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An expression for the pulse wave velocity in a non-linear elastic pressurized arterial tube is derived; in terms of the arterial constitutive (experimentally derived strain energy density function) parameters and the undeformed and deformed arterial diameters. The pulse wave velocity expression is then employed for developing the analysis for invivo determination of the arterial constitutive parameters from arterial imaging data. The analysis provides a method to non-invasively determine the values of the non-linear elastic parameters of the artery by using the invivo monitored values of its diameter and the pulse wave velocity. This Information on the elastic parameters of an artery could characterize the state of the artery and hence a diagnostic indication of the atheromatous involvement of the blood vessel. ? 1981, Walter de Gruyter. All rights reserved ? 1981, Walter de Gruyter. Alle Rechte vorbehalten.

The receptors involved in the pressor and tachycardic effects of catecholamines applied systemically or released from sympathetic nerve endings were compared. Intravenously administered (-)-epinephrine activated alpha-1, alpha-2, beta-1 and beta-2 adrenoceptors as demonstrated in pithed rats, using the alpha-1 sympatholytic drug prazosin, the alpha-2 adrenoceptor blocking substance rauwolscine, the beta-1 and beta-2 sympatholytic agent(-)-propranolol, the predominantly beta-1 adrenoceptor antagonist atenolol and the selective beta-2 adrenoceptor blocking agent ICI 118,551 as tools. (-)-Norepinephrine given i.v. proved to be an alpha-1, alpha-2 and beta-1 adrenoceptor agonist. 1,1-Dimethyl-4-phenylpiperazine iodide (DMPP) releases catecholamines from noradrenergic neurons and the adrenal medulla. The i.v. injection of DMPP into pithed rats caused an increase in diastolic pressure and heart rate by this indirect effect, which has been confirmed by pretreatment with reserpine and removal of the adrenals. After bilateral adrenalectomy, there occurred a release of mainly norepinephrine, only from the neurons. Catecholamines liberated by DMPP activated alpha-1 and beta-1 receptors and, at high doses of DMPP, alpha-2 and beta-2 adrenoceptors as well. Removal of both adrenal glands abolished the alpha-2 and beta-2 adrenoceptor-mediated effects. (-)-Norepinephrine released from neurons stimulated alpha-1 and beta-1 adrenoceptors only, although after i.v. administration of this catecholamine alpha-2 adrenoceptors were also activated. There was no indication for a beta-2 adrenoceptor-mediated vasodilation by neuronally released catecholamines. A beta-2 adrenoceptor-mediated effect, however, could be demonstrated by i.v. injection of (-)-epinephrine. The results can be explained by the presence of predominantly alpha-1 and beta-1 adrenoceptors in the postganglionic sympathetic synapses and an extrasynaptic location of alpha-2 and beta-2 adrenoceptors. The extrasynaptic receptors are possibly controlled by epinephrine from the adrenals.

The receptors involved in the pressor and tachycardic effects of catecholamines applied systemically or released from sympathetic nerve endings were compared. Intravenously administered (-)-epinephrine activated alpha-1, alpha-2, beta-1 and beta-2 adrenoceptors as demonstrated in pithed rats, using the alpha-1 sympatholytic drug prazosin, the alpha-2 adrenoceptor blocking substance rauwolscine, the beta-1 and beta-2 sympatholytic agent(-)-propranolol, the predominantly beta-1 adrenoceptor antagonist atenolol and the selective beta-2 adrenoceptor blocking agent ICI 118,551 as tools. (-)-Norepinephrine given i.v. proved to be an alpha-1, alpha-2 and beta-1 adrenoceptor agonist. 1,1-Dimethyl-4-phenylpiperazine iodide (DMPP) releases catecholamines from noradrenergic neurons and the adrenal medulla. The i.v. injection of DMPP into pithed rats caused an increase in diastolic pressure and heart rate by this indirect effect, which has been confirmed by pretreatment with reserpine and removal of the adrenals. After bilateral adrenalectomy, there occurred a release of mainly norepinephrine, only from the neurons. Catecholamines liberated by DMPP activated alpha-1 and beta-1 receptors and, at high doses of DMPP, alpha-2 and beta-2 adrenoceptors as well. Removal of both adrenal glands abolished the alpha-2 and beta-2 adrenoceptor-mediated effects. (-)-Norepinephrine released from neurons stimulated alpha-1 and beta-1 adrenoceptors only, although after i.v. administration of this catecholamine alpha-2 adrenoceptors were also activated. There was no indication for a beta-2 adrenoceptor-mediated vasodilation by neuronally released catecholamines. A beta-2 adrenoceptor-mediated effect, however, could be demonstrated by i.v. injection of (-)-epinephrine. The results can be explained by the presence of predominantly alpha-1 and beta-1 adrenoceptors in the postganglionic sympathetic synapses and an extrasynaptic location of alpha-2 and beta-2 adrenoceptors. The extrasynaptic receptors are possibly controlled by epinephrine from the adrenals.

