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Biomedical subjects

R Kornowski

Publications and source records attributed to R Kornowski.

At least 91 records · Page 5Linked to original sources
PubMed1996

Reduction of reinfarction and angina with use of low-molecular-weight heparin therapy after streptokinase (and heparin) in acute myocardial infarction.

This study examined whether extending the anticoagulation effect of heparin by low-molecular-weight heparin (clexane) can prevent recurrent myocardial infarction (AMI) treated by streptokinase. On the fifth day after AMI and after heparin therapy cessation, 103 patients were randomly assigned to either treatment with low-molecular-weight heparin (40 mg subcutaneously per day for 25 days, n=43) or control (no treatment, n=60). All patients were followed carefully for 6 months after the infarction date. A total of 32 patients (31%) sustained a cardiac event during the 6-month observation period. There were 12 patients (20%) with reinfarction in the control group versus 2 patients (4.6%) in the low-molecular-weight heparin group during the first 30 days of the study (p=0.02). One additional patient sustained reinfarction at 3 months of followup in the control group, which yielded a total of 13 patients (21.6%) sustaining reinfarction in the control group versus 2 patients (4.6%) in the low-molecular-weight heparin group during 6 months of followup (p=0.01). Angina pectoris after AMI was diagnosed in 13 control patients (21.6%) versus 4 low-molecular-weight heparin-treated patients (9.3%) (p=0.078) during the study period. No major bleeding events were reported in either low-molecular-weight heparin-treated or control patients. Among patients with recently diagnosed AMI treated by streptokinase, extending the anticoagulant effect of heparin for 25 days may prevent recurrent coronary events for at least one month.

Adult↗
PubMed1996

Prediction of renal impairment in elderly patients with congestive heart failure treated with captopril.

This study assessed the usefulness of the oral captopril test in the prediction of renal impairment among elderly patients with congestive heart failure (CHF). Forty-seven patients aged > or = 65 years with CHF (EF < 40%) participated in a prospective nonrandomized series. Blood samples for plasma renin activity (PRA) were drawn before and 60 minutes after 50 mg of oral captopril. Twenty-four hours later, captopril was administered (up to 75 mg/day over a 4 day period), and renal laboratory and clinical assessment were performed at baseline and for a 9 day period. In 7 of 47 patients (14.9%), deterioration of renal function was observed. During the captopril test, the PRA increased significantly after 1 hour in almost all patients and the mean blood pressure decreased from 99.2 +/- 14.6 mmHg to 92.2 +/- 13.7 mmHg (p < 0.001). All patients whose baseline PRA level was < 1.9 ng/ml/hr and whose stimulated PRA was < 3.2 ng/ml/hr maintained a stable renal function throughout the study period. Significant statistical correlation (p < 0.05) was found between the initial PRA, the changes in PRA or mean blood pressure during the captopril test, and the change in plasma creatinine and creatinine clearance in the entire group, and was even more evident in a subgroup of patients with an ejection fraction > or = 30%. All these correlations were not statistically significant in the patients with an ejection fraction < 30%. It is thus concluded that measurement of pretreatment PRA levels might be a useful laboratory tool for predicting the renal safety of captopril use in patients with CHF whose EF > or = 30%.

Administration, Oral↗
PubMed1996

Prognostic Importance of Previous Myocardial Infarction in Patients Receiving Thrombolytic Therapy for Acute Infarction.

