冠状动脉内注入麦角新碱建立猪冠状动脉痉挛模型

目的探讨冠状动脉内注入麦角新碱构建猪冠状动脉痉挛模型及可能引起的心律失常事件。方法18只猪随机分成实验组（n=10）和对照组（n=8），麻醉后经右侧股动脉置入冠状动脉球囊导管至左前降支开1：3，实验组冠状动脉内注入麦角新碱0．3mg／kg，对照组注入等量的生理盐水。结果实验组均出现心电图胸导联ST段明显抬高，其中4例伴有严重室性心律失常，包括频发室性早搏2例、室性早搏合并非持续性室性心动过速1例、持续性室性心动过速合并心室扑动及颤动1例。冠状动脉造影提示血管痉挛致左前降支中远段血管明显狭窄8例、血管闭塞2例；对照组未见明显变化。结论冠状动脉内注入麦角新碱法可简单方便的建立猪冠状动脉痉挛模型。     

A case of acute myocardial infarction after blunt chest trauma in a young man

Coronary artery injury rarely occurs after blunt chest trauma, but it can lead to extensive myocardial infarction and be frequently overlooked. A 16-yr-old man was presented with comatose mental state and rapid respiration rate. He ran into guard rail while riding a motorcycle. In routine examination, his electrocardiogram showed Q wave and 2 mm ST segment elevation in all precordial leads, I and aVL. The cardiac enzymes were also elevated: creatine kinase (CK)-MB was 300 U/L, and cardiac specific troponin I was 5.7 ng/mL. Two-dimensional echocardiography showed anteroseptal akinesia with severely depressed left ventricular function, ejection fraction of 28%. He could not receive any anticoagulation or thrombolytic therapy because of his brain lesion. Three weeks later, his mental state improved. A diagnostic coronary angiogram revealed total occlusion in the proximal left anterior descending artery (LAD) with collaterals from the right coronary artery and left circumflex artery. We successfully performed a percutaneous coronary intervention for the LAD lesion, and the final angiogram showed a good coronary flow without residual stenosis.     

False lumen stent placement during iatrogenic coronary dissection

A 38-year-old woman without significant cardiovascular risk factors was admitted in the coronary care unit with the diagnosis of acute coronary syndrome without ST-segment elevation. In coronary angiography, left coronary artery system was normal in the first contrast injection, but acute occlusion of the left main coronary trunk (LCT) due to iatrogenic dissection was observed in the following. The patient presented marked ST elevation, severe hypotension, hemodynamic collapse, and loss of consciousness. Cardiopulmonary resuscitation (CPR) was initiated, and two drug-eluting stents were consecutively placed in the LCT and the left anterior descending coronary (LAD), but the patient died after 60 min of continuous CPR. The autopsy showed dissection of the LCT and LAD coronaries with both stents placed in the false lumen and hyperacute myocardial infarction in the anterior left ventricular free wall. This case underlines the importance of careful indication of invasive procedures and of taking in consideration their potential risks.     

Evidence for a link between mechanical and electrical alternans in acutely ischaemic myocardium of anaesthetized dogs

In order to examine the relation between mechanical alternans and associated electrical alternans during acute myocardial ischaemia, we determined the effect of a ventricular premature beat and calcium antagonists on mechanical and electrical alternans during acute coronary occlusion in anaesthetized dogs. Isometric contractions and unipolar electrocardiograms were recorded from ischaemic myocardium. During coronary occlusion, mechanical alternans was accompanied by electrical alternans, which was an alternate change in the ST segment elevation, i.e. the higher ST and the lower ST. Electrical alternans was frequently discordant and in some cases accompanied by discordant mechanical alternans. Both discordant electrical and mechanical alternans became concordant and were potentiated after the ventricular premature beat. In all cases, concordant mechanical alternans was accompanied by concordant electrical alternans and vice versa. In this situation, the higher and the lower ST corresponded to the larger and the smaller contractions respectively. Thus, a fixed correspondence was observed between mechanical and electrical alternans. A fixed correspondence was also observed between mechanical alternans and the variation in the time taken for repolarization of the monophasic action potential. Verapamil and diltiazem inhibited both electrical and mechanical alternans. The present results support the idea that a common mechanism, such as a beat-to-beat cycle of the transmembrane and intracellular movement of calcium ions, may play a role in the mechanisms of electrical and mechanical alternans.     

