Occluded Side Research Articles

The occlusal contact mode during lateral excursion

The purpose of this study is to clarify the occlusal contact mode between the upper and lower molars on the working side of group function occlusion during lateral excursion. After the intercuspal position (IP) and two lateral positions (L1, the middle point between IP and L2; L2, the edge-to-edge occlusal position of the molars) on the Gothic arch were defined, occlusal contact relations in these three occlusal positions were recorded, using black silicone. Digital data of real occlusal contacts and visualized data of close (less than 30 microns) occlusal areas, by computer image processing, were analyzed. The conclusions are as follows: 1. Although the numbers of real occlusal contacts and the visualized occlusal area tend to decrease toward L2 during lateral excursion, the former, in some cases, goes up and down. 2. Functional cusps play an important part in occlusal contact at the intercuspal position. 3. Occlusal contact points are on the functional cusps of the upper and lower molars, which can be clinically regarded as certain points, and these points slide on the inclining non-functional cusps of antagonistic teeth during lateral excursion. 4. Each upper and lower molar has 2 to 6 occlusal contact points near the top functional cusps at the intercuspal position, and some of them contact continuously during lateral excursion.

Patterns of cerebrovascular reactivity in patients with carotid artery occlusion and severe contralateral stenosis

There is evidence suggesting that among other factors, an alteration in cerebral hemodynamics plays a relevant role in the occurrence of strokes in patients with carotid disease. The purpose of this study was to investigate patterns of cerebrovascular reactivity in patients with internal carotid occlusion and severe contralateral carotid stenosis and their relationship with symptomatology. Using transcranial Doppler ultrasound, cerebrovascular reactivity to hypercapnia in middle cerebral arteries was evaluated with the breath-holding index (BHI) in 42 patients with internal carotid occlusion and severe contralateral carotid stenosis and in 40 control subjects. A significant decrease of BHI on the occluded side was observed in symptomatic patients with respect to asymptomatic ones (0.12+/-0.1 vs. 0.75+/-0.4, P<0.0001) and with respect to the control group (1.11+/-0.1, P<0.0001). The difference was also significant between asymptomatic patients and controls (P<0.0001). Breath-holding values on the stenotic side were significantly higher (P<0.0001) in asymptomatic patients (1.01+/-0.2) with respect to symptomatic ones (0.39+/-0.1). A significant difference (P<0.0001) was also present between controls and symptomatic patients. The pattern of cerebrovascular reactivity in patients with severe bilateral carotid steno-occlusive disease seems to be strictly dependent on the presence of previous symptoms. Further studies are needed to investigate whether the study of cerebral hemodynamics in patients with bilateral carotid artery disease is important for planning therapeutic strategies.

Inhibition of cyclic AMP-dependent protein kinase in the acute phase of focal cerebral ischemia in the rat