This study evaluated the prognostic significance of reinfarction location by considering the previous site or type of myocardial infarction (MI) among 1601 patients with a history of previous MI who took part in the International (non-Italian) tPA/STK trial and/or the Israeli GUSTO study population. These patients were accordingly divided and hospital mortality was compared by six location groups as follows: acute inferior with previous inferior (8.1% hospital mortality), acute inferior with previous anterior (12.8%), acute anterior with previous inferior (13.3%), acute anterior with previous anterior (11.1%), acute inferior with previous non-Q-wave MI (7.6%), and acute anterior with previous non-Q-wave MI (11.2%) (p = 0.17 for comparison between the six groups). Hospital mortality tended to increase among patients with an anterior reinfarction compared with those with an inferior one (12.1% vs. 9.5%, p = 0.12). Among patients with a reinfarction at a different ECG location from the previous event, mortality tended to be higher compared with patients with two MIs at the same location (13.1% vs. 9.7%, p = 0.07). Recurrent MI following a previous Q-wave MI did not cause a higher mortality compared with a previous non-Q-wave type of MI (11.5% vs. 9.5%, p = 0.24). Among patients sustaining reinfarction, overall mortality did not differ between STK- and tPA-treated patients (11.0% vs. 11.4%, p = NS). In conclusion, the current study identified trends for higher mortality rates in patients with anterior compared with inferior reinfarction, with remote compared with the same ECG location of the two infarctions but not following a previous non-Q-wave compared with Q-wave MI. However, no particular combination of successive MIs location was significantly associated with a higher risk for hospital mortality.

Journal Article↗
PubMed1996

Long-term prognosis of patients after a Q wave compared with a non-Q wave first acute myocardial infarction. Data from the SPRINT Registry.

UNLABELLED: OBJECTIVE, DESIGN AND PATIENTS: Between August 1981 and July 1983, 5839 consecutive myocardial infarction patients were hospitalized in 13 coronary care units in Israel. The present study examines 10 year survival among 4037 consecutive patients with a first myocardial infarction with either Q or non-Q waves. Demographic and medical data were collected from hospital records, and 1 year clinical follow-up was complete for 99% of hospital survivors. Mortality follow-up was extended to June 1992 (mean 10 years of follow-up). RESULTS: Five hundred and eighty patients (14%) had first myocardial infarctions of the non-Q wave type and 3457 of the Q wave type. Hospital mortality was significantly higher in patients with a Q wave (10%) than those with a non-Q wave myocardial infarction (7%) (P < 0.05). One year post-discharge, non-fatal reinfarction and mortality rates were comparable in patients with Q wave (4% and 7%) and non-Q wave myocardial infarctions (4% and 7% respectively). Similarly, 5 to 10 year post-discharge mortality rates were equally high in patients with a non-Q wave (26% and 44%) as in those with a first episode of a Q wave myocardial infarction (22% and 40% respectively). CONCLUSIONS: Patients with a first non-Q wave acute myocardial infarction exhibited relatively better in-hospital survival than counterparts with a first Q wave infarction, but the advantage did not persist after discharge. Patients with a non-Q wave infarction deserve particular attention as their post-discharge mortality risk is similar to counterparts with a first Q wave myocardial infarction.

Aged↗
PubMed1996

High-dose intravenous magnesium attenuates complement consumption after acute myocardial infarction treated by streptokinase.

OBJECTIVE: This study was designed to detect changes in complement levels following acute myocardial infarction and to test whether magnesium sulphate (MgSO4) administration interferes with the complement response that follows acute myocardial infarction. DESIGN: Twenty-nine patients with acute myocardial infarction treated with streptokinase were included and randomly assigned to three treatment groups. In groups A and B, a bolus of 1 g MgSO4 was infused intravenously followed by 4 g (group A) and 14 g (group B) MgSO4 for 24 h while normal saline was administered in group C (control). Blood samples for C3, C4 and CH-100 were obtained at baseline and repeatedly during the 48 h following the initiation of magnesium infusion. RESULTS: In groups A and C, a remarkable decrease in the levels of C3, C4 and CH-100 was observed when measured 1 h after the end of streptokinase infusion and thereafter for the ensuing 48 h compared to baseline values (P < 0.05). In group B, the decrease in these complement elements was attenuated, and a significant (P < 0.05) delayed decrease of C3 and C4 was observed only at 24 h and later up to 48 h. The mean level of CH-100 in group B was significantly depressed compared to baseline from 3 h and thereafter up to 48 h. Mean C3 values plotted against observation time differed between the three groups (P = 0.021). A similar trend was observed for C4 (P = 0.133) but not for CH-100 (P = 0.46). CONCLUSION: (1) Complement elements are being consumed following acute myocardial infarction treated by streptokinase. (2) High-dose intravenous magnesium attenuates the complement process following acute myocardial infarction. (3) These results might signify that magnesium modulates the inflammatory response that follows infarction.

