A review of portal screen-film technology and five radiologists' evaluations of some existing products.

Portal radiographs, radiographs made to document the accuracy of radiotherapy treatment fields, are typically of poor image contrast. Recently, a new portal film and screened-cassette system was marketed, the Kodak EC-L system, with the claim of greatly improved image contrast. This new EC-L system was tested on a canine cadaver exposed to Cobalt-60 teletherapy gamma radiation, and image quality was compared to earlier marketed Kodak portal film products. The EC-L system was found to provide portal images of improved contrast/quality.

Effect of thyroxine on urinary bladder autonomic receptor densities and contractility.

The effect of thyroxine on the response of urinary bladder strips to autonomic drugs and electrical stimulation was studied. Bladder strips from euthyroid, hyperthyroid and thyroidectomized rats were used. Rats were made hyperthyroid by intramuscular injection of thyroxine (250 micrograms/rat for 5 days). Surgical thyroidectomy was performed 12-15 weeks before the experiment. The contractile response of bladder strips from each of the 3 groups of rats to electrical field stimulation and the following drugs was measured: isoproterenol; bethanechol; methoxamine; adenosine triphosphate, and potassium chloride. Isoproterenol produced a significantly greater relaxation in strips from hyperthyroid than from euthyroid rats. The enhanced relaxation response to isoproterenol was accompanied by an increase in beta-adrenergic receptor density. The contractile response to methoxamine, adenosine triphosphate and potassium chloride was unchanged by pretreating the rats with thyroxine. The increase in contraction produced by bethanechol was the same in strips from hyperthyroid and euthyroid rats and the muscarinic receptor densities were also unaltered by thyroxine. Bladder strips from thyroidectomized rats showed the same response as strips from control animals following electrical field stimulation or exposure to isoproterenol, bethanechol, methoxamine, adenosine triphosphate and potassium chloride. These results demonstrate that thyroxine pretreatment enhances the relaxation of urinary bladder strips produced by isoproterenol and that this response is correlated with a hormone-induced increase in beta-adrenergic receptors in this tissue.

Metabolic effects of acarbose in normal and diabetic rats: long- and short-term administration.

The effects of acarbose administration to normal and streptozotocin-diabetic rats were studied in animals given the drug for 3 or 21 days. The acarbose was incorporated into control diets or diets fortified with sucrose and starch. After extirpating the hearts, they were perfused by the Langendorff procedure and ventricular rate and isometric force of contraction were recorded in the presence or absence of isoproterenol. Frozen samples of heart and liver were used for metabolic measurements. At a low dose of isoproterenol (0.01 microgram) the positive inotropic response was the same in control and diabetic animals. With a higher dose of the amine (0.1 microgram) the contractile response was increased further in hearts from normal animals but not enhanced in hearts from diabetic rats. Cardiac phosphorylase activation by isoproterenol was accentuated by diabetes only when the smaller dose of the amine was given. The markedly elevated heart glycogen content of diabetic rats was decreased in response to a high carbohydrate diet. Inclusion of acarbose in the diet prevented this diminution in cardiac glycogen. In normal and diabetic rats fed the high carbohydrate diet for 3 weeks, liver glycogen was elevated. The increase in hepatic glycogen was not observed when acarbose was present in the diet. A comparison of the results of the short- and long term-administration of acarbose show that the onset of action of the drug is prompt and that the effect of the treatment is undiminished over an extended period of time.

Enhanced response of arterioles to oxygen during development of hypertension in SHR.

The goal of this study was to assess the possible role of O2-related local control mechanisms in contributing to an elevated skeletal muscle resistance during the development of hypertension in the spontaneously hypertensive rat (SHR). Diameters of first- (1A), second- (2A), third- (3A), and fourth-order (4A) arterioles were measured by television microscopy in the cremaster muscle of SHR in the early (4- to 6-wk-old) and rapidly developing (8- to 9-wk-old) stages of hypertension and in age-matched normotensive Wistar-Kyoto (WKY) controls. Active neurogenic tone was blocked by superfusing the tissue with 0.1 microgram/ml tetrodotoxin. When superfusion solution PO2 was elevated by changing the gas equilibration mixture from 0 to 5% O2, neurally blocked 3A and 4A of SHR exhibited a significantly greater constriction and a higher incidence of complete closure than those of their age-matched WKY controls. However, there were no significant differences in the constriction of larger arterioles (1A and 2A) in response to elevated superfusion solution PO2. The results suggest that O2-related local control mechanisms could contribute to constriction and closure of small arterioles and to an elevated skeletal muscle vascular resistance early in the development of hypertension in SHR.

Neural and local control of arterioles in SHR.