Binding of cyclic AMP to the regulatory subunit of cyclic AMP-dependent protein kinase is an essential step in cyclic AMP-mediated intracellular signal transduction. In the present study, the binding capacity of cyclic AMP-dependent protein kinase for cyclic AMP was examined by autoradiography with local cerebral blood flow in focal cerebral ischemia in the rat, which was induced by occlusion of the middle cerebral artery using the intraluminal suture method. The binding capacity of cyclic AMP-dependent protein kinase and local cerebral blood flow were assessed by the in vitro [ 3H]cyclic AMP binding and the [ 14C]iodoantipyrine methods, respectively. At 3 h of occlusion, a significant reduction in the binding of cyclic AMP-dependent protein kinase to cyclic AMP was already noted in the lateral region of the caudate–putamen and the parietal cortex. Between three and five hours of occlusion, the area with reduced cyclic AMP binding was significantly expanded to the peri-ischemic regions including the frontal cortex and the medial region of the caudate–putamen. The threshold in local cerebral blood flow for reduced cyclic AMP binding was clearly noted at 5 h of ischemia, and was 45 ml/100 g per min in the cerebral cortices, and 38 ml/100 g per min in the caudate–putamen, respectively. No threshold was noted at 3 h of ischemia, since cyclic AMP binding showed a large variation ranging from reduced to normal values even when local cerebral blood flow was below 20 ml/100 g per min. Recirculation for 3.5 h following 1.5 h of ischemia restored the normal cyclic AMP binding in the cerebral cortices, but failed to normalize cyclic AMP binding in the caudate–putamen despite good recovery of local cerebral blood flow. Western blot analysis suggested that this reduction in cyclic AMP binding was not due to loss or degradation of the subunit protein of cyclic AMP-dependent protein kinase, and may therefore have resulted from conformational changes in the protein. A significant increase in cyclic AMP binding was noted after recirculation in the non-ischemic regions such as the frontal and the cingulate cortices on the occluded side and in the contralateral cortices. These data indicate that cyclic AMP-mediated signal transduction in the brain tissue may be very susceptible to ischemic stress, and the region of disrupted signal transduction may expand progressively from the ischemic core to peri-ischemic regions in the acute phase of ischemia. Such impairment of signal transduction may not be restored in the caudate–putamen even when cerebral circulation is fully recovered after short-term ischemia, suggesting that a regional vulnerability to ischemic stress may also exist in cyclic AMP-mediated signal transduction. A significant increase in cyclic AMP binding after recirculation in regions outside of ischemic area may be closely related with the protective mechanisms of brain tissue, since cyclic AMP has been reported to exert various neuroprotective actions.

Role of the ryanodine receptor in ischemic brain damage--localized reduction of ryanodine receptor binding during ischemia in hippocampus CA1.

1. The ryanodine receptor has recently been shown to play a pivotal role in the regulation of intracellular Ca2+ concentration via Ca(2+)-induced Ca2+ release (CICR). Effects of ischemia on CICR in the brain tissue, however, remain largely unknown since only a few reports have been published on this subject. In this paper we report on work in this area by our group and review related progress in this field. 2. We examined alterations of ryanodine receptor binding and local cerebral blood flow (LCBF) at 15 min, 30 min, and 2 hr after occlusion of the right common carotid artery in the gerbil brain. A quantitative autoradiographic method permitted simultaneous measurement of these parameters in the same brain. The LCBF was significantly reduced in most of the cerebral regions on the occluded side during each time period of ischemia. In contrast, only in the hippocampus CA1 on the occluded side was a significant reduction in ryanodine binding found at 15 min, 30 min and 2 hr after the occlusion. 3. These findings suggest that suppression of ryanodine binding in the hippocampus CA1 may be attributable to a regionally specific perturbation of CICR and that this perturbation may be closely associated with the pathophysiological mechanism that leads to be selective ischemic vulnerability of this region. 4. Other recent studies have also reported an important role for ryanodine receptors in neuronal injury such as the delayed neuronal death in the hippocampus CA1. These data suggest that derangement of CICR is likely to be involved in acute neuronal necrosis as well as in delayed neuronal death in ischemia. 5. Further studies on clarifying the role of CICR in ischemic brain damage are needed in order to develop new therapeutic strategies for stroke patients.

Balloon ischemic percutaneous microwave coagulaion for hepatic tumor of segmental borderline area

In three of 20 patients with liver tumors who underwent baloon-ischemic percutaneous microwave coagulation therapy, computed tomography during arterial portography (CTAP) images with balloon occlusion of the hepatic vein revealed localization of a tumor on the borderline of the middle hepatic vein region and the right hepatic vein region. Patient 1 : had metastatic liver cancer in S5, measuring 20 mm in diameter. Microwave coagulation was performed at 60W for 10 minutes under balloon occlusion of the right hepatic artery and hepatic vein. A coagulation area which measured 40 × 24 mm resembled a CTAP image under right hepatic vein occlusion. Patient 2 : had metastatic liver cancer in S5, measuring 15 mm in diameter. Microwave coagulation was performed at 60W for 5 minutes under balloon occlusion of the middle hepatic vein and proper hepatic artery. A coagulation area which measured 50 × 27 mm protruded hemispherically into the middle hepatic vein region. There was little coagulation of the right hepatic vein region. Patient 3 : had hepatocellular carcinoma in S5, measuring 29 mm in diameter. Microwave coagulation was performed at 60W for 8 minutes under balloon occlusion of the right hepatic vein and embolism with gelatin sponge A5 and A8. A coagulation area which measured 48 × 31 mm expanded to the ischemic, right hepatic vein region. In balloon-ischemic microwave coagulation on a segmental borderline, a microwave coagulation area extends matching to the portal venous blood flow occlusion area with a hepatic vein balloon. The microwave coagulation area expanded clearly on the hepatic vein occlusion side, whereas on the hepatic vein non-occlusion side, the microwave coagulation area was obviously limited.

