NEUTROPHIL PLATELET-ACTIVATING FACTOR PRODUCTION AND ACETYLTRANSFERASE ACTIVITY IN CLINICAL ACUTE MYOCARDIAL INFARCTION

1. Neutrophil function was studied in 10 males presenting with acute myocardial infarction (MI) within 6 h of onset and in 10 normal males. Neutrophil production of platelet-activating factor (PAF), determined by bioassay, that of leukotriene B₄ by HPLC, and the activity of an enzyme involved in the synthesis of PAF, acetyltransferase (AT), were measured before and after stimulation with opsonized zymosan and calcium ionophore, A23187. 2. The neutrophil count was significantly raised at presentation in those with MI (8.2 ± 0.8 vs 2.8 ± 0.3 (s.e.m.) |MX 10⁹ cells/L, P<0.001; t-test, 18d.f.). Production of PAF per neutrophil in response to both stimulants was greater than normal in those with MI (zymosan: 21 ± 4 vs 12 ± 1ng/10⁷ cells, P<0.05; ionophore: 174 ± 18 vs 113 ± 11ng/10⁷ cells, P<0.02) despite normal leukotriene B₄ production and depressed AT activity. By 7 days, the neutrophil count had significantly fallen but it remained greater than normal as did PAF production. 3. Acute MI is associated with increased potential for production of PAF by neutrophils which may be important in the pathogenesis of MI.     

SHORT TERM VITAMIN E SUPPLEMENTATION HAS NO EFFECT ON PLATELET FUNCTION, PLASMA PHOSPHOLIPASE A2 AND LYSO-PAF IN MALE VOLUNTEERS

1. Based largely upon in vitro studies, vitamin E has been reported to inhibit phospholipase A2 activity, to alter phospholipid metabolism and reduce platelet aggregation. 2. The effect of dietary supplementation with D-alpha-tocopherol (1500 iu/day for 14 days) was studied in nine males, 41-63 years old, comparing active treatment with a preceding placebo period. 3. Despite an increase from 2.6 +/- 0.8 (s.d.) x 10(-5) mol/L to 6.0 +/- 1.8 10(-5) mol/L in plasma vitamin E there were no significant changes in the aggregation of diluted whole blood or platelet rich plasma to adenosine diphosphate (ADP) or collagen, in plasma phospholipase A2 activity or plasma lyso-platelet-activating factor (lyso-PAF) (bioassay after in vitro acetylation to PAF). 4. High dose vitamin E dietary supplementation had no effect on these phospholipid and platelet parameters.     

PLASMA PROPRANOLOL CONCENTRATION IN PATIENTS WITH ANGINA AND ACUTE MYOCARDIAL INFARCTION

1. Plasma levels of propranolol were measured fluorometrically in patients with angina pectoris and in patients admitted to the Coronary Care Unit with acute myocardial infarction. 2. In thirty patients with stable angina pectoris, plasma propranolol levels varied almost linearly with doses between 10 and 120 mg during 6-hourly chronic oral administration. Plasma levels greater than 100 ng/ml produced 70–80% reduction in the tachycardia induced by strenous exercise on a treadmill. 3. In nineteen patients with acute myocardial infarction given oral propranolol, 20 mg 6-hourly, peak as well as trough plasma levels of the drug increased progressively but remained below 100 ng/ml in all except two patients during the first 24 h after their admission to the Coronary Care Unit. 4. The data suggest that the use of low and fixed doses of propranolol may not produce adequate plasma levels or significant β-adrenoceptor blockade in the early stages of acute myocardial infarction in man.     

