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Biomedical subjects

N A Svendgaard

Publications and source records attributed to N A Svendgaard.

At least 37 records · Page 2Linked to original sources
PubMed1990

Prevention of cerebral vasospasm in the rat by depletion or inhibition of substance P in conducting vessels.

Cisternal blood injection in the rat induces a biphasic angiographic vasospasm, with a maximal acute spasm at 10 minutes and a maximal late spasm at 2 days after the subarachnoid hemorrhage (SAH). Depletion of substance P-containing sensory nerves to the cerebral arteries with capsaicin prior to SAH prevents the development of both acute and late spasm. Intrathecal administration of the substance P antagonist spantide 2 hours prior to SAH also prevents the development of vasospasm, while spantide administration 1 hour before SAH only hinders the occurrence of late vasospasm. Intracisternal administration of spantide 2 hours post-SAH prevents the development of late vasospasm. This antagonist per se can induce a short-lasting dose-dependent angiographic vasoconstriction. Substance P-containing nerve fibers on the cerebral arteries could constitute the sensory link in a reflex arc system involved in the development of vasospasm in which the presence of blood in the subarachnoid space stimulates sensory substance P-containing nerve fibers on the cerebral arteries inducing a centripetal impulse to the A2-nucleus tractus solitarius setting into motion the events in the brain stem leading to acute and late vasospasm.

Animals↗
PubMed1988

Stellate ganglion innervation of the vertebro-basilar arterial system demonstrated in the rat with anterograde and retrograde WGA-HRP tracing.

Stellate ganglia projections to cerebral arteries have been investigated with wheatgerm-agglutinated horseradish peroxidase (WGA-HRP). Injections of WGA-HRP into the stellate ganglia resulted in labelling of nerve fibres on the vertebral and basilar arteries, and their side branches. The innervation was bilateral, but with an ipsilateral predominance. After WGA-HRP application on the basilar artery, retrogradely labelled cells appeared in both stellate ganglia, but most numerously in the right ganglion (70-75%). Failure to detect stellate projections to cerebral arteries in 6-hydroxydopamine (6-OHDA)-pretreated animals indicates that these fibres are of noradrenergic sympathetic character. It is suggested that the stellate fibres follow the vertebral arteries towards the basilar artery and its branches.

Afferent Pathways↗
PubMed1988

Brain stem terminations of the trigeminal and upper spinal ganglia innervation of the cerebrovascular system: WGA-HRP transganglionic study.

The central projections of the nerve fibers innervating the middle cerebral and basilar arteries were investigated by transganglionic tracing of wheat germ agglutinin conjugated with horseradish peroxidase (WGA-HRP) in the rat. WGA-HRP was applied to the exposed basilar and/or middle cerebral arteries. Sections of the brain, trigeminal and upper spinal ganglia were reacted with tetramethylbenzidine for detection of the tracer. The results demonstrate that trigeminal neurons that innervate the middle cerebral artery project to the trigeminal main sensory nucleus, pars oralis, and the dorsocaudal two-fifths of pars interpolaris of the trigeminal brain stem nuclear complex. Terminals were also visible in the ipsilateral nucleus motorius dorsalis nervi vagi (dmnX) and in the lateral nucleus tractus solitarius (nTs) bilaterally at the level of the obex. The ventral periaqueductal gray, including the dorsal raphe and C2 dorsal horn, were also innervated by nerve fibers from the middle cerebral artery. Ipsilateral trigeminal rhizotomy prior to WGA-HRP application over the middle cerebral artery impeded the visualization of nerve terminations throughout the brain stem. Pretreatment with capsaicin reduced the density of labeled neurons and terminals within the trigeminal ganglion and the brain stem, respectively, following WGA-HRP application over the middle cerebral artery. Basilar artery fibers terminate in the C2 dorsal horn, the cuneate nuclei, dmnX, and nTs bilaterally. A few projections were also labeled in the ventral periaqueductal gray. Unilateral upper two spinal dorsal rhizotomy prior to WGA-HRP application over the exposed basilar artery resulted in terminal labeling within the C2 dorsal horn, the cuneate nucleus, dmnX, and nTs contralateral to the rhizotomy, whereas the ipsilateral side was devoid of any labeling. Bilateral superior cervical ganglionectomy prior to WGA-HRP administration to the middle cerebral and basilar arteries did not alter the visualization of nerve terminations throughout the brain stem.

