for salivary-type enzyme, however, did not support the previously reported finding of higher than usual levels in CF patients. This discrepancy is probably due to differences in analytical methods. It is felt that this procedure will be of value in the investigation of patients for cystic fibrosis and other pancreatic disorders.

Adolescent↗
PubMed1978

Abnormalities of renal transport of sodium o-[131I]iodohippurate (Hippuran) in essential hypertension.

1. Renal function has been studied in 312 hypertensive patients by quantitative renography with sodium o-[131I]iodohippurate (131I-labelled Hippuran) and estimation of overall effective renal plasma flow. In 59% of the patients the results were normal. 2. Severe hypertension was associated not only with reduced effective renal plasma flow but also a characteristic abnormality of Hippuran transport in 10% of the patients in which there was a wider than normal variation in transit times of Hippuran through the kidney, which may reflect non-uniformity of reabsorption of filtrate by different groups of nephrons. 3. Plasma renin activity was higher in a group of 14 patients with multimodal transit time spectra than in a matched hypertensive control group, with very substantial overlap between the two groups. 4. The renographic abnormality was usually reversed by treatment.

Blood Flow Velocity↗
PubMedDate not supplied

Attenuation of the systemic and coronary hemodynamic effects of cocaine in conscious dogs: propranolol versus labetalol.

The interaction of cocaine with myocardial and vascular adrenoceptors is incompletely understood. The systemic and coronary hemodynamic effects of intravenous cocaine (1.5 mg/kg) were examined in dogs with and without pretreatment with propranolol (2 mg/kg i.v.) or labetalol (5 mg/kg i.v.) on different days. A total of 24 experiments was completed (three sets of experiments) using eight dogs chronically instrumented for measurement of aortic and left-ventricular pressure, left-ventricular dP/dt, subendocardial segment length, coronary blood flow, and cardiac output. Myocardial oxygen consumption was estimated from the pressure work index (PWI). Cocaine significantly (p < 0.05) increased heart rate (+51 +/- 17 bpm), mean arterial pressure (+72 +/- 10 mm Hg), left-ventricular systolic and end-diastolic pressures (+56 +/- 9 and +14 +/- 6 mm Hg, respectively), coronary blood flow (+32 +/- 10 ml/min) and the PWI (+10.0 +/- 2.3 ml O2/min/100 g). Significant reductions in stroke volume (-9 +/- 5 ml) and percent segment shortening (-7.1 +/- 1.7) were observed. These changes returned to control after 30 min. After pretreatment with propranolol, the cocaine-mediated increases in mean arterial pressure, left-ventricular systolic pressure, rate-pressure product, and the pressure work index (4.4 +/- 0.7 ml O2/min/100 g) were significantly (p < 0.05) less than those observed with cocaine alone. Cocaine also reduced contractility [dP/dt50 (-341 +/- 80 mm Hg/s)] and increased systemic vascular resistance (+2703 +/- 339 dyn.s.cm-5) in the presence of propranolol. Labetalol abolished the cocaine-mediated increases in heart rate and coronary blood flow and significantly attenuated the increases in mean arterial pressure, left-ventricular systolic pressure, cardiac output, rate-pressure product, and calculated myocardial oxygen consumption when compared to results obtained with cocaine alone. The results demonstrate that a portion of the basic dynamic effects of cocaine is mediated by stimulation of alpha and beta adrenoceptors. Combined alpha and beta adrenergic blockade reduces the hemodynamic effects of cocaine more than beta blockade alone. During antagonism of the sympathomimetic response of cocaine, direct negative inotropic actions of this drug are unmasked.

Animals↗
PubMedDate not supplied

Vasodilator actions of interleukin-1 in the canine coronary circulation.

The effects of intracoronary ultrapure human Interleukin-1 on the regional distribution of coronary blood flow (radioactive microspheres), contractile function (subendocardial ultrasonic length gauges) and systemic hemodynamics were studied in open-chest, anesthetized dogs (n = 7). Bolus doses of Interleukin-1 (10, 20, and 30 u) administered directly into the left anterior descending coronary artery increased coronary blood flow from 43 to 71, 80 and 87 ml/min, respectively. The increase in blood flow produced by Interleukin-1 was distributed uniformly to the subendocardium, midmyocardium, and subepicardium of the left ventricular free wall without effect on regional function or systemic hemodynamics. Indomethacin (1 mg/kg i.v.) attenuated the increase in blood flow, especially to the subepicardium. Due to the selective diminution of the Interleukin-1-mediated increase in subepicardial blood flow by indomethacin, the subendocardial to subepicardial perfusion ratio was increased by Interleukin-1 in the presence of indomethacin. The present results demonstrate that Interleukin-1 has direct coronary vasodilator actions, a portion of which is mediated by a product of cyclooxygenase metabolism.

Animals↗