重组链激酶对急性心肌梗死溶栓治疗临床观察

目的：观察溶栓新药重组链激酶（ｒ－ＳＫ）在急性心肌梗死（ＡＭＩ）静脉溶栓治疗中的临床疗效和不良反应。方法：采用平行随机单盲对照的研究方法,以尿激酶（ＵＫ）为对照比较ｒ－ＳＫ对ＡＭＩ的溶栓治疗效果和不良反应。结果：ｒ－ＳＫ１５０万Ｕ对ＡＭＩ的溶栓再通率为８４．４％,而ＵＫ１５０万Ｕ仅为５６．７％（Ｐ＜０．０５）。不良反应除发冷外其他方面两组无差异。结论：国产ｒ－ＳＫ是一个血管再通率高,不良反应及出血并发症低,安全有效的溶栓药物。     

A1-and A2-PURINOCEPTORS IN THE GUINEA-PIG UTERUS

1. Radioligand binding and functional studies were undertaken to investigate the P₁-purinoceptors present in the separated myometrial layers and the endometrium of the guinea-pig uterus. 2. In preparations of endometrium-denuded circular myometrium, the A₂-selective agonists (2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamido-adenosine (CGS 21680, 100 μmol/L) and N-ethylcarboxamido adenosine (NECA, 1–10 μmol/L) inhibited contractile responses to phenylephrine. In preparations of endometrium-intact circular myometrium, NECA (10 μmol/L) enhanced responses to phenylephrine. NECA did not modulate the spontaneous contractions of longitudinal myometrium. 3. Homogenate binding studies with circular myometrium, longitudinal myometrium and endometrium revealed saturable high affinity [³H]-NECA binding sites. The mean maximal densities of binding sites (B_max) were 2.08, 14.7 and 15.5 fmol/mg protein, and pK_D (neg. log dissociation constant) values were 9.82, 9.19 and 7.44, respectively. 4. (R-) and (S-) -N⁶-(2-phenylisopropyl)adenosine (R- and S-PIA) both competed for two [³H]-NECA binding sites in preparations of circular myometrium. CGS 21680 competed for two [³H]-NECA binding sites in preparations of endometrium and longitudinal myometrium. All other agonist competition was for one site only. The rank orders of potency of high affinity binding were S-PIA ≥ R-PIA ≥ CGS 21680 (circular myometrium), R-PIA ≥ CGS 21680 ≥ S-PIA (longitudinal myometrium) and CGS 21680 > > S-PIA ≥ R-PIA (endometrium). 5. In preparations of circular myometrium, longitudinal myometrium and endometrium the selective A₁-purinoceptor antagonist, 1,3-dipropyl-8-(2-amino-4-chloro)-phenylxanthine (PACPX), competed for two [³H]-NECA binding sites, the non-selective antagonist 3,7-dimethyl-1-propargylxanthine (DMPX), competed for one site only. 6. NECA increased cyclic adenosine monophosphate (CAMP) levels in preparations of both circular myometrium and endometrium. 7. These results indicate that P₁-purinoceptors of the A₂-subtype mediate the inhibitory effects of adenosine analogues on the phenylephrine-induced contractions of the circular myometrium of the guinea-pig, this effect is modified by the presence of the endometrium. There is no evidence that the [³H]-NECA binding sites of the longitudinal myometrium correlate with functional P₁-purinoceptors in this tissue.     

TIME DEPENDENT CONVERSION FROM α1- to β-ADRENOCEPTOR- MEDIATED GLYCOGENOLYSIS IN ISOLATED RAT HEPATOCYTES: ROLE OF MEMBRANE PHOSPHOLIPASE A2 AND PROTEIN KINASE C

1. Incubation of isolated rat liver cells in a serum-free buffer leads to the reduction of the glycogenolytic effect of phenylephrine and the simultaneous emergence of the response to isoprenaline within 4 h. 2. Inhibitors of phospholipase A2 reverse the adrenergic activation of phosphorylase alpha from a beta- to an alpha 1-receptor-mediated event. Conversely activators of phospholipase A2 enhance the conversion. 3. In vitro incubation of hepatocytes leads to a translocation of protein kinase C from the cytosol to the membrane which can be mimicked by phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C. PMA is also associated with transformation from alpha 1- to beta-adrenoceptor-mediated glycogenolysis. 4. It is proposed that coupling of hepatic alpha 1- and beta-adrenoceptors to postreceptor pathways are regulated by changes in membrane phospholipase A2 and protein kinase C activity.     