Carotid artery balloon test occlusion: combined clinical evaluation and xenon-enhanced computed tomographic cerebral blood flow evaluation without patient transfer or balloon reinflation: technical note.

Clinical evaluation was combined with xenon-enhanced computed tomographic (CT) cerebral blood flow (CBF) evaluation during carotid artery balloon test occlusion (BTO), without patient transfer from the angiography suite to the CT scanner or balloon reinflation. Thirteen patients underwent carotid artery BTO. Placement of temporary occlusion balloons was performed with patients positioned on the CT scanner table. If neurological testing revealed no changes within 10 minutes after balloon inflation, patients were positioned within the CT scanner gantry for xenon-enhanced CT CBF evaluation. CBF evaluations were begun 12 to 15 minutes after balloon inflation and required 8 minutes for completion. After completion of CBF evaluation, neurological testing continued during 30 minutes of arterial occlusion. One patient did not tolerate BTO, with the development of reversible hemiparesis. Reliable CBF data were not obtained because of patient motion in one case. Eleven patients clinically tolerated BTO and completed CBF evaluation. For five patients, xenon-enhanced CT scanning revealed no regions with CBF of less than 30 ml/100 g/min. For four patients, xenon-enhanced CT scanning revealed small regions with CBF of less than 30 ml/100 g/min within the anterior frontal lobe on the occluded side. For two patients, ipsilateral CBF decreased dramatically during BTO, with CBF in many regions of less than 30 ml/100 g/min and in some of less than 20 ml/100 g/min. Xenon-enhanced CT CBF evaluation can be combined with clinical testing during BTO without patient transfer, balloon reinflation, or increases in the duration of the procedure. We recognize that the value of CBF evaluation during BTO remains to be proven; our technique does, however, eliminate abbreviated clinical neurological evaluation, patient transfer, and balloon reinflation, which were previously associated with the use of xenon-enhanced CT CBF evaluation during carotid artery BTO.

Qualitative versus quantitative assessment of cerebrovascular reserves.

Quantitative studies of cerebral blood flow (CBF) combined with a vasodilatory challenge have defined a subgroup of patients with symptomatic carotid occlusion who have an increased risk for stroke. These are patients whose CBF paradoxically decreases in response to a vasodilatory challenge. Recent reports suggest that qualitative CBF techniques, such as single photon emission tomography with 99m-hexamethylpropyleneamine oxime, can also define the same high-risk subgroup. To determine whether qualitative measures of CBF are sufficient for predicting the risk of stroke, we converted our quantitative CBF data, obtained with xenon-enhanced computed tomography (Xe/CT), to qualitative ratios in a manner similar to that used with single photon emission tomography data. We analyzed CBF values within the territory of the middle cerebral artery for 94 patients with symptomatic carotid occlusion. Values obtained using Xe/CT before and after the intravenous administration of 1 g of acetazolamide were used to derive an asymmetry index: (Coccl - Cnon)/Cavg x 100. The difference between the postacetazolamide asymmetry index and the baseline asymmetry index was used to classify the patients into groups according to CBF values. The threshold for abnormal qualitative CBF reactivity was defined as a percent change in the asymmetry index of less than -10%. Quantitative (Xe/CT) CBF was considered abnormal ("steal" response) when the response to acetazolamide (percent change) on the occluded side was a decrease of 5% or greater. Of 34 patients whose cerebrovascular reserves were considered compromised based on qualitative criteria, 17 (50%) did not have a steal response as defined by quantitative Xe/CT CBF (i.e., false positive). Eleven of 62 (18%) who were not considered compromised by qualitative criteria had a steal response (i.e., false negative). Our data indicate that a qualitative approach has a 61% sensitivity and a 75% specificity for detecting patients with compromised reserves. Further, the positive predictive value of this method is only 50%. Therefore, the two methodologies do not predict the same patients as having compromised reserves. Previous studies have shown that patients at high risk for stroke can be identified with quantitative CBF methods. This study shows that the important subgroup cannot be accurately defined with qualitative methodology. The implications of using the more reliable methodology are important for individual patient management and for designing clinical trials.