Evidence for a link between mechanical and electrical alternans in acutely ischaemic myocardium of anaesthetized dogs.

In order to examine the relation between mechanical alternans and associated electrical alternans during acute myocardial ischaemia, we determined the effect of a ventricular premature beat and calcium antagonists on mechanical and electrical alternans during acute coronary occlusion in anaesthetized dogs. Isometric contractions and unipolar electrocardiograms were recorded from ischaemic myocardium. During coronary occlusion, mechanical alternans was accompanied by electrical alternans, which was an alternate change in the ST segment elevation, i.e. the higher ST and the lower ST. Electrical alternans was frequently discordant and in some cases accompanied by discordant mechanical alternans. Both discordant electrical and mechanical alternans became concordant and were potentiated after the ventricular premature beat. In all cases, concordant mechanical alternans was accompanied by concordant electrical alternans and vice versa. In this situation, the higher and the lower ST corresponded to the larger and the smaller contractions respectively. Thus, a fixed correspondence was observed between mechanical and electrical alternans. A fixed correspondence was also observed between mechanical alternans and the variation in the time taken for repolarization of the monophasic action potential. Verapamil and diltiazem inhibited both electrical and mechanical alternans. The present results support the idea that a common mechanism, such as a beat-to-beat cycle of the transmembrane and intracellular movement of calcium ions, may play a role in the mechanisms of electrical and mechanical alternans.     

Myocardial infarction in dogs with acute and gradual occlusion of the circumflex or right coronary arteries

This study was designed to quantitate and describe the incidence and magnitude of myocardial infarction in the canine heart following acute and gradual occlusion of the circumflex or right coronary arteries. In animals with acute occlusion, the circumflex artery was ligated just distal to the bifurcation of the left coronary artery for 4 hr (seven dogs). Gradual occlusion was produced by placing an Ameroid occluder on the circumflex artery for 1 month (nine dogs), 3 months (nine dogs), and 5 months (eight dogs) and on the right coronary artery for 3 months (nine dogs). Ten dogs served as controls. At the end of the experiments the dogs were sacrificed, and identification of myocardial infarction was made with an enzyme-mapping technique in dogs with acute occlusion and with histological methods in dogs with gradual occlusion. The volume of ventricular infarction was determined with the use of an Apple II Computer and graphics tablet. After 3 months, gradual occlusion of the right coronary artery produced a 22% incidence of infarction which was significantly less (P <.01, X²) than the 67% incidence observed with 3 months of gradual circumflex occlusion. The average infarct volume produced by gradual right coronary occlusion was 0.94 + 0.69%. The average volume of left ventricular infarction in animals with circumflex acute occlusion was 15.6% + 6.6 and the incidence of infarction was 100%. With gradual occlusion of the circumflex artery for 1, 3, and 5 months, average left ventricular infarction was 2.02 ± 1.01%, 3.13 ± 1.53%, and 2.96 ± 1.35%, respectively. There were no significant differences in the amount of damage observed among the three groups with gradual occlusion, and the average incidence of infarction for these three groups was 76%. In the 1-, 3- or 5- month animals with circumflex occlusion, no additional areas of necrosis subsequent to the original damage were found, indicating that infarction is a single event in this model of gradual occlusion. These results suggest that infarct size is determined primarily by factors at the time of total occlusion and that gradual occlusion allows sufficient time for collateral growth, thereby limiting the extent of myocardial injury.     