BLOOD PRESSURE EFFECTS OF THROMBOXANE A2 BLOCKADE IN SPONTANEOUSLY HYPERTENSIVE RATS

1. The effects of CGS 22652, a thromboxane (Tx) A₂ synthase inhibitor and TxA₂ prostaglandin (PG) H2 receptor antagonist, on blood pressure (BP) were studied in conscious freely moving spontaneously hypertensive rats (SHR). 2. Three groups of 13 male SHR were subcutaneously infused from 5 to 11 weeks of age via osmotic minipumps with CGS 22652 at doses of 5 (SHRa) or 10 (SHRb) mg/ kg per 24 h or with the vehicle only (SHRc). A fourth group (SHRd, n= 13) was orally treated from 3 to 11 weeks of age with CGS 22652 (30 mg/kg) given by gavage once a day. 3. CGS 22652 dose-dependently reduced the age-related increase in systolic BP. The pressor response to noradrenaline (200 ng/kg, i.v.) but not to angiotensin I or II was slightly (P<0.05) diminished in 11 week old SHRb and SHRd compared to SHRc. Acute ganglionic blockade by trimethaphan (10 mg/kg, i.v.), as well as angiotensin converting enzyme inhibition by perindopril (2 mg/kg, i.v.) decreased BP to a similar extent in the four groups. After combined blockade of vasopressin receptors and of the autonomic nervous system and the administration of a direct vasodilator (hydralazine, 3 mg/kg, i.v.), the residual mean BP was identical in the four groups of rats. 4. Chronic treatment with CGS 22652 dose-dependently antagonized the TxA₂ PGH₂ receptors but did not modify the TxA₂ synthesis. The urinary sodium excretion did not differ between groups. 5. In conclusion, at the doses used, CGS 22652 given either orally or subcutaneously exhibited only TxA₂/PGH₂ receptor blocking properties in SHR. Chronic treatment modestly prevented the development of hypertension in SHR, probably through a decrease in the pressor effects of TxA₂ and of noradrenaline.     

EFFECT OF EXERCISE ON PLASMA ADRENOMEDULLIN AND NATRIURETIC PEPTIDE LEVELS IN MYOCARDIAL INFARCTION

1. We investigated the effect of exercise on plasma adreno-medullin, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations and studied the relationship between these peptides and haemodynamic parameters in nine patients with old myocardial infarction (MI) and in eight normal subjects. 2. The exercise protocol consisted of two fixed work loads (40 and 80 W) for 4 min each and venous blood samples were taken at rest, during each exercise stage and after exercise while monitoring the mean arterial pressure (MAP) and heart rate (HR). In MI, pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), left ventricular end-diastolic pressure (LVEDP) and cardiac output (CO) were measured throughout exercise. 3. Adrenomedullin levels did not significantly increase with exercise. Adrenomedullin levels correlated with PAP and PCWP at rest (P < 0.05). Atrial natriuretic peptide levels correlated with PAP, PCWP and LVEDP throughout exercise (P < 0.05) but, on multiple regression analysis, PCWP correlated only with ANP (P < 0.01). Brain natriuretic peptide levels correlated with LVEDP throughout exercise (P < 0.01) and its increment correlated closely with basal BNP levels at rest (P < 0.01). 4. These results suggest that adrenomedullin does not respond to the acute haemodynamic changes of exercise, whereas ANP responds to it and PCWP is the major stimulus factor. Brain natriuretic peptide responds to exercise in proportion to the basal synthesis of BNP in patients with left ventricular dysfunction and LVEDP may play a role in increasing BNP during exercise.     

