Publications by authors named "Innes I"

This study aimed to describe the demographic and clinical characteristics of consecutive referrals to a liaison psychiatry outpatient clinic, based within a National Health Service (NHS) general hospital. All outpatient referrals to the service between January 2005 and January 2008 were subjected to retrospective completion of a proforma for post hoc data collection. Data relating to characteristics of the referral, patients, diagnosis, and nature and extent of contact were extracted for scrutiny.

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Staphylococcus aureus remains an important human pathogen responsible for a high burden of disease in healthcare and community settings. The emergence of multidrug-resistant strains is of increasing concern world-wide. The identification of S.

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Cats anesthetized with pentobarbital sodium were hemorrhaged (1 ml.min-1.kg body wt-1) until arterial pressure declined to 55 mmHg.

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Cats anesthetized with pentobarbital sodium were hemorrhaged (1 ml.min-1.kg body wt-1) until arterial pressure declined to 55 mmHg.

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In cats anesthetized with pentobarbital, hepatic venous pressure was increased to cause drops of exudate to appear on the surface of the liver. These drops were collected during steady-state infusions of small doses of ethanol and galactose when there was a large arteriovenous gradient across the liver. Comparison of the concentrations of these substances in arterial, portal, and hepatic venous blood and exudate showed that the exudate concentrations were slightly higher than the hepatic venous concentrations but markedly lower than arterial and portal blood concentrations.

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The liver has important functions as a blood volume reserve and in uptake and metabolism of many substrates. This study examines whether changes in hepatic blood volume modify the uptakes of model substrates galactose and indocyanine green (ICG) in cats anesthetized with pentobarbital sodium. A hepatic venous long-circuit technique with an extracorporeal reservoir was used to control hepatic flow and venous pressure and to allow repeated sampling of arterial, portal, and hepatic venous blood without depletion of the cat's blood volume.

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Isolated rat hearts exhibited a biphasic contractile response to varying concentrations of ruthenium red. A negative inotropic effect was observed with concentrations of 0.025-0.

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Specific insulin binding sites in cardiac sarcolemmal (SL) and sarcoplasmic reticular (SR) membranes were examined. Under in vitro conditions, the specific insulin binding to SL was two to three times greater than that to SR isolated from myocardium of different species. Insulin binding to these membranes was rapid, saturable, and temperature dependent.

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The ability of hearts to store, distribute, and release norepinephrine (NE) was investigated in rats 8 wk after the induction of diabetes by an injection of streptozotocin (65 mg/kg iv). Chronic diabetes was associated with increased content and concentration of NE in heart and in other tissues such as kidney, brain, and spleen. Reserpine or tyramine treatment resulted in depletion of endogenous cardiac NE in control and diabetic rats.

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Heart hypertrophy in response to increased workload is a complex process in which this organ adapts to the environment by increasing the muscle mass in terms of additional contractile units and formation of different types of contractile proteins (myosin isozymes). In addition, augmentation of membrane function with respect to calcium transport activities of sarcolemma and sarcoplasmic reticulum occurs at early stages of cardiac hypertrophy associated with hyperfunction of the myocardium. However, if cardiac hypertrophy is left unattended beyond a certain period, physiological hypertrophy is converted to pathological hypertrophy whereby the cardiac muscle is unable to generate an adequate amount of contractile activity.

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Cardiac norepinephrine turnover and metabolism were examined in rats 8 weeks after the induction of chronic diabetes by an intravenous injection of streptozotocin (65 mg/kg). Cardiac norepinephrine concentration, norepinephrine turnover, and norepinephrine uptake were markedly increased in chronic diabetes in comparison with control values; these changes were reversible by 28-day insulin therapy. When the animals were exposed to cold for 6 hours, norepinephrine turnover rate constant increased in control and decreased in diabetic animals; cold exposure also increased norepinephrine concentration in diabetic hearts.

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Arterial pressures, portal pressures, and hepatic blood volumes were recorded after hepatic denervation in cats anesthetized with pentobarbital. Bromocryptine (50 micrograms/kg) lowered arterial pressure but did not significantly change portal pressure or hepatic blood volume. However, both portal pressure and hepatic blood volume responses to hepatic nerve stimulation were significantly depressed after bromocryptine especially at low frequencies of stimulation.