Decreased regional contractility in nonischemic myocardium during acute coronary artery occlusion in conscious pigs

The purpose of this study was to use the relationship between end-systolic left ventricular pressure and segment length to assess the inotropic state of nonischemic myocardium during acute coronary artery occlusion in the conscious pig. Eight pigs were chronically instrumented with sonomicrometers to measure midwall segmental shortening and a micromanometer to measure left ventricular pressure. Occlusion of the inferior vena cava with a pneumatic occlusive cuff caused transient decreases in left ventricular pressure so that the relationship of left ventricular pressure and segment length at end systole could be determined over a range of pressures. In preliminary studies using open-chest pigs, this relation was shown to be highly linear and best quantified using a calculated segment length at a left ventricular pressure of 100 mm Hg (ESL100). During acute, 1-min occlusion of the left anterior descending coronary artery, the ESL100 of the nonischemic lateral and posterior walls was significantly increased from 8.75 +/- .18 mm to 9.64 +/- .21 mm (mean +/- SD, p less than .01), indicating a decreased inotropic state. Similarly, during occlusion of the left circumflex coronary artery, the ESL100 of the nonischemic anterior wall increased from 8.44 +/- 2.53 mm to 9.26 +/- 3.12 mm (p less than .05). This was not associated with a change in the amount of shortening during systole. Pharmacological autonomic blockade using atropine and propranolol failed to alter the response of nonischemic zones to acute coronary artery occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of ischemia, hypertrophy, hypoxia, acidosis, and alkalosis on canine defibrillation

Our purpose was to assess the effect of myocardial ischemia, left ventricular hypertrophy, and systemic hypoxia and acid-base abnormalities on the energy requirements for defibrillation. We determined the defibrillation threshold (DFT), the minimum energy required to defibrillate. DFT was not significantly elevated after left anterior descending coronary occlusion, nor was there a relationship between the size of the occluded coronary distribution area (coronary risk area) and the change in DFT in individual animals. Renal hypertension and left ventricular hypertrophy were induced by unilateral nephrectomy and contralateral renal artery stenosis. DFT in left ventricular hypertrophy dogs was not significantly higher than in dogs without hypertrophy. Finally, we induced systemic hypoxia and acid-base abnormalities. Neither respiratory nor metabolic acid-base disturbances affected DFT, but during systemic hypoxia (O2 tension 45 +/- 2) DFT fell from 83 +/- 49 to 58 +/- 28 J (P less than 0.01). Thus in dogs, myocardial ischemia, left ventricular hypertrophy, and acid-base abnormalities do not elevate defibrillation energy requirements, whereas hypoxia reduces the energy needed to defibrillate.     

Mortality after high ligation of the anterior descending branch of the left coronary artery in dogs; effects of various pharmacological agents

Summary Over a period of seven years the anterior descending branch of the left coronary artery was acutely ligated in a total of 93 dogs. Two control series, 1963/1964 and 1969/1970, on 11 and 13 dogs respectively, produced essentially identical survival rates of 9.1% and 7.7% despite variations in the experimental team. Two experimental series performed at the same time with Intensain pretreatment show essentially the same survival rate (62.2%,p<0,05 and 66.7%,p<0.01, respectively.After pretreatment with Persantin the survival rate of 84.7% is likewise significantly higher than in the control animals (p<0.001). After prolonged administration of Carduben, 42.9% of the experimental animals survived coronary occlusion (p<0.05).If young animals of the age of 9 to 12 months are used in the control series, the survival rate of 58.3% is clearly higher than with adult ones (p<0.01). If young animals receive prophylactically Pteridinol (RE 102), the survival rate is increased after acute occlusion of the anterior descending artery to 91.1% (p<0.05). The higher survival rate in young animals may be explained by an improved collateral circulation of the myocardium.The good reproducibility of survical rates following acute coronary occlusion over several years with both controls and treated dogs proves the significance of comparative studies between treated and untreated animals. The experimental conditions, age and living conditions, however, must be comparable.     