This study sought to determine if neural influences and/or alterations in arteriolar responses to oxygen could contribute to an elevated microvascular resistance in spontaneously hypertensive rats (SHR). Diameters of third-order arterioles (3A) and fourth-order arterioles (4A) were measured in the cremaster muscle of 12- to 15-week-old SHR and normotensive Wistar-Kyoto (WKY) controls anesthetized with pentobarbital. The preparation was suffused with physiological salt solution (PSS) equilibrated with various concentrations of oxygen (0% O2, 5% O2, or 10% O2) with and without local neural blockade with 10(-7) g/ml tetrodotoxin (TTX). Total active tone was assessed with 10(-4) M adenosine. SHR 3A (but not 4A) exhibited a smaller resting diameter than WKY, and larger dilations in response to TTX and adenosine. When suffusion solution PO2 was elevated in the presence or absence of TTX, SHR arterioles constricted more than did those of WKY, and SHR 4A exhibited a higher incidence of complete closure. Therefore, both neural influences and local vascular control mechanisms may contribute to an elevated microvascular resistance in SHR.

Metabolic effects of acarbose administration in normal and diabetic rats.

The effect of acarbose on cardiac and hepatic metabolism was investigated in normal and diabetic rats. Groups of rats were fed one of the three following diets for 7 days: (1) ground Purina chow, (2) ground Purina chow fortified with raw corn starch and sucrose, and (3) the above high carbohydrate diet, with added acarbose (40 mg/100 g food). At the end of the dietary period the rats were decapitated, and a sample of liver tissue was removed and frozen in liquid nitrogen. The heart was extirpated for subsequent perfusion by the Langendorff technique. Increases in liver and heart glycogen produced by the high carbohydrate diet in the normal rats were prevented completely when acarbose was incorporated into the food. In diabetic animals, liver glycogen was uniformly lower than normal, irrespective of the diet or the presence of acarbose. With animals fed the control diet, cardiac glycogen was higher in diabetic than in normal rats. The high carbohydrate diet caused a lowering of heart glycogen in diabetic rats and this reduction in glycogen content was reversed by including acarbose in the diet. Effects of isoproterenol on myocardial phosphorylase a activity were determined in hearts from normal and diabetic rats given one of the three diets. The high carbohydrate diet decreased the enzymatic response to the catecholamine in hearts from both normal and diabetic animals, and this phenomenon was prevented by the presence of acarbose in the diet. In diabetic rats fed any of the three diets, the activation of cardiac phosphorylase by isoproterenol was greatly accentuated. Measurements of heart uridine kinase showed that the activity of this enzyme was lower than normal in hearts from diabetic rats given either the control or the high carbohydrate diet. The presence of acarbose in the latter diet resulted in a significant decrease in cardiac uridine kinase activity in hearts from normal rats. The results of this study demonstrate the effectiveness of acarbose in modulating tissue metabolism in normal and diabetic animals.

Interaction between thyroxine and tricyclic antidepressant drugs on cardiac neurotransmitter receptors.

The effect of chronic administration of desmethylimipramine (DMI) and iprindole on cardiac neurotransmitter receptors was studied. In addition, the influence of these drugs on the action of thyroxine (T4) on myocardial receptors was investigated. Administration of iprindole (10 mg/kg i.p., twice daily for 11 days) markedly increased the number of beta- adrenergic receptors in the heart and significantly reduced the affinity of these receptors for (-)[3H]dihydroalprenolol ([3H]DHA). Injection of T4 (500 mg/rat i.m., for 5 days) concomitantly with iprindole resulted in a lower beta-adrenergic receptor density that with iprindole treatment alone, but significantly higher than that measured in control rats. Affinity of the receptors for (-)[3H]quinuclidinyl benzilate ([3H]QNB) in heart membrane preparations of animals pretreated with T4 alone or with T4 plus iprindole was not different from control. Neither pretreatment with DMI nor with iprindole affected the density of cholinergic muscarinic receptors in the heart or their affinity for [3H]QNB. The decrease in cardiac cholinergic receptors induced by administration of T4 was not prevented by simultaneous injections of DMI. Combined administration of iprindole and T4 caused a reduction in the affinity of myocardial cholinergic muscarinic receptors, but restored the number of these receptors to normal. The results demonstrate distinct differences between DMI and iprindole in their effects on cardiac neurotransmitter receptors and in the influence of these drugs on the actions of T4 on receptors in the heart.

Inhibitory effects of desmethylimipramine on the action of thyroxine on cardiac beta-receptors and myocardial phosphorylase.

The influence of chronic administration of desmethylimipramine (DMI) on the actions of thyroxine (T4) on rat heart was studied. Administration od DMI (10 mg/kg, i.p., twice daily) for 7 days did not alter the cardiac beta-adrenergic receptor density or the affinity for (-)[3H]dihydroalprenolol (3H-DHA) but diminished the activation of myocardial phosphorylase produced by isoproterenol. Chronic injections of T4 (500 microgram/rat) for 5 days caused an increase in the number of beta-adrenergic receptors in the heart and potentiated the stimulatory effect of isoproterenol on cardiac phosphorylase alpha activity. When DMI was administered concomitantly with T4, there was no increase in the density of myocardial beta-adrenergic receptors and the T4-induced potentiation of the activation of heart phosphorylase by isoproterenol was abolished. However, simultaneous treatment of the rats with DMI and TR4 did not diminish the positive chronotropic effect of T4. It was concluded that DMI, while not affecting the population of cardiac beta-adrenergic receptors by itself, prevents the increase in these receptors produced by T4 and obviates the T4-induced potentiation of phosphorylase activation by isoproterenol. That the tachycardia caused by T4 persists in hearts in which DMI has impeded the increase in myocardial beta-receptors suggests that the increase in heart rate is not dependent on cardiac beta-adrenergic receptor density.