Adult↗
PubMed1996

Enhancement of recombinant tissue-type plasminogen activator thrombolysis with a selective factor Xa inhibitor derived from the leech Hirudo medicinalis: comparison with heparin and hirudin in a rabbit thrombosis model.

OBJECTIVE: To compare the efficacy of Yagin, a factor Xa inhibitor derived from the leech Hirudo medicinalis, with those of heparin and hirudin as adjuncts to recombinant tissue-type plasminogen activator (rTPA) thrombolysis in a rabbit thrombosis model. METHODS: Thirty-one animals were allocated randomly to three groups, all administered four boluses of 0.25 mg/kg rTPA every 10 min for 30 min, 17 mg/kg aspirin intravenously, and heparin (as a 100 IU/kg bolus followed by infusion of 50 IU/kg heparin per h), hirudin (as a 2 mg/kg bolus followed by infusion of 1 mg/kg hirudin per h), or Yagin (as an 80 micrograms/kg bolus followed by infusion of 43 micrograms/kg Yagin per h). RESULTS: Administration of Yagin was associated with a significant acceleration of the reflow time, this time being 14.5 +/- 1.2 min with Yagin, 25.8 +/- 5.2 min with heparin (P < 0.0001, versus Yagin), and 28.7 +/- 16.0 min with hirudin (P = 0.012, versus Yagin). Overall patency did not differ significantly among the three groups. CONCLUSIONS: At the indicated single doses, inhibition of factor Xa by a relatively low concentration of Yagin was found to be superior than that with either heparin or hirudin for accelerating rTPA thrombolysis.

Animals↗
PubMed1996

The effect of low molecular weight heparin (fragmin) on myocardial neutrophil accumulation and infarct size in a rat model of myocardial infarction.

BACKGROUND: Heparin molecules possess immunomodulating properties, which are thought to complement their established antithrombotic activity. The purpose of this study was to evaluate whether the antiinflammatory properties of low molecular weight heparin (LMWH) can attenuate polymorphonuclear neutrophil accumulation and infarct size in a rat model of myocardial infarction. METHODS: Myocardial infarction was induced by ligating the left main coronary artery. LMWH (fragmin 500 anti-FXa u/kg) or vehicle (saline) were administered subcutaneously thirty minutes prior to coronary artery occlusion. Significant anticoagulant activity was attained with LMWH for more than eight hours. Twenty-four hours later, neutrophil accumulation and infarct size were determined by measuring left ventricular free wall myeloperoxidase and residual creatine kinase activity, respectively. RESULTS: As compared with rats administered vehicle, myeloperoxidase activity was insignificantly decreased in rats treated with LMWH (1.24 +/- 0.28 u/g vs 1.66 +/- 0.15 u/g, P = 0.16. Infarct size was also not significantly different between the groups (62.48 +/- 3.5% and 50.67 +/- 7.2% of left ventricular free wall with vehicle and LMWH, respectively, P = 0.1). CONCLUSION: The authors conclude that LMWH does not significantly reduce myocardial neutrophil accumulation and infarct size twenty-four hours after myocardial infarction in the rat.

Animals↗
PubMed1995

Intensive home-care surveillance prevents hospitalization and improves morbidity rates among elderly patients with severe congestive heart failure.

The purpose of this study was to examine the impact of intensive home-care surveillance on morbidity rates of elderly patients with severe congestive heart failure. Forty-two patients aged 78 +/- 8 years who had severe congestive heart failure (New York Heart Association functional classes III through IV, mean ejection fraction 27% +/- 6%), were examined at least once a week at home by internists from the district hospital and by a trained paramedical team. The year before entry to the home-care program was compared to the first year of home surveillance. The mean total hospitalization (hosp) rate was reduced from 3.2 +/- 1.5 hosp/yr to 1.2 +/- 1.6 hosp/yr and duration from 26 +/- 14 days/yr to 6 +/- 7 days/yr (p < 0.001 for both). Cardiovascular admissions decreased from 2.9 +/- 1.5 hosp/yr to 0.8 +/- 1.1 hosp/yr and duration from 23 +/- 13 days/yr to 4 +/- 4 days/yr (p < 0.001). The vital status (ability to perform daily activities, expressed in a 1 to 4 scale) was improved from 1.4 +/- 0.9 to 2.3 +/- 0.7 (p < 0.001). In conclusion, an intensive home-care program was associated with a marked decrease in the need for hospitalization and improved the functional status of elderly patients with severe congestive heart failure. Such a service might also have a cost-effective advantage and a major impact on health expenditure.