Animals↗
PubMed1988

The role of vasopressin in acute cerebral vasospasm. Effect on spasm of a vasopressin antagonist or vasopressin antiserum.

An experimental model of subarachnoid hemorrhage (SAH) in the Sprague-Dawley rat induces angiographically demonstrable, reproducible biphasic vasospasm of the vertebrobasilar system. The acute vasospasm is maximum at 10 minutes and the maximum late vasospasm occurs 2 days after the SAH. Brattleboro rats, which are deficient in arginine vasopressin (AVP), do not have acute vasospasm after SAH but exhibit a degree of late vasospasm that is not significantly different from that seen in Sprague-Dawley rats. Cisternal injection of AVP induced acute vasospasm in Sprague-Dawley rats with a duration similar to that seen after cisternal blood injection; however, at 2 days, the vessel diameter was normal. Intravenous AVP antagonist or intracisternal AVP antiserum administered prior to the SAH prevented the development of acute vasospasm without affecting the late phase. The data suggest that an increased release of AVP in the cerebrospinal fluid is involved in the development of acute cerebral vasospasm.

Acute Disease↗
PubMed1987

Cerebrovascular and metabolic changes during the delayed vasospasm following experimental subarachnoid hemorrhage in baboons, and treatment with a calcium antagonist.

A model has been designed in baboons for simulating the clinical situation during the late phase of vasospasm in patients with subarachnoid hemorrhage (SAH). A total amount of 14-33 ml autologous blood was injected into the cisternal system on 3 occasions in the course of 4 days. Neurological symptoms were seen, and the mortality rate was 29%. Angiography 3 days after the last injection showed arterial vasoconstriction amounting to 23% in the vertebro-basilar system, and 11% (right) and 18% (left) in the carotid system. Cerebral blood flow (CBF) measured by the intra-arterial 133Xe technique and the cerebral metabolic rate of oxygen (CMRO2) were reduced by 18% and 11%, respectively. The hypercapnic CBF response was significantly impaired, from a mean of 3.90 ml/100 g/min to 1.72 ml/100 g/min of flow increase for each mm Hg elevation of paCO2. Autoregulation, tested by administration of angiotensin II, was also significantly affected as evidenced by a pressure-dependent increment of CBF during hypertension in 5 out of 7 animals tested. The impaired autoregulation was reflected in the autoregulatory index, which in the whole group increased from 0.06 ml/100 g/min for each mm Hg increase in MABP in the pre-SAH animals to 0.29 ml/100 g/min per mm Hg post-SAH. Treatment with the calcium antagonist, nimodipine (0.5 microgram/kg/min i.v. during 45 min), enhanced CBF significantly by 17% before experimental SAH, whereas after SAH the effect was slight and did not reach statistical significance; CMRO2 was not significantly affected in either group. Intravenous nimodipine combined with hypertension resulted in a marked increase in the autoregulatory index to 1.58 ml/100 g/min per mm Hg in pre-SAH animals and a less pronounced increment to 0.58 ml/100 g/min per mm Hg following experimental SAH. The beneficial effect of nimodipine reported in SAH patients is therefore, in view of our findings, more likely due primarily to a protective mechanism at the cellular level than to an influence on the vascular bed.

Animals↗
PubMed1987

Effect of selective lesions of medullary catecholamine nuclei on experimental cerebral vasospasm in the rat.

Intracisternal injection of blood in the rat induces an angiographically demonstrable, biphasic cerebral vasospasm of the vertebrobasilar system, with a maximal acute spasm at 10 min and a maximal late spasm at 2 days after the subarachnoid hemorrhage (SAH). Selective lesioning of the A1 nuclei in the medulla oblongata prior to the SAH prevents the development of the late spasm, but the acute spasm develops to the same extent as in sham-lesioned animals. Lesions of the medullary A2 nuclei not only prevent the development of both acute and late spasm, but give rise to a dilatation of the vertebrobasilar arteries at day 2 post-SAH. The study indicates that both the A1 and A2 nuclei participate in the development of vasospasm post-SAH. The contrasting patterns of spasm after A1 and A2 lesions suggest a different mechanism for acute and late spasm.

Adrenergic Fibers↗
PubMed1987

Effect of neonatal 6-hydroxydopamine treatment on experimental vasospasm following a subarachnoid hemorrhage in the rat.

