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Biomedical subjects

T A McCalden

Publications and source records attributed to T A McCalden.

At least 19 recordsLinked to original sources
PubMed1978

Cerebrovascular effects of cerebrospinal fluid removal.

The effects on cerebral blood flow of withdrawal of graded volumes of cerebrospinal fluid (CSF) from the cisterna magna were studied in 12 barbiturate-anaesthetized baboons. The results show that withdrawal of CSF was accompanied by a decreased CSF pressure, an increased CSF PCO2, a decreased CSF PO2 and an increased cerebral blood flow. The possible clinical significance of these findings is pointed out.

Animals↗
PubMed1978

Impaired skeletal muscle vasomotor response to infused noradrenaline in baboons with obstructive jaundice.

1. We have measured muscle blood flow by a 133Xe clearance technique, and its response to noradrenaline in baboons before and 2 weeks after ligation of the bile ducts when they were jaundiced. 2. In the normal baboons, the response to noradrenaline was a dose-dependent decrease in muscle blood flow. 3. Bile-duct ligation caused no significant alteration in skeletal muscle blood flow but the response to noradrenaline in the jaundiced baboons was significantly attenuated. This effect was not observed in four sham-operated baboons.

Animals↗
PubMed1978

Potentiation of the cerebrovascular response to intra-arterial 5-hydroxytryptamine.

Infusion of 5-hydroxytryptamine (5HT) into the internal carotid artery of normal baboons was not accompanied by alteration of gray matter cerebral blood flow. In animals pretreated with depot estrogen and progesterone (dosage equivalent to oral contraceptive preparations), infusion of 5HT produced a marked decrease in gray matter blood flow. A similar decrease in flow was obtained when the 5HT was infused with a concentrate of beta-lipoprotein. Steroid substances appear to enhance the cerebrovascular constrictor responses to 5HT. A further series of six experiments has shown that the monoamine oxidase inhibitor tranylcypromine similarly produced constrictor responses to 5HT. It is possible that the steroids, the beta-lipoprotein, and the tranylcypromine produced constrictor responses to 5HT by the same mechanism (inhibition of cerebrovascular monoamine oxidase).

Animals↗
PubMed1978

The effect of intracarotid infusion of dexamethasone and 5-hydroxytryptamine on cerebral blood flow and metabolism in baboons.

The effect of intracarotid infusion of dexamethasone on cerebral blood flow and cerebral oxygen utilization was measured in baboons using the xenon-133 clearance technique. The cerebrovascular response to intracarotid infusion of 5-hydroxytryptamine (5-ht) was then determined during simultaneous infusion of the steroid. Infusion of dexamethasone alone and infusion with 5-HT produced no significant change in cerebral blood flow or cerebral oxygen utilization when compared to baseline values. The study indicates that neither dexamethasone nor 5-HT with dexamethasone modify cerebral blood flow when infused via the internal carotid artery.

Animals↗
PubMed1977

The interaction between noradrenaline and 5-hydroxytryptamine in the isolated perfused rat hindlimb.

The vascular response to bolus injections of 5-hydroxytryptamine (5HT) over the range 0.01-10.0 microgram was measured in isolated perfused rat hindlimbs. The hindlimb vasculature displayed a vasoconstrictor response to 5HT, which was potentiated by the addition of 0.01 microgram/ml noradrenaline (NA) to the perfusate at all doses tested. The response to 5HT was also enhanced by the monoamine oxidase (MAO) inhibitor, tranylcypromine (0.05 mg/ml), suggesting that MAO located in the vascular wall is involved in the termination of the response to 5HT in the peripheral circulation. MAO inhibition abolishes the potentiation of 5HT by NA, indicating that this potentiation results from competition for MAO by both amines, leaving more amine intact to activate membrane receptors. Corticosterone (0.01 mg/ml), catecholamine extraneuronal uptake inhibitor, did not alter the response to 5HT, nor the increase of this response by NA, it thus appears that 5HT and NA have different membrane transport systems in the peripheral vasculature.

Animals↗
PubMed1977

Barrier and uptake mechanisms in the cerebrovascular response to noradrenaline.

Cerebral blood flow (CBF) was measured in 20 baboons by the intra-arterial xenon-133 injection method. The CBF responses to intra-arterial infusions of noradrenaline (NA) were determined. These responses were normally found to be vasodilator and mediated by beta adrenoreceptors. After infusion of substances blocking extraneuronal uptake of NA or opening of the blood-brain barrier, this vasodilation was either abolished or converted to an alpha-receptor mediated vasoconstriction. This suggests that normally the cerebral circulation is protected against noradrenergic vasoconstriction by mechanisms reducing the concentration of NA in the tunica media to below threshold for alpha-adrenoreceptor stimulation.

Animals↗
PubMed1976

Cerebrovascular response to infused noradrenalin and its modification by a catecholamine metabolism blocker.