Correlation of Continuous EEG Monitoring with [O-15]H2O Positron Emission Tomography Determination of Cerebral Blood Flow during Balloon Test Occlusion of the Internal Carotid Artery

The purpose of this paper was to evaluate the utility of continuous electroencephalography (EEG) during balloon test occlusion (BTO) of the internal carotid artery (ICA). Continuous EEG monitoring and [O-15] H2O PET cerebral blood flow (CBF) studies were completed in 34 patients undergoing BTO of the ICA. CBF determinations were obtained as a baseline without carotid occlusion, and following balloon occlusion, with continuous EEG monitoring. Patients were divided into three groups based on clinical and CBF response to BTO. Group I had no clinical signs or symptoms and had a CBF decrease less than 10 ml/l00 g/min ipsilateral to the occlusion. Group II had no symptoms but CBF fell to 35 to 25 ml/l00 g/min on the occluded side. Group III were clinically unable to tolerate occlusion or CBF fell to less than 25 ml/l00 g/min on the occluded side. The results of continuous 21 channel EEG monitoring were assessed at the time of the examination and retrospectively reviewed for changes in the EEG pattern indicative of ischaemia. On the basis of PET CBF, eighteen patients were classified as Group I, four as Group II, and twelve as Group III. EEG evidence of ischaemia was seen in three patients, all members of Group III. Of the three patients, only one patient had clinical signs or symptoms of ischaemia. All four patients in Group II had PET quantitated CBF levels indicating carotid sacrifice should be done with caution or following a presacrifice by-pass procedure, and nine patients in Group III with PET quantitated CBFs below eligibility for carotid sacrifice, were not identified by EEG monitoring. Even when CBF falls below 25 ml/100 g/minute continuous EEG monitoring is insensitive to reduction in perfusion. Reliance upon EEG for detection of cerebral hypoperfusion in interventionl neuroradiological procedures will significantly underestimate ischaemic risk.

O-15]H2O Positron Emission Tomography Determination of Cerebral Blood Flow Reserve after Intravenous Acetazolamide during Balloon Test Occlusion of the Internal Carotid Artery

The purpose of this paper was to evaluate the effects of acetazolamide on cerebral blood flow (CBF) measured by [O-15]H2O positron emission tomography (PET) during balloon test occlusion (BTO) of the internal carotid artery (ICA). [O-15]H2O PET cerebral blood flow studies were completed in 20 patients undergoing BTO CBF determinations were obtained without carotid occlusion as a baseline, following balloon occlusion, and as a third scan with balloon occlusion after an intravenous acetazolamide bolus. The balloon was left deflated between scans, and was only inflated immediately before and during the 90 second period of time needed for CBF determination. Significance was determined at the P < 0.05 level. Two of twenty studies were technical failures. Prior to acetazolamide there was a significant decrease in CBF (P < 0.0007) ipsilateral to the occlusion. After acetazolamide administration there was no statistically significant change in flow on the occluded side (P < 0.3047); however, there was a significant increase in cerebral blood flow (P < 0.0002) on the non-occluded side. In this patient population, there was no acetazolamide-induced CBF decompensation (steal) phenomenon or haemodynamically significant risk in CBF ipsilateral to the occlusion.