Intracisternal injection of blood in the rat produces an angiographically demonstrable biphasic cerebral arterial vasospasm. Systemic 6-hydroxydopamine (6-OHDA) treatment in the neonatal stage, which causes a depletion of noradrenaline (NA) from both sympathetic and central NA-containing nerve fibers, prevents the development of the late spasm phase, while the acute spasm occurs to the same extent as in normal animals. The occurrence of acute spasm can be prevented by lesioning in the mesencephalon of the ascending catecholamine fibers originating in the lower brainstem and projecting to the hypothalamus. It is suggested that 6-OHDA treatment results in the altered spasm pattern via its effect on catecholamine fibers projecting between the medullary A1 and A2 nuclei and the hypothalamus. The occurrence of acute but not late spasm indicates that there is a different pathway underlying the two spasm phases.

Animals↗
PubMed1987

Nerves containing serotonin, its interaction with noradrenaline, and characterization of serotonin receptors in cerebral arteries of monkey.

1 Immunohistochemistry was applied to study the presence of 5-hydroxytryptamine (5-HT) and dopamine-beta-hydroxylase (DBH) in cerebrovascular nerves of monkeys, and serotonergic receptors were characterized in the vessels by in vitro pharmacology. 2 A well-developed plexus of 5-HT immunoreactive fibres was found to supply the pial arteries at the base of the brain. The network closely resembled the distribution of neural DBH, used as an index for noradrenergic nerves. 3 5-HT contracted the basilar artery (BA) and middle cerebral artery (MCA) with equal potency and intrinsic activity. The effect was not antagonized by phentolamine or propranolol. 4 The 5-HT2 receptor antagonist, ketanserin, inhibited the response to 5-HT in a competitive manner in both vessels, with pA2 values obtained from Schild plots of 9.15 in BA and 9.40 in MCA. 5 Electrical field stimulation elicited a neurogenic contraction that was completely blocked by 3 X 10(-7) M tetrodotoxin, 3 X 10(-6) M guanethidine, and 10(-6) M phentolamine. The response was also antagonized by ketanserin, but only in concentrations higher than those inhibiting the response to 5-HT. 6 In accordance with the findings during nerve stimulation, noradrenaline (NA) contracted the pial arteries, particularly MCA where the intrinsic activity closely resembled the value obtained with 5-HT. Ketanserin antagonized the response, but less efficiently than that induced by 5-HT. 7 5-HT had no effect on the (noradrenergic) neurogenic contraction obtained during electrical stimulation. Nor did 5-HT affect the contraction induced by exogenous NA. 8 It is concluded that 5-HT and NA may be co-localized in perivascular nerves of the monkey brain. 5-HT contracts pial arteries through postjunctional 5-HT2 receptors, but does not seem to interfere prejunctionally with the noradrenergic nerves or with exogenous NA.

Animals↗
PubMed1987

Prediction and prevention of delayed ischemic dysfunction after aneurysmal subarachnoid hemorrhage and early operation.

Mean hemispheric cerebral blood flow (CBF) was studied after the intravenous administration of xenon-133 in 20 anesthetized patients with aneurysmal subarachnoid hemorrhage. Before early aneurysm operation, repeated CBF measurements were made to evaluate the cerebral vascular reactivity to controlled hyperventilation. Thirteen individuals received intravenous treatment with the calcium channel blocker nimodipine, whereas the other seven patients did not receive such specific antiischemic treatment. Five of the latter patients had an impaired CO2 response, and three showed delayed ischemic deterioration (DID), whereas none of the seven nimodipine-treated patients with impaired CO2 response showed DID. One nimodipine-treated patient with a preserved CO2 response, in whom operation was complicated, developed DID. The observed findings indicate that DID after uncomplicated early aneurysm operation may be associated with an early disturbance of cerebral vasoreactivity. Treatment with nimodipine may counteract the development of DID in patients with an impaired CBF CO2 response.

Adult↗
PubMed1986

Origin and distribution of cerebral vascular innervation from superior cervical, trigeminal and spinal ganglia investigated with retrograde and anterograde WGA-HRP tracing in the rat.

