Ipsilateral Carotid Artery Ligation Research Articles

In vivo neuroprotective effects of ACEA 1021 confirmed by magnetic resonance imaging in ischemic stroke

The neuroprotective activity of ACEA 1021 (5-nitro-6,7-dichloro-1,4-dihydro-2,3-quinoxalinedione; licostinel), a selective antagonist at the strychnine-insensitive glycine site associated with the NMDA receptor complex, has been investigated in various models of focal cerebral ischemia. In isoflurane-anaesthesised Wistar rats with permanent ipsilateral carotid artery ligation and transient middle cerebral artery occlusion (duration of occlusion, 2 h) followed by reperfusion (24 h), intravenous administration of ACEA 1021 (bolus: 10 mg/kg, 15 min after the onset of middle cerebral artery occlusion; infusion: 7 mg/kg/h for 6 h beginning 30 min after occlusion of the artery) produced a 32% reduction in infarct volume. Similarly, in Sprague–Dawley rats with transient middle cerebral artery occlusion (2 h) followed by 24 h of reperfusion, identical treatment with ACEA 1021 decreased infarct size by 39%. Magnetic resonance imaging (MRI) confirmed these effects in the transient model, in that infarct volume observed using apparent diffusion coefficient (ADC) maps was significantly smaller after 24 h in the ACEA 1021-treated rats compared with Tris-treated controls. Furthermore, the increase in perfusion signal intensity after reperfusion was more pronounced in the ACEA 1021-treated rats than in controls. In Fisher 344 rats with permanent occlusion of the middle cerebral artery, ACEA 1021 induced a dose-related decrease in infarct volume, which was associated with an improvement in neurological outcome as measured by the rope suspension procedure. Administration of the same dose regimen, as above, in Fisher rats with permanent middle cerebral artery occlusion reduced infarct volume by 68%. This dose was as effective when administration was delayed for 2 h. In mice with permanent middle cerebral artery occlusion, ACEA 1021 (5 mg/kg, i.v., 5 min after occlusion; 30 mg/kg, s.c., 1 and 4 h post-middle cerebral artery occlusion) decreased infarct size by 42%. The consistent anti-ischemic effects of ACEA 1021 make it a valuable compound for exploratory stroke research.

Treatment of Trapped CCF by Direct Puncture of the Cavernous Sinus by Infraocular Trans-SOF Approach

We present a case of recurrent carotid-cavernous fistula after prior ipsilateral carotid artery ligation. Due to lack of endovascular access, embolization was performed by direct puncture of the cavernous sinus via a transorbital approach. Operative technique and an anatomical basis for treatment are described.

Perinatal Brain Iron Deficiency Increases the Vulnerability of Rat Hippocampus to Hypoxic Ischemic Insult

Fetal brain iron deficiency occurs in human pregnancies complicated by diabetes mellitus or intrauterine growth retardation. Because neurocognitive deficits are more common in the offspring of these pregnancies, we tested the hypothesis that perinatal brain iron deficiency predisposes the neonatal hippocampus, a structure important for memory processing, to injury. Brain iron concentration was reduced by 45% in 45 neonatal rats by maternal dietary iron restriction during gestation. Right-sided neuronal injury in four hippocampal subareas was induced by hypoxic-ischemic insult (ipsilateral carotid artery ligation and subsequent hypoxia on postnatal d 7) and was quantified histochemically on d 8 by cytochrome c oxidase activity (n = 30), and on d 14 by Nissl staining (n = 15). Acute right-sided cytochrome c oxidase activity loss occurred in CA1 (P = 0.02), CA3c (P < 0.001) and dentate gyrus (P < 0.001) in the iron-deficient group, whereas only CA1 (P = 0.003) was affected in the iron-sufficient group. Long-term right-sided Nissl substance loss occurred in CA1 (P = 0.001), CA3a,b (P < 0.001) and dentate gyrus (P = 0.008) in the iron-deficient group, but only in CA1 (P = 0.004) in the iron-sufficient group. No increase in right-sided free-iron staining was present in either group. Perinatal iron deficiency predisposes the neonatal hippocampus to a greater acute loss of neuronal metabolic activity after an hypoxic-ischemic event, suggesting compromised cellular energetics. The subsequently greater loss of hippocampal neuronal integrity suggests poorer recoverability after injury in the perinatal iron-deficient brain.

Anterior Segment Ischemia Syndrome Following Rectus Muscle Transposition

Two patients developed clinically significant anterior segment ischemia following full tendon transposition of the superior and inferior recti muscles nine and 20 years after they underwent horizontal rectus muscle surgery. Ipsilateral carotid artery ligation in one patient and possible hyperlipoproteinemia type II in the other were discovered postoperatively and may have contributed to the circulatory disturbances observed. In adult patients with paretic strabismus, the most important function of the paretic muscle may be maintenance of circulation to the anterior segment of the eye.

Effect of carotid ligation on cerebral blood flow in baboons. 2. Response to hypoxia and haemorrhagic hypertension.

Cerebral blood flow (CBF) measurements were carried out in two groups of anaesthetized normocapnic baboons. In the first group of five animals the effect of hypoxia on the CBF before and after ipsilateral carotid artery ligation was studied. The results showed that, although after ipsilateral carotid ligation there was little change in the CBF at normal PaO(2), at hypoxia there was only 20% rise in the CBF as compared with an 80% rise before the carotid ligation. In the second group of 10 animals, effects of haemorrhagic hypotension on the CBF after ipsilateral carotid artery ligation were estimated. The results indicated impairment of autoregulatory response of the cerebral circulation.

Effect of carotid ligation on cerebral blood flow in baboons. I. Response to altered arterial PCO2.

Measurements of cerebral blood flow (CBF) were made in anaesthetized baboons before and after ipsilateral carotid artery ligation and also after bilateral carotid ligation. Results showed that at normocapnia (PaCO(2) 38-39 mmHg) there was little change in cerebral blood flow on ipsilateral carotid ligation, but when both carotid arteries were tied the blood flow to the brain fell significantly. At hypercapnia (PaCO(2) 58-60 mmHg) the CBF/CO(2) gradient fell significantly on ipsilateral carotid ligation; on bilateral carotid ligation there was only minimal rise in cerebral blood flow in response to the rise in PaCO(2). At hypocapnia (PaCO(2) 20-21 mmHg) the gradients of fall in the CBF were similar before and after ipsilateral carotid ligation; after bilateral carotid ligation there was minimal change in the CBF in response to the fall in the PaCO(2). It is suggested that, although cerebral blood flow may be normal after ipsilateral carotid ligation, the circulatory reserve of the brain is not sufficient to meet physiological challenges. This may be the reason for the development of delayed neurological complications after carotid artery ligation.