内頚動脈閉塞症における立位負荷の脳循環への影響 頚部超音波ドプラ法と脳ＳＰＥＣＴによる検討

The present study was performed to examine the influence of head-up postural change on cerebral circulation in patients with internal carotid artery occlusion (ICAO) . Duplex ultrasonography was used to measure blood flow velocity (FV) and pulsatility index (PI) of the common carotid artery (CCA) in 11 men with unilateral ICAO (aged 63.0±7.2 yr) while they were lying flat, as well as standing up. In addition, the change in cerebral blood flow (CBF) after becoming upright was evaluated using SPECT. No patient showed any sign of orthostatic hypotension. FVs and PI on the nonoccluded side and systolic FV on the occluded side remained unchanged, while mean, end-diastolic (ED) FVs on the occluded side decreased, and the PI on the occluded side increased. Thus, the side-to-side ratio of EDFV (ED ratio) increased in all cases. A decrease in CBF was observed in 7 out of 9 patients when they were standing upright. The degree of the increase in the ED ratio was associated with worsening of hypoperfusion in upright SPECT. Our results suggest that head-up postural change increases the relative resistance of the CCA against the decrease in carotid arterial pressure due to gravity in carotid occlusive disease, and that cerebral dysautoregulation might then occur. Duplex ultrasonography and SPECT are both safe and useful methods for evaluating the hemodynamic influence of head-up postural change on cerebral circulation in such patients, and the upright test is helpful in diagnosing ICAO using Doppler sonography because of the conspicuous laterality of the FVs.

Cerebral hemodynamics in patients with Moyamoya disease and in patients with atherosclerotic occlusion of the major cerebral arterial trunks

To determine the difference in cerebral hemodynamics between Moyamoya disease and atherosclerotic occlusion of the major cerebral arterial trunks, we measured local cerebral blood flow (CBF) and local CO2 reactivity (CO2R) by xenon-enhanced computed tomography (CT). A total of 11 adult patients with Moyamoya disease (mean age, 39.6±7.8 years) and eight patients with atherosclerotic occlusion of the major arterial trunks (mean age, 62.4±15.4 years) were studied. Regions of interest were frontal, temporal and occipital cortex, caudate, putamen and thalamus in each hemisphere. In patients with Moyamoya disease, local CBF values in the internal carotid artery territory (frontal and temporal cortex, caudate, putamen) were significantly higher than those in the occluded side of patients with atherosclerotic occlusion. Local CO2R values in the caudate and putamen were significantly higher than those in the occluded side of patients with atherosclerotic occlusion. These results suggest that the cerebral hemodynamics of Moyamoya disease differ from those of atherosclerotic occlusion of the major cerebral arterial trunks, and may be a result of the abundant collateral circulation through basal `Moyamoya' vessels.

Acute ischemic vulnerability of PKA in the dendritic subfields of the hippocampus CA1

Alterations of [3H]cyclic AMP (cAMP) binding, an indicator of the binding activity of particulate cyclic AMP-dependent protein kinase (PKA), were examined after 15 and 30 min of ischemia in the gerbil brain. Severe hemispheric cerebral ischemia was induced by occluding the right common carotid artery. Significant reductions in cAMP binding were noted only in the dendritic subfields of the hippocampus CA1 such as the strata oriens, radiatum and lacunosum-moleculare, on the ischemic side after 15 min of ischemia. After 30 min ischemia cAMP binding was significantly decreased not only in each dendritic subfield of the hippocampus CA1, but also in the layer of pyramidal cell bodies (stratum pyramidale) on the occluded side; other brain regions such as the hippocampus CA3, dentate gyrus and cerebral cortices revealed no significant changes in cAMP binding. These findings suggest that derangement of PKA may begin in the dendritic subfields of the hippocampus CA1 after as little as 15 min of severe ischemia, and proceed centrally to the neuronal cell bodies of the hippocampus CA1.