清醒心肌缺血模型的可控冠状动脉狭窄程度

BACKGROUND:Anesthesia is a protective measure to animals in animal experiments, but the use of the corresponding anesthetic drugs will have different effects on the experimental results. OBJECTIVE:To analyze the differences of various indexes and the therapeutic effect of myocardial ischemia canine model of coronary stenosis under the condition of consciousness and anesthesia. METHODS:Twenty Beagle canine myocardial ischemia models were equally assigned to five groups, and prepared according to the complete orthogonal Latin square arrangement for the experiment. Intervention procedures included the normal observation (normal control for 10 minutes, observation for 30 minues), conscious model (after normal control, coronary artery stenosis for 10 minutes, and observation for 30 minutes), conscious treatment (after normal control, coronary artery stenosis for 10 minutes, 50 μg/kg nitroglycerin sublingually buccal, and observation for 30 minutes), anesthesia model (animals received anesthesia; after normal control, coronary artery stenosis for 10 minutes, and observation for 30 minutes), anesthesia treatment (animals received anesthesia; after normal control, coronary artery stenosis for 10 minutes, 50 μg/kg nitroglycerin sublingually buccal, and observation for 30 minutes). We recorded canine electrocardiogram, blood pressure, heart rate and body temperature level when animals were conscious after coronary artery stenosis, and mean arterial blood pressure, body temperature, heart rate, electrocardiogram ST segment changes in conscious and anesthetic states in myocardial ischemia dogs, and observed the therapeutic effect of nitroglycerin on conscious and anesthetic states in myocardial ischemia dogs. RESULTS AND CONCLUSION:The electrocardiogram, blood pressure, heart rate and body temperature were changed after the coronary artery stenosis in conscious dogs, and the ST segment of electrocardiogram was significantly increased. The blood pressure and heart rate were significantly higher than that in the conscious state (P < 0.05), and the ST segment of electrocardiogram in dogs was significantly increased in conscious and anesthetic states. After the treatment of nitroglycerin, the effect was obvious in the myocardial ischemia model in conscious state. The results showed that the model of myocardial ischemia and the clinical fitting degree were higher, which could reduce the effect of anesthesia on the experimental results.     

Multivessel coronary thrombosis resulting from heparin induced thrombocytopenia

Thrombosis associated with a drop in the platelet count may occur in 33-50% of the patients who develop heparin-induced thrombocytopenia (HIT) during treatment with unfractionated heparin. We report the case of a 63-year-old man who was treated with unfractionated heparin following a non-ST segment elevation myocardial infarction (NSTEMI). He developed an acute ST segment elevation infarction (STEMI) on day 3 with an associated severe thrombocytopenia. He was successfully treated with percutaneous intervention and aspiration of coronary thrombus from the right coronary artery and the left circulflex artery, followed by an infusion a direct thrombin inhibitor lepirudin/bivalirudin. He made an excellent recovery.     

The effect of chronic hypoxemia on regional myocardial blood flow in the conscious dog after acute coronary artery occlusion

Chronic hypoxemia was produced in 16 dogs by surgical transposition of the caudal vena cava to the left atrium to determine if chronic hypoxemia would alter the response of the myocardium to acute ischemia. An electromagnetic aortic flow probe, left atrial tube, and occlusive cuff on the left circumflex coronary artery were permanently implanted in 11 hypoxemic and 26 normal control dogs. The animals were studied in the conscious state after recovery from the surgery. Dogs with hypoxemia had a blood hematocrit value of 54.3 ± 1.0% (SE), arterial PO₂ of 43.2 ± 1.4 mm Hg, and 80.2 ± 1.6% oxygen saturation. There was no difference from control animals in the ratio of left ventricular weight to body weight, but the right ventricular weight was significantly decreased in the hypoxemic dogs. Cardiac output from the left ventricle was twice that of the right ventricle. Aortic blood flow was 3.68 ± 0.22 liters/min in hypoxemic animals and 2.64 ± 0.19 liters/min in normal dogs. Myocardial blood flow measured with 15-μ diameter tracer microspheres was increased from 79 ± 10 and 59 ± 8 ml/100 g/min in left ventricular endocardial and epicardial halves, respectively, in normal dogs to 212 ± 48 and 172 ± 39 in dogs with chronic hypoxemia. There were no deaths in 10 hypoxemic dogs within 24 hours after complete circumflex coronary artery occlusion; 7 of 26 (27%) normal dogs died after circumflex coronary artery occlusion during the conscious state. Gross infarct size was extremely variable in both groups. Median infarct size was smaller in dogs with hypoxemia and was directly correlated with arterial PO₂ in hypoxemic dogs. There was a mild, but statistically not significant, increase in the anastomotic index of hypoxemic dogs compared with that of normal animals, suggesting that a metabolic adaptive change rather than increased collateral circulation may have been responsible for the decreased mortality and smaller infarct size in hypoxemic dogs.     

