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Biomedical subjects

C J Mathias

Publications and source records attributed to C J Mathias.

At least 253 records · Page 14Linked to original sources
PubMed1984

Growth hormone response to clonidine is impaired in patients with central sympathetic degeneration.

Serum growth hormone (GH) levels before and after intravenous clonidine (1.5 mcg/Kg) were measured in normal subjects and patients with chronic idiopathic autonomic failure (AF) due to central sympathetic degeneration. Normal subjects showed a rise in plasma GH from 2 +/- 1 mU/l to 27 +/- 12 mU/l. Basal levels were similar but there was no rise in GH levels in the AF patients. There was no difference in sedation in the two groups, indicating similar central nervous system penetration of the drug. Systolic blood pressure fell in both groups. Diastolic blood pressure fell significantly in normals but not in the AF patients. Clonidine-induced growth hormone release may be a potentially useful neuroendocrine marker indicating derangement of certain components of the central alpha-adrenergic system in man.

Autonomic Nervous System Diseases↗
PubMed1983

Comparison in animal models of 18F-spiroperidol and 18F-haloperidol: potential agents for imaging the dopamine receptor.

Fluorine-18-labeled haloperidol and spiroperidol have been prepared by an exchange reaction using the corresponding non-labeled compound or the nitro analog. Studies in rats have shown that the distribution of labeled spiroperidol has a high striatum to cerebellum ratio which is not observed with haloperidol. A ratio of 10.66 +/- 1.6 is obtained two hours after administration of the 18F-spiroperidol. When 18F-spiroperidol was administered to a baboon and tomographic images obtained, the dopamine receptor rich areas were clearly visualized two hours after administration.

Animals↗
PubMed1983

Autonomic neuropathy.

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Autonomic Nervous System Diseases↗
PubMed1983

Clonidine lowers blood pressure independently of renin suppression in patients with unilateral renal artery stenosis.

The effects of 300 micrograms of oral clonidine were studied in nine patients with unilateral renal artery stenosis proved by selective renal arteriography. Blood pressure, heart rate, plasma renin activity (PRA) levels, plasma noradrenaline levels, and sedation were measured before and for eight hours after dosage. After clonidine administration, both systolic and diastolic blood pressure fell within the first hour, was maximum in the fourth hour, and remained lower than predosage levels even in the eighth hour. There was a fall in heart rate, maximum in the fourth hour. There were minimal changes in PRA levels after giving the clonidine. Plasma noradrenaline levels fell, with the maximum fall in the sixth hour. Sedation occurred within one hour of dosage and was maximum in the second hour. We conclude that in patients with unilateral renal artery stenosis clonidine causes a substantial and prolonged fall in blood pressure not accompanied by suppression of PRA levels but by a reduction in plasma noradrenaline levels. This suggests a role for central pressor mechanisms, probably linked to angiotensin II and central sympathetic activation, in the maintenance of hypertension in patients with renal artery stenosis.

Adult↗
PubMed1983

Clonidine in unilateral renal artery stenosis and unilateral renal parenchymal disease--similar antihypertensive but different renin suppressive effects.

The effects of 300 micrograms oral clonidine were studied in 15 hypertensive patients with unilateral renal involvement -nine had renal artery stenosis and six renal parenchymal disease. After clonidine blood pressure fell substantially in both groups, with the maximum fall in the fourth hour and effects persisting after 6 h. Levels of plasma renin activity were considerably higher in the renal artery stenosis patients and remained unchanged during the study; there was a progressive fall in levels in each of the patients with renal parenchymal disease. Plasma noradrenaline levels fell in both groups. Clonidine therefore lowers blood pressure in patients with unilateral renal artery stenosis and renal parenchymal disease. The known pharmacological effects of clonidine would thus favour either an increase or an inappropriate maintenance of central pressor activity as a contributory factor to the hypertension in both groups. The central mechanisms raising blood pressure may result not only from high angiotensin II levels but to other less well defined effects, from an ischaemic or diseased kidney. The lack of fall of plasma renin activity in the renal artery stenosis patients probably indicates the greater influence of ischaemia and renal baroreceptor stimulation over sympathetically mediated renin release.

Adolescent↗
PubMed1983

Noninvasive detection of coronary thrombi with In-111 platelets: concise communication.