Middle cerebral artery occlusion alters neurotransmitter activities in ipsilateral and contralateral rat brain regions: an ex vivo voltammetric study

Differential pulse voltammetry with treated carbon fibre micro-electrodes has been successfully employed in in vivo analysis of neurotransmitter release and metabolism. This methodology has been now applied to ex vivo preparations (brain slices) in order to study diverse neurotransmitter activities in various brain regions ipsilateral and controlateral to a middle cerebral artery (MCA) occlusion performed in anaesthetised adult male rats. Data demonstrated that significant changes of voltammetric ascorbic acid levels related to the ischaemic state were monitored within the ipsilateral to MCA occlusion frontal cortex, striatum, nucleus accumbens and hippocampus which were the brain area studied. Furthermore, it appeared that voltammetric catecholaminergic and 5-hydroxy indolaminergic values measured within the nucleus accumbens controlateral to MCA occlusion differ significantly from the results monitored with the same technique in brain slices obtained from sham rats. In various studies, the brain regions contralateral to MCA occlusion are generally considered as control areas, however, the present data suggest that the nucleus accumbens contralateral to the MCA occlusion side is specifically affected by the ischaemic state.

Rapid reduction in ryanodine binding of hippocampus CA1 in cerebral ischemia.

Ryanodine receptors located on the sarcoplasmic or endoplasmic reticulum, play an important role in the regulation of the intracellular Ca2+ level via the mechanism of Ca(2+)-induced Ca2+ release (CICR). Perturbation of intracellular Ca2+ regulation has been considered to be one of the most important mechanisms underlying acute ischemic neuronal damage. The ryanodine binding, an indicator of intracellular channels of CICR, and local cerebral blood flow (LCBF) were therefore examined at 15 min post-ischemia in the gerbil brain. The autoradiographic method developed in our laboratory enabled us to determine both parameters within the same brain. Severe hemispheric cerebral ischemia was induced by occluding the right common carotid artery. LCBF was measured at the end of the experiment using [14C]iodoantipyrine method. The ryanodine binding was evaluated autoradiographically in vitro using [3H] ryanodine. A group of gerbils who underwent a sham procedure served as controls. LCBF was found to be significantly decreased in most cerebral regions on the occluded side. In contrast, a significant reduction in ryanodine binding was noted only in the hippocampus CA1 on the occluded side. Taken together, these findings indicate that the CICR in the hippocampus CA1 may be especially susceptible to acute ischemic stress, and be closely associated with the pathophysiological mechanisms of the selective vulnerability of this region.

Patency of intermediate size side branches after Palmaz-Schatz stent implantation.

The immediate and long-term patency of intermediate size side branches was assessed by serial coronary angiography in 47 patients with 48 lesions to determine whether the presence of these side branches (1-2 mm in diameter) is unsuitable for Palmaz-Schatz stent implantation. Coronary angiography was performed at baseline, after conventional balloon angioplasty, immediately after stent implantation, at 1 week, and at 6-month follow-up. Sixty-eight lesion-associated side branches that were 1-2 mm in diameter, 11 with branch ostial stenosis (Group A) and 57 without ostial stenosis (Group B) were studied. After stent implantation, 9 (13%) branches became totally occluded and coronary flow deteriorated in 13 branches (19%). The incidence of side branch occlusion during the procedure in group A was greater than in group B (55% vs. 12%; p < 0.005). One (2%) patient suffered persistent chest pain, but no procedure was complicated by Q-wave myocardial infarction or significant elevation of creatine kinase concentration. Flow improved in 82% of the occluded side branches after 1 week and in 90% after 6 months. These results suggest that the presence of intermediate size side branches is not a contra-indication to Palmaz-Schatz stent implantation.

Relationship between the flow pattern and vasomotor reactivity in the ophthalmic artery, siphon and vessels within the circle of Willis in the unilateral internal carotid artery occlusion.