Dissociation between cardiac cyclic AMP and myocardial contractility induced by verapamil, calcium and magnesium ions.

Isolated, perfused rat hearts were used to study the effects of verapamil, excess calcium ions or excess magnesium ions on changes in heart cyclic AMP and myocardial force of contraction. Verapamil caused a dose-dependent decrease in force of contraction and a nondose-related reduction in cyclic AMP. Perfusion of hearts with medium containing 5 mM calcium produced a significant rise in cyclic AMP, but no change in contractile force. The depressant effects of verapamil on contractility and cyclic AMP were reversed by 5mM calcium; excess calcium in the perfusion fluid also containing verapamil prevented the myocardial depressant effects of verapamil. Acutely elevating the magnesium concentration in the perfusion medium decreased force of contraction, accentuated the negative inotropic effect of verapamil, but did not decrease cyclic AMP or enhance the verapamil-induced reduction in cyclic AMP.

Pituitary-adrenal function in thyroparathyroidectomized male and female rats.

The influence of thyroid hormones on pituitary-adrenal function was assessed by studying several aspects of adrenocortical function approximately 30 days after thyroparathyroidectomy (TPTx). Both male and female rats showed evidence of rhythmic adrenocortical activity; peak plasma corticosterone levels occurred just before the dark phase of the lighting schedule. Only the amplitude of the rhythm appeared altered by TPTx. Peak plasma corticosterone levels in TPTx male and female animals were less (P less than 0.05) than corresponding levels in intact control rats. Both sexes showed significant responses to stress, but the morning stress response in TPTx females was less (P less than 0.01) than the stress response in intact controls. Concomitant with the reduced stress response, the adrenocortical response to exogenous ACTH was reduced in TPTx female rats.

Effects of verapamil on myocardial contractility, cardiac adenosine 3,'5'-monophosphate and heart phosphorylase.

The effects of verapamil on myocardial isometric force on contraction, cardiac adenosine 3,'5'-monophosphate (cyclic AMP) and heart phosphorylase alpha activity were studied in the isolated perfused rat heart. When hearts were perfused with verapamil (5.98 times 10- minus 8 M), force of contraction was reduced approximately 50% within 4 to 5 minutes; at this point, the concentration of cyclic AMP was significantly lower than control but phosphorylase alpha activity was unchanged. In hearts perfused continuously for 60 minutes with verapamil, force of contraction and cyclic AMP levels returned to normal within 20 minutes after administration of verapamil was begun. Isoproterenol (0.355 nmol/min) reversed the depressant effect of verapamil on cardiac contractility and restored heart cyclic AMP levels to normal. Methoxamine (35.5 nmol/min) given to verapamil-depressed hearts, caused contractile force to return to normal, but cardiac cyclic AMP levels remained low. Mephentermine (23.0 nmol/min) had no effect on cardiac contraction, cyclic AMP or phosphorylase alpha activity in hearts depressed by verapamil. It was concluded that with the concentration of verapamil used in these experiments, the drug caused a transient decrease in force of contraction and myocardial cyclic AMP. Both the depression in myocardial contractility and in cardiac cyclic AMP caused by verapamil were reversed promptly by isoproterenol, whereas methoxamine overcame acutely only the negative inotropic effect of verapamil. Mephentermine had no effect on hearts depressed by verapamil.

Metabolic and inotropic effects of verapamil in perfused rat heart.

The effect of verapamil on myocardial contractility, heart adenosine 3', 5'-monophosphate (cyclic AMP) and cardiac phosphorylase a activity was studied in isolated perfused rat hearts. In a concentration of 0.025 mug/ml, verapamil decreased force of contraction 50% and caused a significant fall in heart cyclic AMP within 4 to 5 min after perfusion with the drug was begun. When perfusion of the heart with medium containing verapamil was continued for 60 min, contractile force gradually returned to control. at the end of 60 min of perfusion with verapamil, the myocardial concentration of cyclic AMP was not different from that measured in hearts perfused with contro medium for a similar time period. Isoproterenol, given at the point of maximal contractile depression induced by verapamil, restored normal force of contraction and raised cardiac cyclic AMP to the same level as that observed when the catecholamine was given to untreated hearts; When methoxamine was administered to hearts depressed by verapamil, contractility returned to normal, but cyclic AMP content remained below control values.