Activities of Daily Living↗
PubMed1995

Exogenous insulin-like growth factor II enhances post-infarction regional myocardial function in swine.

OBJECTIVES: Insulin-like growth factor II (IGF-II) promotes cardiac myocyte growth and contractility in vitro. This study was designed to investigate the effect of exogenous IGF-II on regional myocardial function at the area of infarct in the pig. METHODS: Myocardial infarction was induced in 12 female anaesthetized pigs by affigel blue beads, embolizing microvessels of the left anterior descending coronary artery distribution. In the experimental group (n = 6), IGF-II (0.12 microgram.kg-1 in two animals and 0.6 microgram.kg-1 in four) was incorporated into the beads and delivered by them to the infarct area. Myocardial function was followed echocardiographically, and the excised heart was analysed immunohistochemically and histopathologically. RESULTS: Myocardial function in injured zones, inversely related to an echocardiographic segmental wall motion score (mean +/- SEM), was similar between the two groups at baseline, but at 4 weeks post-infarction was significantly (P = 0.008) reduced in the control group (0.58 +/- 0.38 vs 3.42 +/- 0.84), in contrast to nearly baseline values in the experimental group (0.58 +/- 0.33 vs 1.17 +/- 0.42, P = 0.41). Cardiac performance in injured segments was significantly better after myocardial injury in the experimental group (P = 0.04). Tissue samples from both groups (4 weeks post-infarction), stained with haematoxylin and eosin demonstrated peri-infarct myocyte hypertrophy, corresponding to regions selectively stained by an antibody for CD56, which highlights growing cardiac myocytes. By image analysis semi-quantification, staining for CD56 was significantly (P = 0.04) higher in the peri-infarct region of the experimental group, as compared with controls (106.5 +/- 2.8 vs 92 +/- 4.4 gray level units). Microvessels stained for von-Willebrand factor were similar in number in both groups (P = 0.8), as were mesenchymal cells stained for vimentin (P = 0.7). CONCLUSIONS: Exogenous IGF-II, delivered to the infarct area ameliorates regional cardiac function in the pig, perhaps by inducing peri-infarct myocyte growth.

Animals↗
PubMed1995

Beneficial effect of nitroglycerin on arterial rethrombosis after thrombolysis. Results from a rabbit thrombosis model.

BACKGROUND: Although nitroglycerin (NTG) is commonly administered to patients with acute myocardial infarction, its effect on concomitant thrombolytic therapy has not been fully elucidated. We examined whether NTG administration further optimizes thrombolysis with rt-PA, combined with aspirin and heparin. METHODS AND RESULTS: Blood clots were produced in a rabbit femoral artery with endothelial damage and distal stenosis. rt-PA was administered in repeated bolus i.v. injections of 0.3 mg.kg-1 every 10 min for 50 min. Femoral artery flow was measured continuously for 2 h. Fourteen rabbits were randomized into two groups (group A and B), both receiving aspirin (i.v. 17 mg.kg-1) and heparin (i.v. 200 units.kg-1) prior to the first rt-PA bolus injection. NTG was administered in group B only, 10 min prior to the first rt-PA bolus, at 10 micrograms.kg-1.min-1 for 130 min. Reperfusion at the end of the 120 min observation period occurred in 5/7 group A and 6/7 group B rabbits (P = ns). In 3/7 group A rabbits, re-flow was achieved but persistent re-occlusion subsequently developed in 1/3 and oscillatory re-flow and re-occlusion cycles (cyclic re-flow) with subsequent patency developed in the remaining two rabbits. These flow patterns were not observed in any of group B rabbits. Overall patency duration was significantly prolonged with NTG (group B; 578/840 min) compared to controls (group A; 258/840 min) (P < 0.001). The mean recanalization time (group A; 30.8 +/- 9.3 vs group B; 22.5 +/- 4.7 min, P = 0.16) as well as mean rt-PA boluses needed to achieve complete recanalization (group A; 4.3 +/- 0.7 vs group B; 3.3 +/- 0.6 boluses/rabbit, P = 0.3) did not differ between groups. However, NTG infusion was associated with increased restored femoral flow following recanalization (expressed as % of stenotic flow value over observation time) compared to control group (P = 0.025 by repeated measures ANOVA). CONCLUSION: Adding NTG to a thrombolytic regimen with rt-PA, aspirin and heparin increases the magnitude of restored flow and total patency duration following recanalization in a rabbit model of arterial thrombosis.