INTERACTION BETWEEN PLATELET-RELEASED SEROTONIN AND THROMBOXANE A2 ON HUMAN DIGITAL ARTERIES

Synergism between the contractile effects of platelet-derived serotonin (5HT) and thromboxane A2 (TXA2) on a human blood vessel has been investigated by incubating strips of digital arteries in subcontractile concentrations of either 5HT or the TXA2-mimetic agent U46619. Either agonist U46619 or 5HT, in subcontractile concentrations, significantly potentiated the contractile response to the other. The 5HT antagonist ketanserin (10 mumol/l), the Ca2+ antagonist drugs verapamil (3 mumol/l), or nifedipine (10 nmol/l), or a Ca2+-free bathing medium, reduced the contractile responses to 5HT, but had no effect on the potentiation mediated by U46619. The interaction between TXA2 and 5HT derived from platelets was studied by measuring responses to platelets 1 min after aggregation (in the absence or the presence of ketanserin 10 mumol/l), and 20 min after aggregation. The results indicated that the response to platelets mediated by TXA2 and 5HT was greater than the sum of those mediated by TXA2 or 5HT separately. It is concluded that synergism between the contractile effects of 5HT and U46619 occurs in human blood vessels; that this is mediated by enhanced utilization of intracellular, rather than extracellular calcium; and that synergism can also occur when 5HT and TXA2 are released from stimulated human platelets.     

CHARACTERIZATION OF THROMBOXANE A2 RECEPTORS IN THE HUMAN FETAL PLACENTAL VESSELS AND UMBILICAL VEIN

An in vitro examination has been made of the thromboxane A2 receptors in human fetal placental villous vessels and umbilical veins utilizing the TxA2 agonist U46619 and its competitive antagonist AH22921. U46619 was a potent constrictor of both preparations. The EC50 were 25.3 nmol/l (s.e.m. = 2.5, n = 8) for causing constriction of perfused villous vessels and 22 nmol/l (s.e.m. = 5, n = 17) for contraction of the venous longitudinal strip. AH22921 competitively antagonized responses to U46619 in both preparations. The pA2 values were not significantly different and their 95% confidence limits, obtained for its ability to antagonize responses to U46619 in villous vessels and the umbilical vein, were 8.0 (7.3-8.8) and 7.1 (6.3-7.9) respectively. It is concluded that TxA2 receptors in both the human fetal placental villous vessels and umbilical vein may be similar. They also may be similar to those in human platelets and pulmonary blood vessels.     

不同年龄组急性心肌梗塞溶栓治疗的对比研究

４７例急性心肌梗塞（ＡＭＩ）患者按发病年龄随机分成三组，进行尿激酶（ＵＫ）溶栓疗效的对比研究。结果表明，１２小时内溶栓的４７例ＡＭＩ患者再通率、死亡率和并发症发生率分别为５５．３％、１４．９％和８．５％。６小时内溶栓再通率老年组（５０％）明显低于青年组（８０％）和老年前期组（７０％）。老年组住院病死率为２５．９％，且有出血并发症发生，而青年组和老年前期组无一例死亡且无一例出血并发症发生。提示ＵＫ溶栓疗效与患者年龄有关，老年人溶栓疗效较差，病死率和出血并发症发生率较高。     

EFFECT OF ACUTE AND SUBACUTE TREATMENT OF CLONIDINE ON BLOOD pH, Pco2 AND Po2 IN MICE

Measurements were made on blood pH, .Pco₂ and Po₂ in mice after a single injection and following five weeks continuous clonidine hydrochloride treatment. A single injection of clonidine hydrochloride exerts no effect on blood pH, Pco₂ and Po₂ but five weeks of continuous clonidine hydrochloride treatment lowers the blood pH and Pco₂ and raises blood Po₂, suggesting acidosis has taken place. The acidosis may be attributed to rebound hypertension as a result of withdrawal of clonidine treatment.     