Peripheral sources of cerebral vascular innervation have been investigated with retrograde and anterograde neuronal tracing of wheat germ agglutinin conjugated with horseradish peroxidase (WGA-HRP) in the rat. For retrograde identification of sources of innervation, WGA-HRP was applied to the exposed basilar artery through a fine slit in the overlying meninges, and sections of brain and peripheral ganglia were reacted with tetramethylbenzidine for detection of the tracer. A high density of tetramethylbenzidine reaction product was observed around the basilar artery and in the surrounding pial tissue, but the application sites were not completely selective since some tracer always had spread into the ventral brain stem. Retrogradely labelled cell bodies were identified in the superior cervical, stellate, first and second spinal, and trigeminal ganglia, i.e. these ganglia may represent origins of basilar artery innervation. In a second series of experiments, microinjections of WGA-HRP were placed into the indicated ganglia to obtain anterograde labelling of nerve fibres on whole-mounts of the cerebral vessels. Injections into trigeminal ganglia labelled nerve fibres on the ipsilateral half of the circle of Willis, as well as the contralateral anterior cerebral artery and the rostral part of the basilar artery. The first and second spinal ganglia projected to the vertebrobasilar arteries, while the ipsilateral part of the internal carotid (outside the circle of Willis) received fibres from the second spinal ganglion. Nerve fibres originating in trigeminal and spinal ganglia were organised in bundles, and between these a sparse plexus of thin single fibres appeared. Injection of WGA-HRP into superior cervical ganglion labelled a plexus of nerve fibres on the ipsilateral circle of Willis and the (rostral) basilar artery. These experiments demonstrated the origin and distribution of sympathetic and sensory innervation to major cerebral arteries in the rat.

Animals↗
PubMed1986

Subarachnoid hemorrhage in the rat: cerebral blood flow and glucose metabolism during the late phase of cerebral vasospasm.

A double-isotope technique for the simultaneous measurement of CBF and CMRglu was applied to a subarachnoid hemorrhage (SAH) model in the rat. Cisternal injection of 0.07 ml blood caused a rather uniform 20% reduction in CBF together with an increase in glucose utilization of 30% during the late phase of vasospasm. In one-third of the SAH animals, there were focal areas where the flow was lowered to 30% of the control values and the glucose uptake increased to approximately 250% of control. We suggest that blood in the subarachnoid space via a neural mechanism induces the global flow and metabolic changes, and that the foci are caused by vasospasm superimposed on the global flow and metabolic changes. In the double-isotope autoradiographic technique, [14C]iodoantipyrine and [3H]deoxyglucose were used for CBF and CMRglu measurements, respectively, in the same animal. In half of the sections, the [14C]iodoantipyrine was extracted using 2,2-dimethoxypropane before the section was placed on a 3H- and 14C-sensitive film. The other sections were placed on x-ray film with an emulsion insensitive to 3H. The validity of the double-isotope method was tested by comparing the data with those obtained in animals receiving a single isotope. The CBF and metabolic values obtained in the two groups were similar.

Animals↗
PubMed1986

Subarachnoid hemorrhage in the rat: cerebral blood flow and glucose metabolism after selective lesions of the catecholamine systems in the brainstem.

A double-isotope autoradiographic technique was used to evaluate CBF and glucose metabolism 2 days after a subarachnoid hemorrhage (SAH) in rats with lesions in the lower brainstem. Lesioning in the mesencephalon of the ascending catecholamine pathways from locus ceruleus and from the A1 and A2 nuclei, or lesioning in the medulla oblongata of the ascending fibers from A1 and A2, prevents the development of the global changes in flow and metabolism seen in normal animals post SAH. Also the focal low-flow areas with markedly elevated deoxyglucose uptake, which can develop in normal animals 2 days post SAH, were not seen in the lesioned animals after the SAH. The findings indicate that the A1 and A2 nuclei, which project to the hypothalamus-pituitary, are essential for the flow and metabolic changes after an SAH. The lesions per se did not change baseline flow and metabolism as compared with sham-lesioned animals.

Animals↗
PubMed1986

Effect of selective lesions in the hypothalamic-pituitary region on the development of cerebral vasospasm following an experimental subarachnoid hemorrhage in the rat.