The aim was to study a relationship between the flow pattern in the ophthalmic artery (OA), the siphon and vessels within the circle of Willis. 27 patients, 22 males and 5 females, mean age 63 +/- 15 years (SD) with unilateral occlusion of the internal carotid artery (ICA) were examined by 3-dimensional Transcranial Doppler scanner. Flow signals from the OA, the siphon and intracranial vessels were registered before and after i.v. injection of 1 g acetazolamide. Pathological flow pattern was found in 18 patients in the OA on the occluded side consisting of 12 retrograde and 6 isoelectric flow directions. After acetazolamide injection retrograde systolic velocities (SV) increased significantly (p < 0.01), but anterograde velocities remained unchanged as did 3 isoelectric flow patterns, 2 turned to retrograde and one to anterograde flow direction. In the siphon lower resting anterograde mean velocities (MV) were found on both sides (p < 0.05) compared to normal subjects. Six patients had the same retrograde flow as in the OA. After acetazolamide MV in the siphon increased (p < 0.01) only on the nonoccluded side. Baseline retrograde ophthalmic SV and MV in the siphon correlated (p < 0.01 and p < 0.05 respectively) with MV in the middle cerebral artery (MCA) according to linear regression analysis (r = 0.78 and 0.59 respectively). All patients, having impaired vasomotor reactivity (VMR) < or = 11% in the anterior cerebral artery (ACA) on the occluded side, had pathological flow pattern in the OA. Patients with greatest difference (delta) between MV in the ACA on the nonoccluded and occluded side had a tendency to anterograde flow (r = 0.56, p < 0.05). Pulsative index (PI) in the ACA on the occluded side was lowest in the category with retrograde flow in the OA (0.67 +/- 0.14) and differed (p < 0.05) from normals and from the category with isoelectric and anterograde flow. Correlation of retrograde flow direction in the OA and baseline MV in the MCA and low PI in the ACA on the occluded side indicates a supplying ophthalmic collateral to the anterior brain circulation. Impaired VMR in the ACA on the occluded side in connection with pathological flow pattern in the OA may reflect an exhaustion of the ACA as a supplying vessel.

Focal cerebral ischaemia increases the levels of several classes of heat shock proteins and their corresponding mRNAs

The induction of focal cerebral ischaemia in rats by middle cerebral artery occlusion has previously been shown to increase, over time, the mRNA levels of the heat shock proteins (HSPs) 27 and 70. However, the levels of HSP90 mRNA remain constant. In contrast, during global ischaemia, HSP70 and HSP90 mRNA levels are both raised, particularly in the CA1 neurons in the hippocampus, an area that is resistant to the insult in comparison to the surrounding regions. HSP27 mRNA is raised in the neuroglia in the subregions of the hippocampus. However, the protein levels of HSP27, 70 and 90 have not been characterised in focal ischaemia. With this data in mind, we have carried out a comparative study of HSP27, 56, 60, 70 and 90 mRNA and protein levels during focal cerebral ischaemia in rats, up to 24 h post-occlusion. We have shown that HSP70 and HSP27 mRNA levels are increased and also that HSP60 mRNA levels (which had also not previously been characterised in this model of focal ischaemia) are significantly raised. HSP90 and HSP56 mRNAs were not significantly elevated. On Western blot analysis, the inducible HSP72 protein was first detected at 8 h post-occlusion, HSP27 protein was detected only at 24 h post-occlusion and HSP60 protein, although constitutive, appeared to increase at 24 h post-occlusion. HSP56 protein levels appeared to rise on the occluded side, but HSP90 protein levels remained constant.

Stenting of aortopulmonary collaterals in complex pulmonary atresia.

The optimal treatment of patients with complex pulmonary atresia remains controversial. Surgical unifocalization programs are increasing popular but have not previously or currently gained universal acceptance. Furthermore, not all patients are suitable for attempts at biventricular correction. These patients may become increasingly symptomatic and require palliation. We attempted to palliate 12 patients with progressive symptomatic hypoxemia. Each had at least one stenotic but balloon-dilatable collateral supplying at least three lung segments. It was impossible to traverse the stenotic area with the stent in 1 patient, despite two attempts. Twelve stents were thus deployed in 11 patients. There was no effect in 1 patient who had multiple stenoses distal to the stented area. There was excellent palliation in the remainder, arterial oxygen saturation 45% to 79% before stenting (mean, 64 +/- 12%) rising to 67% to 90% (mean, 78 +/- 10%, P < .01) at discharge from hospital. One patient was referred for surgery to secure blood flow to a nearly totally occluded side branch to the right upper lobe traversed by the stent. There was an excellent symptomatic response in the remainder, with an early increase in exercise duration (P < .01). Late arterial desaturation occurred in 2 patients. In 1, there was pulmonary arterial hypertension in the lung segments supplied by the stented vessel. A stenosis had developed within the stent in the other patient, who was noncompliant with anticoagulation therapy. Stenting of stenotic aortopulmonary collaterals can achieve excellent palliation in the majority of this highly selected subgroup of patients with complex pulmonary atresia.