THE 5-HT2 RECEPTOR ANTAGONIST SARPOGRELATE REDUCES URINARY AND PLASMA LEVELS OF THROMBOXANE A2 AND URINARY ALBUMIN EXCRETION IN NON-INSULIN-DEPENDENT DIABETES MELLITUS PATIENTS†

1. Therapeutic effects of a 5-HT2 receptor antagonist sarpogrelate on microalbuminuria and thromboxane (TX)A2 biosynthesis were examined in non-insulin-dependent diabetes mellitus (NIDDM) patients. 2. In protocol I, the ankle-brachial pressure index (API; an indicator of peripheral blood flow) and urinary albumin excretion (UalbV; an indicator of renal function) were determined in 42 NIDDM patients who had been treated with 300 mg/day sarpogrelate for 8 weeks. In an analysis of the results, the NIDDM patients were divided into four groups based on the severity of either vasculopathy or nephropathy as follows: group A, API < 0.9, UalbV > or = 100 mg/day; group B, API < 0.9, UalbV < 100 mg/day; group CAPI > or = 0.9, UalbV > or = 100 mg/day; and group D, API > or = 0.9, UalbV < 100 mg/day. 3. In protocol II, 10 NIDDM patients with UalbV values > 100 mg/day were divided into two groups to further confirm the effect of sarpogrelate on albuminuria: group E, the sarpogrelate treatment group (n = 5); and group F, the no treatment group (n = 5). 4. In protocol I, the incidence of a cold sensation in the lower extremities was reduced from 45.2 to 21.4% following sarpogrelate treatment. In patients with UalbV > or = 100 mg/day (groups A and C), UalbV was significantly decreased independent of API, while it did not change in patients with UalbV < 100 mg/day (groups B and D). Plasma TXB2 levels were significantly decreased following sarpogrelate treatment, whereas plasma 6-keto-prostaglandin F1 alpha levels were not. 5. In protocol II, in the sarpogrelate treatment group (group E), albuminuria was significantly improved and both plasma levels TXB2 and urinary TXB2 excretion were significantly decreased. In contrast, in the untreated group (group F), neither plasma levels TXB2 nor urinary TXB2 excretion was changed. 6. In conclusion, microalbuminuria was improved by treatment with the 5-HT2 receptor antagonist sarpogrelate independent of latent vasculopathy. Blockade of 5-HT2 receptors is suggested to be beneficial for the treatment of nephropathy in NIDDM patients. It is possible that the inhibition of TXA2 biosynthesis is involved in the therapeutic effect of 5-HT2 receptor antagonists.     

HYPOTHESIS: ISCHAEMIC PLAQUE NECROSIS AS THE INITIATOR OF UNSTABLE ANGINA/ACUTE MYOCARDIAL INFARCTION?

1. Coronary atherosclerotic plaque complications are important in precipitating acute coronary events such as unstable angina and myocardial infarction. 2. The hypothesis is put forward that plaque complications are initiated by increases in local coronary artery tone sufficient to cut off the vasa vasorum blood supply to the plaque and result in its ischaemic necrosis.     

THROMBOXANE A2 RECEPTOR STIMULATION SIMILARLY POTENTIATES PRESSOR RESPONSES TO 5-HYDROXYTRYPTAMINE IN PERFUSED HINDQUARTERS OF NON-DIABETIC AND ALLOXAN DIABETIC RATS