The need for rapid, definitive identification of coronary thrombosis has been intensified by the advent of thrombolytic therapy and by interest in the role of thrombosis in the etiology of coronary artery disease. To determine whether platelet thrombi can be detected noninvasively with In-111 platelets, a method was developed in which Tc-99m-tagged red blood cells were used to correct for activity within the blood attributable to platelets circulating but not associated with thrombus. In 18 dogs coronary thrombi were induced closed-chest with a copper coil introduced into the coronary artery. Indium-111 platelets and Tc-99m RBCs were administered either before or 1 hr after induction of thrombus, and serial scintigrams obtained. Coronary thrombus was identified readily in the processed scintigrams. In six dogs, thrombolysis was achieved with intracoronary streptokinase. In each case serial scintigraphy demonstrated resolution of the clot. The dual radiotracer technique should permit serial noninvasive delineation of the temporal relationship between platelet deposition and coronary heart disease in patients, and should facilitate the evaluation of interventions designed to prevent platelet aggregation or to lyse existing thrombi.

Animals↗
PubMed1982

Perturbed angular correlation studies of 111In-labelled platelets.

Indium-111, as the 8-hydroxyquinoline and acetylacetone complexes, has been used to label cellular blood components. Because of the gamma-ray cascade emitted following the decay of indium-111, perturbed angular correlation studies can be used to investigate the environment of the indium nucleus. Perturbed angular correlation studies have been carried out on the indium at various steps in the procedure used to label platelets with indium using both 8-hydroxyquinoline and acetylacetone as the ligand. Similar values of the integral correlation coefficient were obtained in both cases, suggesting identical labeling mechanisms. Following lysis of the platelets the values of (G22(infinity)) changed, suggesting that the intracellular complex is relatively weak.

Blood Platelets↗
PubMed1982

Indium-111 platelet scintigraphy in cerebrovascular disease.

We obtained scintigraphic images of the neck from 100 patients with suspected cerebrovascular disease after injecting indium-111-labeled autologous platelets. One or more focuses of increased activity, implying local platelet accumulation, were seen along the course of the cervical carotid arteries in 52 patients. In 64 patients, there was a highly significant correlation between the results of scintigraphy and carotid arteriography (p = 10(6)). There was no significant correlation between the scintigraphic findings and the previous or subsequent occurrence of transient ischemic attack or cerebral infarction in the carotid circulation. These data suggest that factors other than the simple formation of platlet thrombi in the cervical carotid arteries are of primary importance in the pathogenesis of stroke.

Adult↗
PubMed1981

Cardiovascular and autonomic reflexes in haemodialysis patients.

1. Blood pressure and heart rate responses to head-up tilt, standing, the Valsalva manoeuvre, sustained handgrip and cutaneous cold were measured in 27 haemodialysis patients (10 of whom had episodes of haemodialysis-induced hypotension) and 15 control subjects to assess autonomic nervous function. Plasma noradrenaline levels were measured at rest and during head-up tilt. 2. Mean resting supine blood pressure, heart rate and plasma noradrenaline levels were higher in haemodialysis patients than in the control subjects. There was no fall in blood pressure during head-up tilt or standing. The ratio of the R--R intervals of the thirtieth and the fifteenth heart beat after standing (30:15) was lower in the patients; this may be related to their higher resting heart rate. Head-up tilt raised plasma noradrenaline levels in both groups. Heart rate responses to the Valsalva manoeuvre were similar in the patients and control subjects. 3. Systolic blood pressure and heart rate responses to sustained handgrip were similar in both groups. Diastolic and mean blood pressure changes, however, were lower in the patients. The blood pressure and heart rate responses to cutaneous cold were similar in the patients and control subjects. 4. We conclude that generalized autonomic nervous dysfunction does not appear to cause haemodialysis-induced hypotension in patients with chronic renal failure on maintenance haemodialysis.

Adult↗
PubMed1981

Renin and aldosterone release during sympathetic stimulation in tetraplegia.

1. The effect of endogenous sympathetic stimulation (induced by urinary bladder stimulation) and intravenous infusion of noradrenaline and isoprenaline on blood pressure, heart rate and levels of plasma renin activity and plasma aldosterone were studied in six tetraplegic patients. Data from infusion studies were compared with data from six normal subjects studied in an identical manner. 2. Bladder stimulation in the tetraplegic patients caused a marked rise in blood pressure and fall in heart rate, but no change in plasma renin activity or plasma aldosterone. 3. Noradrenaline infusion resulted in an enchanced pressor response in the tetraplegic patients when compared with the normal subjects. Heart rate fell in both groups. Plasma renin activity and plasma aldosterone did not change in either group. 4. Isoprenaline infusion caused a fall in both systolic and diastolic blood pressure in the tetraplegic patients, unlike the normal subjects in whom there was a rise in systolic and a fall in diastolic blood pressure. Heart rate and plasma renin activity rose in both groups. Plasma aldosterone did not change in either group. 5. We conclude that in tetraplegic patients neither endogenous sympathetic stimulation by bladder stimulation nor infusion of noradrenaline raises plasma renin activity. Isoprenaline increases plasma renin activity to the same extent as in normal subjects. Renin release mechanisms in tetraplegic patients therefore do not appear to be hypersensitive to catecholamines. Plasma aldosterone is not influenced by any of the stimuli.

