Transcranial cerebral oximetry and carotid cavernous fistula occlusion

Summary Different methods have been used in the evaluation and monitoring of the cerebral oxygen supply during neuro-interventional therapies. Attenuation of near-infrared light by the chromophores oxyhemoglobin and deoxyhemoglobin have shown to be useful in the study of the cellular oxygen metabolism and oxygen delivery to the brain. Transcranial cerebral oximetry (TCCO) has the advantage of providing real-time information regarding regional brain oxygen saturation (rSO₂) by using wavelengths in the near-infrared range.We present a patient with a carotid cavernous fistula who underwent balloon occulusion and concurrent continuous TCCO monitoring. TCCO was found to be a useful tool providing immediate rSO₂ values during the angiographic and interventional procedures. Initial balloon occlusion of a carotid cavernous fistula resulted in partial occlusion of the internal carotid artery lumen causing an immediate decrease in rSO₂ which correlated with angiographic findings. Subsequent reocclusion of the fistula produced a slower and smaller degree of decrease in rSO₂ with clinical improvement in the patient. Changes in rSO₂ were detected before any adverse clinical event was observed. TCCO was reliable, safe, sensitive, and provided a real-time assessment tool for the monitoring of brain oxygen supply in a patient undergoing a neuroendovascular procedure.     

选择性髂内动脉结扎与栓塞对盆腔血供的影响

目的：旨在探讨选择性髂内动脉结扎与栓塞两种方法对盆腔血供的影响。方法：将两组犬在膀胱上动脉分支以下之髂内动脉分别行结扎与栓塞，对比观察两组膀胱创面出血、盆腔动脉造影及盆腔脏器组织学变化，以确定其盆腔脏器的血供情况。结果：①结扎组膀胱创面出血明显大于栓塞组；②结扎组髂内动脉侧支循环建立时间明显早于且数目多于栓塞组；③两组盆腔脏器均未见缺血坏死。结论：栓塞组阻断髂内动脉侧支循环的数目多于结扎组，故对盆腔血供的影响大于结扎组。避免髂内动脉阻断范围过广可减少盆腔脏器缺血坏死的机会。     

Urgent coronary artery bypass surgery in the presence of Dressler's syndrome

The clinical features of Dressler's syndrome which developed in a patient following a third myocardial infarction responded to a short course of prednisolone. However, angina at rest precipitated urgent coronary artery bypass surgery and pericardectomy.     

缺血性脑血管病与颈动脉粥样硬化及其危险因素的关系

目的探讨缺血性脑血管病(ICVD)与颈动脉粥样硬化及其危险因素的关系。方法对186例ICVD患者与194例非脑血管病患者和正常体检者(对照组)行颈部血管超声检查和血液生化检查;比较两组间的颈动脉硬化程度及脑卒中危险因素的差异。结果ICVD组年龄[(69±7)岁]和患有高血压(66.1%)、糖尿病(53.4%)、代谢综合征患者(44.6%)的比率非常明显高于对照组[(61±5)岁、48.8%、15.2%、12.9%](均P<0.001)。ICVD组颈动脉粥样硬化分级计分≥2分(斑块发生率)、≥3分(血管狭窄发生率)分别为69.3%、20.4%,明显高于对照组的33.5%和5.1%(均P<0.05)。结论颈动脉粥样硬化是ICVD的危险因素之一;各种危险因素的聚集对ICVD的发生起重要作用。     

Percutaneous transcatheter occlusion of coronary artery fistulas using detachable balloons

Three pediatric patients underwent successful transcatheter coronary artery fistula occlusion using the Debrun system. This latex balloon system offers several advantages over other occlusion systems. First, the balloon delivery and release is controlled. Second, “test occlusions” can be performed that allow simultaneous balloon inflation, coronary cineangiography, and electrocardiographic monitoring. Third, because the balloons are flow-directed, they are easily positioned in properly chosen locations. Finally, the balloons can be constructed to suit the size of the fistula. In this study, two patients received only one balloon; in the other patient two balloons were placed in the same fistula. All fistulas drained into either the right atrium or ventricle and were successfully occluded. After a follow-up period of up to 3 years, no local or systemic reactions to the balloons were recognized. We conclude that detachable balloon occlusion of coronary artery fistulas is a safe, effective alternative to surgical ligation in selected pediatric patients.     