1. Dose-response curves were obtained to bolus injections of 5-hydroxytryptamine (5-HT) in Krebs'-perfused hindquarters of male Wistar rats. Vasoconstrictor responses to 5-HT (5.7-363 nmol/kg) were significantly attenuated in hindquarters of alloxan-treated 14 day diabetic rats compared with non-diabetics. 2. Infusion of the thromboxane A2 (TxA2)-mimetic U46619 (317 and 31.7, but not 3.17 nmol/L) significantly potentiated vasoconstrictor responses to 5-HT in Krebs'-perfused hindquarters of non-diabetic and diabetic rats. The degree of potentiation was similar for both groups. 3. In Krebs'-perfused hindquarters of non-diabetic rats, infusion of the alpha 1-adrenoceptor agonist methoxamine (8.96 mumol/L, which caused a rise in perfusion pressure intermediate in magnitude to that produced by infusion of 31.7 and 317 nmol/L U46619) did not significantly affect responses to bolus injections of 5-HT. 4. The same concentration of methoxamine did not cause a significant potentiation of vasoconstrictor responses to 5-HT (except for the two highest 5-HT doses, 182 and 363 nmol/kg) in hindquarters of diabetic rats. This potentiation was significantly less than that due to 317 nmol/L U46619, although there was no significant difference between the rise in basal perfusion pressures produced by these concentrations of methoxamine and U46619. 5. Infusion of the TxA2 receptor antagonist AH23848 (111 nmol/L) inhibited the potentiating effect of U46619 (317 nmol/L) on responses to 5-HT in both non-diabetic and diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

NITRIC OXIDE DEFICIENCY INDUCES MYOCARDIAL INFARCTION IN HYPERCHOLESTEROLAEMIC STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RATS

1. To observe the effect of nitric oxide (NO) on the myocardium, the NO synthesis inhibitor N^G-nitro-L-arginine (L-NNA) was administered to hypercholesterolaemic stroke-prone spontaneously hypertensive (SHRSP) rats. 2. Hypercholesterolaemic SHRSP were produced by feeding SHRSP a high fat and high cholesterol diet (HFC) for 2 weeks. The rats were then divided into three groups: (i) the N group, which were fed the HFC diet containing 0.023% L-NNA and 1% NaCl in their drinking water (n = 10); (ii) the NH group, which were fed the HFC diet containing 0.023% L-NNA and 1% NaCl in their drinking water which also contained 80 mg/L hydralazine (n = 10); and (iii) the C group, which were fed the HFC diet and 1% NaCl in their drinking water (n = 10). 3. All rats in the N and NH groups died within 35 days of the initiation of L-NNA administration. Rats in the N and NH groups had significantly increased serum creatine phosphokinase, lactate dehydrogenase, glutamic oxaloacetic transaminase and serum total cholesterol levels compared with rats in the C group. 4. Fibrosis in response to necrosis was histopathologically observed in the hearts of all rats in the N and NH groups without exception. Occlusion or intimal thickening in the arteries adjacent to the necrotic regions was also observed. 5. These results suggest that nitric oxide deficiency induces myocardial infarction in hypercholesterolaemic SHRSP. These NO-deficient hypercholesterolaemic SHRSP offer a new model of myocardial infarction in rats.     

藻酸双酯钠和甘糖酯对急性心肌梗死患者红细胞变形能力保护作用的机制探讨

为探讨藻藻酯双酯钠(PSS)和甘糖酯(PGMS)对急性心肌梗死(AMI)患者红细胞变形能力(ED)保护作用的机制,检测了52例AMI患者红细胞滤过指数(EFI)、红细胞膜Na~ ,K~ -ATP酶和谷胱甘肽过氧化物酶GSH-Px活性及红细胞膜脂质过氧化物(LPO)的变化,同时观察了PSS和PGMS在体外对ED、Na~ ,K~ -ATP酶、GSH-Px和LPO的影响。结果显示,AMI患者EFI、LPO明显增高,Na~ ,K~ -ATP酶和GSH-Px活性明显降低,与对照组比较差异有极显著性(P<0.001)。AMI患者红细胞与PSS或PGMS在体外温育24h后,EFI、LPO明显降低,Na~ ,K~ -ATP酶和GSH-Px活性明显增高。与温育前比较差异有极显著性(P<0.001),与对照组比较差异无显著性(P>0.05)。提示PSS和PGMS具有保护和提高AMI患者ED的作用,其机制与增强红细胞膜ATP酶和抗氧化酶活性有关。     