Risk factors for stroke in patients undergoing coronary artery bypass grafting

Objective: To determine predictors of stroke in patients undergoing first-time coronary bypass grafting, we prospectively collected data on 1631 consecutive patients. Methods: Patients with a history of stroke and/or central nervous system symptoms ( n = 134) and/or carotid bruits ( n = 95) underwent carotid Doppler evaluation. Stenosis greater than 70% was considered significant. Patients with symptomatic disease or asymptomatic bilateral disease were referred for combined coronary bypass and carotid endarterectomy ( n = 21). Patients with neurologic symptoms after the operation were assessed by a neurologist and underwent a computed tomographic scan. Events were classified as reversible transient ischemic attack, reversible ischemic neurologic deficit, or irreversible stroke. Results: There were 19 strokes (1.2%) and 20 deaths (1.2%) in this series. In patients with carotid screening, risk of stroke increased with severity of carotid disease and ranged from 0% in patients without stenosis, to 3.2% (1/31) in those with greater than 70% stenosis, and to 27.3% (6/22) in those with carotid occlusion. By stepwise logistic regression analysis six variables were identified as risk factors for stroke. The most important predictor was carotid occlusion with or without contralateral stenosis (odds ratio = 28, 95% confidence interval (8,105). In this group, four of five strokes occurred on the occluded side. Other risk factors were presence of ascending aortic disease at the time of surgery (odds ratio = 12.8, confidence interval 3,48), perioperative myocardial infarction (odds ratio = 8.2, confidence interval 2,33), poor left ventricular function (odds ratio = 4.6, confidence interval 1,19), peripheral vascular disease (odds ratio = 3.2, confidence interval 1,9), and age >60 years (odds ratio = 2.9, confidence interval 0.8,11). Conclusion: We conclude that risk factors for perioperative stroke in patients undergoing coronary artery bypass grafting are multiple. Carotid scanning in patients with neurologic symptoms or carotid bruits can identify patients at increased risk. Patients with carotid occlusion are at high risk for stroke on the occluded side. (J T HORAC C ARDIOVASC S URG 1996;112:1250-9)

Alteration of ryanodine receptor in the hippocampus CA1 after hemispheric cerebral ischemia.

Alterations in ryanodine binding and local cerebral blood flow (LCBF) were examined at 30 minutes and 2 hours post-ischemia in the gerbil brain in order to evaluate the influence of cerebral ischemia on the intracellular channels of Ca2+-induced Ca2+ release (CICR). Severe hemispheric cerebral ischemia was induced by occluding the right common carotid artery. LCBF was measured at the end of the experiment using [14C]iodoantipyrine method, and the ryanodine binding was evaluated in vitro using [3H]ryanodine as a specific ligand for CICR channels. An autoradiographic method developed in our laboratory enabled us to determine both parameters within the same brain. A group of gerbils who underwent a sham procedure served as controls. LCBF was found to be significantly reduced in most of the cerebral regions on the occluded side at both 30 minutes as well as 2 hours post-ischemia. In contrast, a significant reduction in ryanodine binding was noted only in the hippocampus CA1 on the occluded side at 30 minutes and 2 hours after the occlusion. These findings suggest that regionally specific changes of CICR may be the cause of decreased ryanodine binding in the hippocampus CA1, and that these changes may be related to the pathophysiological mechanisms that cause this region to be particularly vulnerable to ischemia.