肌酸激酶MBmass对急性心肌损伤早期诊断的实验研究

目的：连续测定犬急性心肌损伤动物模型血清中肌酸激酶MBmass（CK-MBmass）、CK-MB活性、CK活性等心肌酶学标志物,观察CK-MBmass对急性心肌损伤早期诊断的价值。方法：采用球囊堵闭左冠状动脉前降支中远端的方法建立犬急性心肌损伤动物模型。在诸闭前、堵闭后每10min直至90min连续采静脉血各2ml,3000r／min离心10min取血清测定或置-40℃保存待测。采用微粒子酶联免疫分析法测定CK-MBmass。免疫抑制法测定CK-MB活性,速率法测定CK活性。观察急性心肌损伤后CK-MBmass、CK-MB活性、CK活性等心肌酶学标志物的动态变化及损伤心肌的组织学改变。结果：冠状动脉堵闭90min后,心电图可见明显心肌损伤性ST段上抬改变;血清CK-MBmass、CK-MB活性、CK活性等指标皆超出个体值的2倍以上,但未超出实验参考值的2倍;出现异常值时间CK-MBmass、CK-MB活性、CK活性分别为（30-45）min、（30-60）min、（45-90）min。结论：CK-MBmass可早期诊断急性心肌损伤。     

Effect of tachycardia on left ventricular blood flow distribution during coronary occlusion.

The effect of heart rate on the amount and distribution of collateral blood flow was determine in open-chested dogs 1 h after coronary artery ligation. Flows to ischemic and nonischemic regions of left ventricle were measured with 7- to 10- mum diam radioactive microspheres during base-line conditions (118 +/- 6 beats/min) and again during atrial pacing at rates 20 and 40% above control (141 +/- 7 and 165 +/- 9 beats/min). During pacing aortic and left atrial pressures and cardiac output did not change significantly, whereas ST segment elevation in epicardial electrograms increased markedly. In nonischemic myocardium, mean flow increased approximately in proportion to the increase in rate, but subepicardial (EPI) flow increased somewhat more than subendocardial (ENDO) flow. In ischemic myocardium, overall flow did not change significantly, but a redistribution from ENDO to EPO was seen. At the faster rate ENDO flow fell 25% (P less than 0.02), EPI flow increased slightly, and ENDO/EPI fell in 8/9 animals (mean 0.54-0.43, P less than 0.01). The ENDO/EPI maldistribution present in ischemic muscle is thus accentuated by tachycardia; this may account for part of the harmful effect of tachycardia in acute myocardial infarction and may help explain the disproportionate ENDO ischemia seen in angina pectoris.     

青年男性ST段抬高急性心肌梗塞的特点及院内转归

目的探讨青年男性ST段抬高急性心肌梗塞（AMI）患者的危险因素、冠脉造影特点、临床特点及院内转归。方法对年龄≤44岁的青年男性AMI患者（61例，青年组）与同期同病同性别年龄≥65岁、〈75岁（老年组）的AMI患者（61例）就其危险因素、冠脉造影、临床特点及院内转归进行对比分析。结果冠心病危险因素青年组高血压、糖尿病明显少于中年组；吸烟青年组高于老年组，低密度脂蛋白胆固醇、阳性家族史两组无明显差别；冠脉造影青年组单支病变多，累及回旋支（LCX）多，右冠状动脉（RCA）少；老年组双支及双支以上病变多，多累及LCX，RCA。与老年组相比，青年组住院天数、心肌酶、机械并发症及死亡构成差别无统计学意义。结论年轻心梗患者大量吸烟者多，单支病变多，有糖尿病、高血压病史者少，但年轻心梗患者院内转归与老年组相似。     