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Intravenous administration of hypotensive doses (30-200 micrograms/kg) of nifedipine to cats anesthetized with pentobarbital caused an increase in cardiac output accompanied by hepatic venoconstriction. The hepatic venoconstriction and the increase in cardiac output were abolished in animals in which the hepatic sympathetic nerves were cut, the adrenal glands were excluded, and the kidneys were removed. This contrasts with the indirect hepatic venoconstrictor action of isoproterenol which was shown previously not to be abolished by these procedures.

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The use of insulin by diabetics has largely removed the threat of death from ketotic coma but cardiovascular dysfunction remains a major cause of death in patients with diabetes. Recent research has indicated a generalized membrane defect, which may cause abnormalities of calcium metabolism in nerves, cardiac and smooth muscle as well as endothelial cells and thus may lead respectively to the development of neuropathy, primary cardiomyopathy, microangiopathy and atherosclerosis in the diabetic population. Each of these pathogenic processes, which are associated with insulin deficiency, alone or in combination with others, may result in cardiac dysfunction in chronic diabetes.

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Hemodynamic relationships between flows, pressures, and blood volume have been examined in the denervated liver of cats anesthetized with pentobarbital. Portal and hepatic lobar venous pressures, portal and total hepatic flows, and hepatic blood volume were recorded when portal flow was varied from 0 to 240 ml X min-1 X 100 g liver-1 and when hepatic outflow pressure was varied from 0 to 9.5 mmHg, before, during, and after intravenous infusion of norepinephrine (2 micrograms X min-1 X kg body wt-1).

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The effects of cumulative doses of seven arteriolar vasodilators were examined in cats anesthetized with pentobarbital. Cardiac output was measured by a thermodilution technique and hepatic venous compliance by plethysmography. All the drugs produced dose-related decreases in total peripheral resistance.

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The effect of sulfinpyrazone (Anturane) on the extent of myocardial lesions caused by coronary ligation or isoproterenol, 5 mg/kg subcutaneously, was determined in the rat. Treatment was with sulfinpyrazone, 15 mg/kg twice daily for 5 days before the cardiac insult, or 21 days after the insult, or both. Pretreatment with sulfinpyrazone reduced isoproterenol-induced lesions by 42%.

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The uptake of (3H)dopamine into nerve endings (synaptosomes) isolated from cortex and brain stem of rats under various stages of ethanol intoxication were studied. Acute or chronic ethanol treatment inhibited the high affinity uptake of dopamine into both regions by about 30% when rats were still under ethanol. The inhibition in brain stem persisted even after 120 h of withdrawal from ethanol.

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This study attempted to measure the extent to which the carotid sinus baroreceptor reflex attenuates the acute changes in arterial pressure during infusions of phenylephrine and nitroprusside, and to express these effects as equations which could be used in a simple computer model of the circulation. Arterial pressure and cardiac output were measured in vagotomized cats anesthetized with chloralose or pentobarbital. The carotid arteries were perfused to allow sinus pressure either to follow changes in systemic arterial pressure or to be held at the preinfusion control level, thereby eliminating the effects of the reflex.

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The effects of veratramine on transmembrane potentials of the isolated right atrial preparation of the cat were examined. Veratramine slowed spontaneous rate and precipitated a characteristic rhythm consisting of alternating periods of asystole and normal atrial rhythm (periodic rhythm). After large doses or continued exposure to low doses of veratramine electrical and mechanical activity of the atria ceased; subsequently activity resumed only in a discrete area within which action potentials were consistent with pacemaker characteristics.

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1 Noradrenaline caused a small contraction of the cat isolated spleen strip bathed in a calcium-free solution; this contraction was greatly potentiated by cocaine. This potentiation was also present in isolated spleen strips where noradrenaline stores were depleted by reserpine. The maximum response of the spleen strip to noradrenaline in the absence of extracellular calcium was also increased by cocaine.

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Cat spleen capsular smooth muscle, depleted of potassium and enriched with sodium by cold storage in a potassium free medium, relaxed and underwent transient reduction in responsiveness to noradrenaline when potassium was introduced into the bathing medium. Both these effects could be blocked by ouabain, lithium substitution for sodium or low ambient temperature, suggesting possible involvement of the sodium pump. In the continued presence of potassium, relaxation was maintained but sensitivity to noradrenaline increased, possibly due to restoration of normal intracellular sodium and potassium concentrations.

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