Adult↗
PubMed1981

beta-Receptor numbers and thermodynamics in denervation supersensitivity.

1. Denervation supersensitivity to adrenergic agonists occurs after degeneration of the sympathetic nervous system in the disease called multiple system atrophy (MSA) or the Shy Drager Syndrome.2. Supersensitivity to the chronotropic effect of i.v. isoprenaline on the heart was demonstrated in eight subjects with sympathetic nervous system degeneration and MSA.3. There was an increased number of beta-receptors present in MSA as measured by [H(3)]dihydroalprenolol ([H(3)]DHA) binding to beta-receptors on lymphocytes isolated from venous blood taken from the MSA subjects compared with [H(3)]DHA binding to lymphocytes from seven normal subjects. There was no difference in the affinity of lymphocyte beta-receptors for [H(3)]DHA in MSA.4. [H(3)]DHA binding to lymphocytes from MSA subjects was decreased at lower temperatures but was unaffected by lower temperatures in lymphocytes from normal subjects.5. Equilibrium constants for [H(3)]DHA binding to normal and MSA lymphocytes were similar, indicating that the affinity of the beta-receptors was similar in both groups. The equilibrium constants were little affected by cooling from 37 to 4 degrees C suggesting that the heat of reaction (enthalpy) for [H(3)]DHA binding was low. The Gibbs free energy change on binding was negative and similar in quantity for both normal and MSA lymphocytes. There was a similar, large, increase in entropy on binding of [H(3)]DHA to both normal and MSA lymphocytes, showing that the binding reaction was entropy driven.6. If lymphocyte beta-receptors reflect the status of cardiac beta-receptors, increased numbers of cardiac beta-receptors may contribute to the denervation supersensitivity to isoprenaline in MSA with sympathetic degeneration.

Adult↗
PubMed1981

Positron tomographic imaging of the liver: 68 Ga iron hydroxide colloid.

A new radiopharmaceutical, 68Ga ion hydroxide colloid, for hepatic imaging by positron emission tomography was prepared from the eluate of a 68Ge-68Ga solvent extraction generator. In rats, 84% of the administered dose of colloid localized in the liver and 4.6% accumulated in the spleen. Initial imaging studies in normal dogs showed close correspondence of the findings by positron tomography and transmission computed tomography. Emission tomography with 68Ga-colloid was performed in 10 patients with hepatic metastases demonstrated by conventional 99mTc sulfur colloid scintigraphy. All focal defects noted on the conventional scintigrams were easily identified and generally were seen more clearly by positron tomography. In one patient, additional lesions not identified on the initial 99mTc sulfur colloid images were demonstrated. The positron tomographic images were compared with those obtained by transmission computed tomography in seven patients; the two studies showed comparable findings in five patients, whereas positron tomography more clearly showed multiple lesions in two. Our results suggest that positron emission tomography is a suitable technique for obtaining high contrast, cross-sectional images of large abdominal organs.

Animals↗
PubMed1980

Severe hypertension in patients with high spinal cord lesions undergoing electro-ejaculation--management with prostaglandin E2.

Intra-arterial blood pressure (BP) and heart rate (HR) were continuously recorded in five patients with spinal cord injuries at different levels who were undergoing electro-ejaculation. In three patients with lesions at C7, C5 and T4 insertion of the electrode and electrical stimulation caused severe hypertension and bradycardia. In a patient with a T7/8 lesion and in another with a T10 lesion there were either moderate or minimal cardiovascular changes. Severe hypertension during electro-ejaculation is a serious problem in patients with high lesions and is probably part of the syndrome of autonomic dysreflexia. In the three patients with high spinal cord lesions the procedures were repeated during an intravenous infusion of Prostaglandin E2. Resting BP was lowered and resting HR raised. The level of BP recorded during electrical stimulation was substantially reduced. This enabled larger stimuli to be used for a longer period and resulted in successful ejaculation in two patients.

Adult↗