槲皮素磷酸酯钾对实验性心肌梗塞的影响

iv10～20mg/kg(木解)皮素磷酸酯钾使兔急性心肌梗塞范围明显缩小,ST段明显降低,并能对抗冠脉结扎后引起的血清CPK含量增加及心律失常,这些作用与普萘洛尔相似。但iv40mg/kg后作用不明显。     

比伐卢定对ST段抬高型心肌梗死病人急诊介入治疗术后超敏C反应蛋白、脂蛋白相关磷脂酶A2、白细胞介素-4水平的影响

目的 研究比伐卢定对ST段抬高型心肌梗死(STEMI)病人急诊介入治疗(PCI)术后超敏C反应蛋白(hs-CRP)、脂蛋白相关磷脂酶A2(Lp-PLA2)、白细胞介素-4(IL-4)水平的影响。 方法 选取2015年2月至2017年2月于邢台市第三医院接受PCI术治疗的STEMI病人100例。根据病人术中所用抗凝药物种类不同分为观察组与对照组,每组50例。观察组则采用比伐卢定进行抗凝,对照组采用普通肝素进行抗凝。分别比较两组治疗前与治疗3 d后血清hs-CRP、Lp-PLA2、IL-4水平,治疗前与治疗30 d后心功能指标水平,MACE发生情况以及出血事件发生情况。 结果 治疗3 d后两组病人血清hs-CRP、Lp-PLA2、IL-4水平均明显低于治疗前,而观察组hs-CRP、IL-4水平分别为(22.7±5.4)mg/L、(2.0±0.5)pg/mL,均明显低于对照组的(32.8±5.6)mg/L、(3.7±0.9)pg/mL,均差异有统计学意义(均P＜0.05)。治疗30 d后观察组LVEF水平为(46.8±3.9)%,明显高于对照组的(43.2±4.0)%,而BNP水平为(284.5±113.8)ng/L,明显低于对照组的(462.8±103.7)ng/L,均差异有统计学意义(均P＜0.05)。治疗30 d后观察组病人MACE发生率为2.00%(1/50),明显低于对照组的14.00%(7/50),差异有统计学意义(P＜0.05)。观察组出血事件发生率为4.00%(2/50),明显低于对照组的18.00%(9/50),差异有统计学意义(P＜0.05)。     

REGIONAL O2 SUPPLY/CONSUMPTION IN NORMAL AND ISCHAEMIC RABBIT MYOCARDIUM: EFFECT OF NIFEDIPINE

The effect of nifedipine infusion on myocardial O2 supply and consumption in flow-restricted and normal regions of the left ventricle was tested in anaesthetized open-chest rabbits after ligation of the left anterior descending coronary artery for one hour. Ten min after occlusion, nifedipine-treated animals were given either a low or high dose of the drug: a 5 micrograms/kg bolus followed by 1 micrograms/kg per min infusion or a 10 micrograms/kg bolus and 10 micrograms/kg per min infusion, respectively. Regional blood flow was measured before and after occlusion using radioactive microspheres and O2 saturation was measured microspectrophotometrically; the Fick Principle was then employed to determine regional O2 consumption. After a 60 min occlusion, blood flow was reduced overall to 51% of pre-ligation flows in the occluded region, and treatment with nifedipine or vehicle did not significantly alter this flow reduction. Blood flow in nonoccluded regions increased 1.6-fold only with the high dose of nifedipine and was unchanged in all other groups. Microspectrophotometric analysis of low dose nifedipine and control hearts showed that O2 extraction was greater in occluded than in normal myocardium (9.0, s.d. = 0.9, ml O2/100 ml blood vs 7.2, s.d. = 0.7, respectively) and that subendocardial extraction exceeded subepicardial. These data suggest that nifedipine administration at this dose had no apparent beneficial effect on O2 supply or O2 consumption in normal or flow-restricted regions of the left ventricle during 1 h of coronary artery occlusion.