Animals↗
PubMed1995

Noninvasive evaluation of microcirculatory hemodynamic changes during hemorrhage followed by saline or blood transfusion.

The purpose of the study was to examine the ability of a system combining laser Doppler flowmetry (LDF), photoplethysmograph (PPG), and transcutaneous oxygen tension (tc-PO2) to follow changes in the microcirculation during hemorrhage and following blood or saline return, and to test the hypothesis that such changes precede and might predict changes in the systemic blood pressure. Measurements were performed on the skin of anesthetized rabbits (n = 10) during mild (0-8%), moderate (9-24%), and severe (25-30% of blood volume) hemorrhage, and following complete volume restitution by blood or saline. We found the following: 1) hemorrhage caused typical changes in the LDF, PPG, and tc-PO2 signals that could be formulated by mathematical models, 2) these signals identified blood as being more efficient than saline for volume restitution following hemorrhage, and 3) microcirculatory changes precede and might predict systemic hemodynamic events.

Acute Disease↗
PubMed1995

Clinical predictors of reinfarction among men and women after a first myocardial infarction. SPRINT Study Group. Secondary Prevention Reinfarction Israeli Nifedipine Trial.

Independent clinical factors predicting reinfarction in the 1st year following an initial myocardial infarction were identified among 900 women and 2,795 men. Women were older (65.8 vs. 59.3 years; p < 0.001) but tended to suffer from reinfarction at a rate similar to that of men (6.9 vs. 5.6%, p = 0.17). Cumulative 1-month, 1- and 5.5-year all-cause mortality following the first infarction was higher among women who sustained reinfarction (43, 52 and 74%, respectively) than among men (29, 30 and 51%, respectively, p < 0.01 for each). Independent clinical predictors for recurrent myocardial infarction among women were (adjusted relative odds): peripheral vascular disease (3.2), postinfarction angina (2.3), diabetes mellitus (2.2), radiographic evidence of cardiomegaly (1.9), anterior location of the first infarction (2.0), congestive heart failure (1.8), prior angina (1.6) and age (10 years) increment (1.2). Predictive variables for men were: anterior infarct location (1.7), peripheral vascular disease (1.6, prior stroke (1.5), prior angina (1.4), systemic hypertension (1.3) and age (10 years) increment (1.1). Our data indicate (a) different cardiac risk factors for reinfarction among men and women after a first myocardial infarction, and (b) a prognostic advantage for men over women following reinfarction.

Aged↗
PubMed1995

Ischemic stroke following an intramuscular injection of diclofenac. Case report.

Nonsteroidal antiinflammatory drugs (NSAIDs) have arterial vasospastic properties. The authors report a stroke that occurred within minutes following an intramuscular injection of diclofenac. A sixty-one-year-old man, a heavy smoker, was admitted for an acute onset of mild hemiparesis thirty minutes after a single intramuscular injection of diclofenac. The neurologic deficit was resolved at one month of follow-up. The authors suggest a temporal causal relationship between the cerebrovascular event and the injection of diclofenac. The mechanism of stroke might be related to a synergistic vasospastic property shared by the use of an NSAID and heavy smoking.

Acute Disease↗
PubMed1994

Endothelin and myocardial ischemia.