In a group of 21 cats, the middle cerebral artery pressure (MCAP) was recorded by means of a catheter introduced into the artery at its origin, just distal to the occlusion. The effects of hypertension, hypercapnia, and hypocapnia were studied. In a group of five cats, both middle cerebral arteries (MCA) were catheterized and the pressure was recorded simultaneously on both sides. In another group of five cats, O2 tension measurements were made with the aid of oxygen electrodes in the brain tissue, the occluded MCA, and the common carotid artery. Some of the results obtained in this study are compared with the results of a previous study where monkeys were used as experimental animals. Chemicals/CAS: carbon dioxide, 124-38-9, 58561-67-4; Oxygen, 7782-44-7

The local EEG, the local cerebral blood flow (lCBF), and the flow in the distal stump of the occluded middle cerebral artery were simultaneously recorded in 28 acute experiments in cats. Nembutal anesthesia was used eleven times, and Halothane anaesthesia 17 times. The recordings were made via platinum electrodes: 12 in the ischaemic hemisphere, and 2-3 in the opposite non-ischaemic hemisphere. The flow in the occluded middle cerebral artery was recorded via a platinum electrode introduced into this artery via the transorbital approach. The changes in lEEG, lCBF, and middle cerebral artery flow were studied during normotension, hypertension, and hypotension. A beneficial effect of hypertension was noted in the acute phase of brain ischaemia. Hypertension counteracted also the 'diaschisis' in the non-ischaemic part of the ischaemic hemisphere and in the opposite non-ischaemic hemisphere. A correlation between lEEG changes and lCBF changes were noted. In addition an interesting discrepancy was observed between the rapid H2 clearance in the middle cerebral artery stump and the much slower H2 clearance in the ischaemic brain area. Significant differences between experiments under Halothane and experiments under Nembutal anaesthesia were noted. In the acute phase those changes are probably the result of the different levels of blood pressure in those two groups. Chemicals/CAS: Metaraminol, 54-49-9; Nitroprusside, 15078-28-1

In a group of 21 cats, the middle cerebral artery pressure (MCAP) was recorded by means of a catheter introduced into the artery at its origin, just distal to the occlusion. The effects of hypertension, hypercapnia, and hypocapnia were studied. In a group of five cats, both middle cerebral arteries (MCA) were catheterized and the pressure was recorded simultaneously on both sides. In another group of five cats, O2 tension measurements were made with the aid of oxygen electrodes in the brain tissue, the occluded MCA, and the common carotid artery. Some of the results obtained in this study are compared with the results of a previous study where monkeys were used as experimental animals. Chemicals/CAS: carbon dioxide, 124-38-9, 58561-67-4; Oxygen, 7782-44-7

The local EEG, the local cerebral blood flow (lCBF), and the flow in the distal stump of the occluded middle cerebral artery were simultaneously recorded in 28 acute experiments in cats. Nembutal anesthesia was used eleven times, and Halothane anaesthesia 17 times. The recordings were made via platinum electrodes: 12 in the ischaemic hemisphere, and 2-3 in the opposite non-ischaemic hemisphere. The flow in the occluded middle cerebral artery was recorded via a platinum electrode introduced into this artery via the transorbital approach. The changes in lEEG, lCBF, and middle cerebral artery flow were studied during normotension, hypertension, and hypotension. A beneficial effect of hypertension was noted in the acute phase of brain ischaemia. Hypertension counteracted also the 'diaschisis' in the non-ischaemic part of the ischaemic hemisphere and in the opposite non-ischaemic hemisphere. A correlation between lEEG changes and lCBF changes were noted. In addition an interesting discrepancy was observed between the rapid H2 clearance in the middle cerebral artery stump and the much slower H2 clearance in the ischaemic brain area. Significant differences between experiments under Halothane and experiments under Nembutal anaesthesia were noted. In the acute phase those changes are probably the result of the different levels of blood pressure in those two groups. Chemicals/CAS: Metaraminol, 54-49-9; Nitroprusside, 15078-28-1

Since two different types of α-adrenoceptors (α1- and α2-) subserve vasoconstriction in pithed rats and noradrenaline behaves as a non-selective agonist of both receptors (for review see Timmerman and van Zwieten, 1981), we have investigated this interaction between noradrenaline and captopril in more detail to identify the class of α-adrenoceptor involved. This study confirms the findings reported recently (Antonaccio and Kerwin, 1981; Clough et al., 1981) that captopril inhibits postjunctional vasocontrictor responses to noradrenaline in pithed rats. However, captopril interfered with the vasoconstriction elicited by noradrenaline only in those animals in which the vascular postsynaptic α2-adrenoceptor system could be triggered (saline-and prazosin-treated rats). Captopril was without effect after removal of the contribution of post-synaptic α2-adrenoceptor stimulation to the in vivo vascular smooth muscle contraction due to (-)-noradrenaline (rauwolscine-treated rats). These results indicate that captopril selectively impairs the vasoconstriction subserved in vivo by postjunctinal α2-adrenoceptors. The vasoconstrictor process initiated by α1-adrenoceptor activation is not affected by captopril.