Variant of the left coronary artery with an unusual origin and course: Anatomic and postmortem angiographic findings

This study demonstrates anatomic and postmortem angiographic findings characterizing the origin of the left coronary (LC) artery arising in common trunk with the right coronary (RC) artery from the right aortic sinus and its course via the ventricular septum (VS) to the left heart. This anomaly was a single finding observed among 388 angiographies and 60 corrosion castings. The course of the LC was divided in four segments. The first three form a curve that is upward concave. Large branches to the septomarginal trabecula (ST), VS, diagonals (DS), and the small anterior interventricular (anterior descending) artery originated from the outer part of this curve. In the anteroposterior x-ray, the above curve resembles a deep-bottom pot with a handle corresponding to the fourth segment. In the right anterior oblique, the first and second segments form a large erect angle. The third segment occupies the lower part of the absent proximal anterior interventricular artery, and the fourth crosses the outflow tract and the first segment in the middle. The course of these four segments of LC resembles the shape of the number 6. These findings are important for interpreting coronary angiographies in patients with this anomaly. Clin. Anat. 11:367–371, 1998. © 1998 Wiley-Liss, Inc.     

Combined effects of reduced connexin 43, depressed active generator properties and energetic stress on conduction disturbances in canine failing myocardium

To show that reductions in connexin43 (Cx43) can contribute, in association with electrophysiological alterations identified from unipolar recordings, to conduction disturbances in a realistic model of heart failure, canines were subjected to chronic rapid pacing (240/min for 4 weeks) and progressive occlusion of the left coronary circumflex artery (LCx) by an ameroid constrictor. Alterations identified from 191 epicardial recordings included abrupt activation delay, functional block, ST segment potential elevation, and reduced maximum negative slope (−dV/dt _max). The LCx territory was divided into apical areas with depressed conduction velocity (LCx1: 0.06 ± 0.04 m/s, mean ± SD) and basal areas with relatively preserved conduction (LCx2: 0.28 ± 0.01 m/s). Subepicardial Cx43 immunoblot measurements (percent of corresponding healthy heart measurements) were reduced in LCx1 (∼40%) and LCx2 (∼60%). In addition, −dV/dt _max was significantly depressed (−3.8 ± 3.3 mV/ms) and ST segment potential elevated (23.3 ± 14.6 mV) in LCx1 compared to LCx2 (−9.5 ± 3.4 mV/ms and 0.3 ± 1.4 mV). Anisotropic conduction, Cx43 and ST segment potential measurements from the left anterior descending coronary artery territory, and interstitial collagen from all regions were similar to the healthy. Thus, moderate Cx43 reduction to “clinically relevant” levels can, in conjunction with regional energetic stress and depression of sarcolemmal active generator properties, provide a substrate for conduction disturbances.     

Functional Development of the Coronary Collateral Circulation During Coronary Artery Occlusion in the Conscious Dog

We studied changes in the coronary collateral circulation during coronary artery occlusion in 14 conscious dogs by: a) determining simultaneous changes in peripheral coronary pressure (PCP) and retrograde flow (RF) after abrupt coronary artery occlusion; b) correlating these functional indices with quantitative anatomic indices (AI) of coronary collateral development (Menick et al: Am Heart J 82:503-510, 1971); and c) observing changes in these indices after repeated reocclusions of a coronary artery. These dogs were subjected to left circumflex coronary artery (LCCA) occlusions for 2 hours to 8 days; pressure tubes were implanted in the aorta and LCCA, the latter tube placed distal to an occlusive cuff for PCP and RF measurements. Afterwards the animals were sacrificed, their hearts injected with a modified Schlesinger's gelatin mass, and AI determined. During 2 to 24 hour LCCA occlusions (11 dogs) mean PCP rose to levels 50 to 80% of prevailing aortic pressure. During repreated 2- to 24-hour occlusions (2 dogs) in the same dog, the rate at which PCP rose increased. Retrograde flow was unchanged during 2- to 24-hour occlusions. Anatomic indices of these dogs were in the same range as those observed in unoccluded controls. When LCCA occlusion was maintained for more than 4 days (3 dogs), mean PCP rose during the first 24 hours and then remained stable; RF did not change until 4 days into occlusion and then increased. Anatomic indices of dogs occluded for more than 4 days were significantly greater (P < 0.001) than those of the 2- to 24-hour occlusion groups. Our study shows that: a) the early PCP rise after occlusion is not associated with an increase in RF, b) RF is a better index of collateral function and c) RF correlated well with the anatomic development of the collateral bed.     