Despite many studies, the cerebrovascular action of infused noradrenalin is still unclear. The study reported here tested the hypothesis that infused noradrenalin is prevented from reaching the adrenoreceptors by being avidly taken up and metabolized in the vascular smooth muscle. Cerebral blood flow was measured by the xenon133 clearance technique in nine baboons before and during blockade of the enzyme catechol-O-methyl transferase, which is known to be important in inactivation of circulating noradrenalin. The cerebral blood flow responses to noradrenalin infused at 8, 16, and 32 mug per minute were also determined. Responses indicated vasodilatation before but vasoconstriction after blockade, with a significant noradrenalin. It is suggested that the cerebral circulation is normally protected against sympathetic vasoconstriction by the avid uptake and metabolism of noradrenalin in extraneuronal and possibly neuronal sites.

Animals↗
PubMed1975

The effects of jaundiced plasma and hypercholesterolaemic plasma on vascular sensitivity to injected noradrenaline.

Jaundiced plasma and plasma from hyperlipidaemic patients was perfused into an isolated artery or kidney preparation. The responses of the artery to doses of noradrenaline when Krebs solution was perfused were compared to the responses when the plasmas were perfused. It was found that both jaundiced and hyperlipidaemic plasmas potentiated the effects of noradrenaline on the isolated arteries and kidneys.

Animals↗
PubMed1975

Effects of jaundiced plasma on vascular sensitivity to noradrenalin.

Alterations in renal perfusion have been shown in a variety of liver diseases. We have examined the possibility that the syndrome is due to a renal vascular hypersensitivity to noradrenalin (NA). Isolated perfused kidneys and segments of rabbit femoral artery were used. Potentiation of the pressor effects of injected NA occurred in all (five artery and five kidney) preparations when jaundiced baboon plasma was perfused. These changes were significant (P less than 0.05) in nine out of the ten experiments. Controls to which normal baboon plasma was administered showed no such change. No correlation was found between the degree of NA potentiation and the plasma concentrations of bilirubin (total and conjugated), serum glutamic oxaloacetic transaminase, blood urea nitrogen, serum glutamic pyruvic transaminase, alkaline phosphatase, Na+ ions or K+ ions in the jaundiced plasma. Plasma renin levels were not significantly changed. When arteris were perfused with Krebtentiation of NA was found. Perfusion of sodium taurocholate or sodium deoxycholate (400 mug/ml) yielded no potentiation. Thus, the altered renal perfusion associated with jaundice may be attributed to a potentiated pressor response to NA which may be caused by an increased level of cholesterol carried on the beta-lipoprotein.

Animals↗
PubMed1975

The inhibitory action of oestradiol-17-beta and progesterone on venous smooth muscle.

1 The in vitro action of oestradiol-17-beta (0.1, 1.0 and 10.0 mug/ml) and progesterone (0.1, 1.0 and 10.0 mug/ml) on the spontaneous activity of the portal veins in female rats at different stages of gestation was studied. 2 Progesterone caused the spontaneous mechanical activity in the rat portal vein to decrease in amplitude and increase in frequency. This action was dose-dependent and the sensitivity of the tissue decreased throughout pregnancy. 3 Oestradiol-17-beta had a biphasic effect on spontaneous mechanical activity in the rat portal vein. At 0.1 mug/ml the vessel was stimulated while a similar effect to progesterone occurred with higher concentrations. The tissue was more sensitive to oestradiol at 7 days of gestation than at either the 10-14 or 17-21 day periods of gestation. 4 These effects of oestradiol and progesterone were still seen after blockade of the beta-adrenoceptors. 5 Hydrocortisone (10 mug/ml) had no inhibitory effect on the spontaneous mechanical activity of the vein. 6 The veins from the 17-21 days pregnant animals showed a smaller amplitude of contraction than comparable non-pregnant females.

Adrenergic beta-Antagonists↗
PubMed1975

The effects of hypercholesterolaemic plasma on vascular sensitivity to noradrenaline.

1. The pressor responses to injected noradrenaline (NA) of 42 isolated perfused femoral arteries of the rabbit were studied. 2. Potentiation of the responses was found when hypercholesterolaemic plasma was perfused through the arteries. No change was found with normal plasma. 3. Potentiation of the responses was found when isolated beta-lipoprotein in Krebs solution was perfused. No change was found with similar amounts of bovine-albumen. 4. Pure cholesterol dissolved directly into normal plasma, and dissolved via propanol into Krebs solution or plasma caused no potentiation. Propanol alone in Krebs or plasma had no effect. 5. Potentiation was caused by a decreased equilibrium coefficient (Keq) for the NA-adrenoceptor interaction and an increased maximal pressor response (Rmax). 6. It is concluded that cholesterol carried on its apoprotein is capable of potentiating the pressor effects of noradrenaline.

Animals↗
PubMed1975

Modification of the cerebrovascular response to noradrenaline by bile duct ligation.

The effects of intracarotid infusions of noradrenaline on the cerebral vasculature were studied in seven baboons with bile duct ligation. Infusion of 8 mug and 16 mug/min of noradrenaline resulted in a significant decrease in cerebral blood flow in the jaundiced animals. In normal baboons, these doses produced cerebrovascular dilatation. These results indicate that there is an increased cerebrovascular sensitivity to noradrenaline in the obstructive jaundice which follows bile duct ligation. It is postulated that noradrenaline smooth muscle uptake mechanisms are disturbed allowing a greater concentration of the amine at the receptor sites.

Animals↗