Editorial

Aim: Wall stress‐independent signalling pathways were studied for endothelin‐1 (ET‐1)‐induced c‐fos expression in rat intact mesenteric small arteries. Methods: Arteries were kept unmounted in Krebs buffer, equilibrated for 1 h and stimulated with vasoactive substances for 15–60 min. The c‐fos mRNA expression was determined by real‐time polymerase chain reaction. Results: Stimulation with fetal bovine serum (FBS), phorbol 12‐myristate 13‐acetate (PMA) and ET‐1 caused about a doubling of c‐fos mRNA. The ET‐1‐induced c‐fos expression was steady (15–60 min) and was inhibited by the inhibitor of the ET_A receptor, BQ‐123. Platelet‐derived growth factor‐B, angiotensin II and U46619 did not cause increased c‐fos mRNA levels. The broad specificity inhibitor staurosporine inhibited the response to ET‐1, but inhibitors of Rho‐A kinase and phosphatidylinositol 3‐kinase had no effect. However, inhibitors to tyrosine kinases, the MAP kinases [extracellular signal‐regulated kinase 1/2 (ERK1/2), c‐Jun amino‐terminal kinase, p38], and to conventional protein kinase C showed no inhibition. Consistent with these findings, ET‐1 did not cause activation of ERK1/2, a finding also seen in vessels held under pressure. In contrast, ET‐1‐induced c‐fos expression was inhibited by the calcium chelator BAPTA, suggesting a role for intracellular calcium. This possibility was supported by the finding that raising the extracellular K⁺ concentration caused increased expression of c‐fos in a concentration‐dependent manner. Conclusion: The results suggest that in the absence of wall stress, ET‐1 is able to induce increased expression of c‐fos independent of traditional growth pathways, such as MAP kinase. The mechanism appears to be calcium‐dependent.     

经导管动脉内溶栓治疗急性动脉血栓栓塞

5例急性动脉血栓栓塞患者行经导管动脉内溶栓治疗 ,其中 4例一次溶栓成功 ,1例经两次溶栓成功 ,无一例出现并发症。对于急性动脉血栓形成的治疗过去常用静脉滴注溶栓剂的方法 ,小剂量效果不明显 ,加大剂量又易发生出血并发症。而采用经动脉插管至局部血栓部位灌注溶栓药物 ,并发症少 ,效果明确     

Influence of melatonin on bovine pulmonary vascular and bronchial airway smooth muscle tone

The influence of melatonin on tension of isolated bovine pulmonary vascular and bronchial smooth muscle rings were examined in these experiments. Melatonin caused a dose-dependent relaxation of precontracted (30 mM KCl) pulmonary artery and vein, although the effect is greater in arterial smooth muscle. This relaxant response was blocked by preincubating vessels with antagonists of vasoactive intestinal peptide or Substance P. In bronchial smooth muscle, melatonin caused a small contractile response. These experiments demonstrate that in response to melatonin the pulmonary vasculature relaxes, while in airway smooth muscle the reverse, constriction, occurs. It is hypothesized that nocturnal exaggeration of asthma may, in part, be due to changes in circulating levels of melatonin.     

Altered neuropeptide Y Y1 responses in mesenteric arteries in rats with congestive heart failure

The aim of the present study was to elucidate if the potentiating effect of neuropeptide Y on various vasoactive agents in vitro is (1) altered in mesenteric arteries from rats with congestive heart failure and (2) mediated by the neuropeptide Y Y₁ receptor. The direct vascular effects of neuropeptide Y and its modulating effects on the contractions induced by endothelin-1-, noradrenaline-, 5-hydroxytryptamine (5-HT)-, U46619-(9, 11-dideoxy-11, 9-epoxymethano-prostaglandin F₂) and ATP, and acetylcholine-induced dilatations were studied in the presence and absence of the neuropeptide Y Y₁ antagonist, BIBP3226 (BIBP3226{(R)-N2-(diphenylacetyl)-N-[(4-hydroxyphenyl)methyl]- -arginine-amide}). Neuropeptide Y, per se, had no vasoactive effect in the arteries. The potency of endothelin-1 was significantly decreased in congestive heart failure rats. Neuropeptide Y and neuropeptide Y-(13–36) potentiated the endothelin-1-induced contraction in congestive heart failure mesenteric arteries. In 20% of the congestive heart failure rats, sarafotoxin 6c induced a contraction of 31±4%. Neuropeptide Y also potentiated U46619- and noradrenaline-induced contractions but not 5-HT-induced contractions in congestive heart failure arteries. In sham-operated animals neuropeptide Y potentiated noradrenaline- and 5-HT-induced contractions. These potentiations were inhibited by BIBP3226. Acetylcholine induced an equipotent relaxation in both groups which was unaffected by neuropeptide Y. In conclusion, neuropeptide Y responses are altered in congestive heart failure rats. The potentiating effect differs between vasoactive substances. Neuropeptide Y Y₁ and non-neuropeptide Y₁ receptors are involved.