Inhibition of arterial baroreceptor reflex during coronary artery occlusion.

The sensitivity of baroreceptor reflex during myocardial ischemia induced by acute occlusion of left anterior descending coronary artery (LAD) was studied in anesthetized, artificially ventilated, and thoracotomized dogs. Occlusion of LAD attenuated the baroreflex mediated changes in heart rate (HR) in response to changes in arterial pressure (AP) in the animals with intact autonomic nervous system (ANS). The HR increased significantly with the time of occlusion of LAD in control (ANS) as well as in beta-blocked group, suggesting vagal inhibition. In atropinized and vagotomized animals, the HR remained unchanged following LAD occlusion. In control group, the sensitivity of baroreflex mediated tachycardia response to hypotension and bradycardia response to hypertension, after 4 h of LAD occlusion, was reduced. In beta-blocked animals, the tachycardia response after LAD occlusion was drastically reduced to almost zero. The peak sensitivity of baroreflex bradycardia response was reduced in atropinized and vagotomized animals while the peak sensitivity of baroreflex tachycardia response increased after vagotomy. In contrast, bradycardia response was increased after beta-blockade. These data indicate that acute LAD occlusion attenuates arterial baroreflex control of HR and reduction of baroreflex sensitivity is mediated by parasympathetic efferents.     

Effect of ridogrel,a combined thromboxane A2 synthase inhibitor/ prostaglandin endoperoxide receptor antagonist,on the lysis of platelet-rich coronary arterial thrombi with recombinant tissue-type plasminogen activator in a canine model

The effect of ridogrel, a combined thromboxane A₂ synthase inhibitor/prostaglandin endoperoxide receptor antagonist, on the lysis of platelet-rich thrombi with recombinant tissue-type plasminogen activator (rt-PA) was studied in everted (inside-out) femoral arterial grafts inserted in the left anterior descending coronary arteries of heparinised dogs. Thrombotic occlusion of the everted segment graft with a platelet-rich thrombus, persisting for at least 30 min, occurred spontaneously within 4.3±3.9 min (mean±SD). These dogs were then heparinised and randomised to 1 of 4 blinded treatment groups: double placebo infusion, bolus injections of 0.5 mg/kg rt-PA, repeated at 15 min intervals until recanalisation occurred or up to 4 doses, ridogrel infusion (5 mg/kg bolus followed by continuous infusion of 5 mg/kg over 150 min), or the combination of rt-PA and ridogrel. In the control group, stable occlusion as measured with an electromagnetic flow probe was maintained throughout the observation period. rt-PA produced reperfusion in 3 of 5 dogs, associated with cyclic reocclusion and reflow in 1 dog. Ridogrel administration did not produce recanalisation in any of the animals. The combined administration of ridogrel and rt-PA produced stable reperfusion without reocclusion in all of 5 dogs (p<0.003 vs control groups), within 41±17 min. Coronary blood flow after recanalisation was significantly higher (p<0.05) in dogs given rt-PA and ridogrel (29±6 ml/min after 10 min and 30±9 ml/min after 60 min) than in dogs given rt-PA alone (10±5 ml/min after 10 min and 14±6 ml/min after 60 min). Ridogrel, alone or in combination with rt-PA, prolonged the template bleeding time from approximately 3.5 min to more than 20 min, whereas rt-PA alone did not significantly affect the bleeding time. The results indicate that ridogrel enhances and sustains recanalisation of platelet-rich arterial thrombosis with rt-PA.