Intracisternal injection of blood in the rat induced an angiographically demonstrable biphasic cerebral vasospasm with a maximal acute spasm at 10 min and a maximal late spasm at 2 days after the subarachnoid hemorrhage. Systemic administration of 6-hydroxydopamine, which destroys catecholamine fibers in the circumventricular areas characterized by the absence of a blood-brain barrier, prevented the development of both the acute and the late spasm. Isolation or removal of one of the circumventricular organs, the pituitary, from the brain via a stalk transection or a hypophysectomy did not affect the degree of vasospasm. Lesion of the median eminence, another region without a blood-brain barrier, prevented the development of both types of spasm. The median eminence receives projections from the A1 and A2 nuclei in the medulla oblongata. It is suggested that the projections of these nuclei to the internal layer of the median eminence underlie the development of spasm.

Animals↗
PubMed1985

The effect on the development of cerebral vasospasm in the rat of lesioning of the peripheral and central catecholamine systems.

An experimental SAH was produced in the rat by the intracisternal injection of blood. The animals were examined with bilateral vertebral angiography or autoradiographic CBF- and CMRgI-studies. A biphasic vasospasm was seen with a maximal acute spasm at ten minutes and a maximal late spasm at two days post SAH. On day two post SAH, CBF studies demonstrated focal low flow areas in the cortex and caudate-putamen. The CMRgI examinations revealed focal areas with deoxyglucose accumulation corresponding to the low flow areas, suggesting an anaerobic glycolysis. Adrenal demedullation did not change the degree of spasm. Cranial sympathectomy reduced the degree of late spasm by about 50%. Lesioning of the ascending CA pathways in the mesencephalon prior to the SAH, prevented the development of both the acute and the late spasm. It also prevented the development of the focal CBF and CMRgI changes.

Adrenal Medulla↗
PubMed1983

Late cerebral arterial spasm: the cerebrovascular response to hypercapnia, induced hypertension and the effect of nimodipine on blood flow autoregulation in experimental subarachnoid hemorrhage in primates.

1. Late cerebral arterial spasm was induced by repeated injections of autologous blood in a total amount of 14-33 ml into the basal cisterns of baboons to mimick subarachnoid hemorrhage (SAH). Regional cerebral blood flow (CBF), sagittal sinus pressure, cerebral arterial caliber from angiograms, and cerebral metabolic rate of oxygen (CMRO2) were measured before and after the experimental SAH to determine responses to hypercapnia and induced hypertension. The effect of the calcium antagonist, Nimodipine, on CBF autoregulation pre- and post-SAH was tested. 2. One week after the blood injections were started there was about 10-20% reduction, depending on territory measured, in the arterial diameter of the carotid and vertebral systems. This was associated with an 18% reduction in CBF and 9% decrease in the brain metabolism. 3. During hypercapnia before and after experimental SAH the flow increased with a mean of 3.7 and 1.8 ml, respectively, for each mm Hg elevation of PaCO2. In control animals, graded angiotensin-induced hypertension did not overtly affect CBF. Following SAH, the CBF autoregulation was impaired in 5 of 6 animals tested. 4. I.v. infusion of Nimodipine markedly curtailed the CBF autoregulation in pre-SAH animals and, to a somewhat slighter extent, also in post-SAH animals.

Animals↗
PubMed1982

Treatment of severe cervical spine injuries by anterior interbody fusion with early mobilization.

A follow up study of 24 patients treated for severe injury of the cervical spine is presented. The dislocation was initially reduced by skull traction, which was later replaced by anterior fusion using a tibial graft. Solid fusion occurred in all patients. The neurological improvement was unaffected by the operation. Our conclusion is that anterior fusion as opposed to conservative treatment leads to earlier mobilization, shorter hospitalization, and less costly rehabilitation.

Adolescent↗
PubMed1978

Redundant nerve roots of the cauda equina. A report of five cases.

Five personally examined cases of redundant nerve roots of the cauda equina are added to the 13 hitherto on record. Except for segmental neurological deficits, intermittent claudication-like symptoms of the cauda equina dominated the histories of four of our five cases. The diagnosis was confirmed at surgical exploration, which included laminal and dural decompression. At follow-up (two months--three years) the neurological deficit, or the intermittent claudication, or both, had improved in all our patients. The pathogenesis of root redundancy is obscure. It seems that the symptoms arise through the action of at least two factors viz compression of the spinal content and the existence of one or more redundant roots. Wider use of diagnostic aids and surgical exploration would probably show that redundant roots are more common than hitherto supposed.

Aged↗