Endothelin is a potent vasoconstrictor with a wide range of effects on the heart. Changes in myocardial and circulating levels of endothelin have been described in various experimental models of myocardial ischemia, and in humans with acute myocardial infarction and different forms of angina pectoris. The role played by endothelin in the different states of myocardial ischemia is unclear. However, myocardial damage has been shown to be reduced in several experimental models of myocardial infarction by administering agents that block the action of endothelin. The aim of this review article is to present the current literature concerning the interaction between endothelin and the various forms of myocardial ischemia, and to explore the significance of such interactions.

Angina Pectoris↗
PubMed1994

Low molecular weight heparin (Fragmin) prevents early reocclusion following femoral artery thrombolysis with rt-PA in rabbits.

The purpose of this study was to evaluate the effect of low molecular weight heparin Fragmin on thrombolysis with tissue-type plasminogen activator (rt-PA) and to compare its effect to that of standard heparin. A rabbit thrombosis model was used, consisting of a blood clot produced in an isolated femoral artery segment with superimposed endothelial damage and distal stenosis. Thirty rabbits were randomized to three treatment groups with rt-PA (30 micrograms.kg-1.min-1 for 60 min and no additional therapy), rt-PA with i.v. standard heparin (200 IU.kg-1 bolus and then 70 IU.kg-1 hourly) and rt-PA with s.c. Fragmin (a single dose of 500 IU.kg-1) prior to rt-PA administration. In six of 10 rabbits given rt-PA only, recanalization was observed which was persistent in three. In eight of 10 rabbits given rt-PA with intravenous heparin, reflow was achieved, which was persistent in three. Fragmin resulted in recanalization in eight of 10 rabbits, with persistent patency in each recanalized rabbit. Reflow time was not shortened with either standard heparin or Fragmin compared with rt-PA alone (64 +/- 41, 56 +/- 18, 50 +/- 23 min respectively), (P = 0.7). Persistent reocclusion after reflow was not observed with Fragmin (0/8) but was present with both standard heparin (5/8, P = 0.03 vs Fragmin) and rt-PA alone (3/6, P = 0.05 vs Fragmin). Thus, in the femoral artery of the rabbit, Fragmin, unlike standard heparin, was found to prevent reocclusion following rt-PA thrombolysis.

Animals↗
PubMed1994

Does external ultrasound accelerate thrombolysis? Results from a rabbit model.

BACKGROUND: Prior in vitro and in vivo studies have reported that external ultrasound accelerates thrombolysis at intensities too low to have a direct effect on clot dissolution in the absence of a thrombolytic agent. The present study was undertaken to examine the ultrasound effect on thrombolysis and reocclusion in a rabbit thrombosis model. METHODS AND RESULTS: Blood clots were produced in a femoral artery segment with endothelial damage and distal stenosis. Recombinant tissue-type plasminogen activator (rTPA) was infused at 30 micrograms.kg-1.min-1 for 60 minutes. Femoral artery flow was measured every 5 minutes for 2 hours. Rabbits were randomized to four groups with continuous wave ultrasound on or off with or without intravenous injection of 17 mg/kg aspirin (+US/-US/+Asp/-Asp). Ultrasound frequency and intensity were 1 MHz and 6.3 W/cm2. In seven of eight and five of five rabbits given rTPA and -US/-Asp or -US/+Asp, respectively, reflow was observed, persisting to the end of the observation period. In five of nine and four of five rabbits given rTPA and +US/-Asp or +US/+Asp, reflow was achieved, but persistent reocclusion was subsequently observed in five of five and two of four of these rabbits, respectively. Overall, femoral artery patency was worse and reocclusion occurred more often when ultrasound was added to rTPA (P = .002 by nonparametric ANOVA). However, initial reflow occurred more rapidly with ultrasound exposure (21 +/- 10 and 33 +/- 6 minutes for the +US/+Asp and +US/-Asp groups, respectively) compared with without ultrasound (46 +/- 13 and 74 +/- 14 minutes for the -US/+Asp and -US/-Asp groups, respectively) (P = .03 by ANOVA). CONCLUSIONS: Although time to initial reflow was shortened by ultrasound, it was associated with less reperfusion and more reocclusion in this model. A possible explanation for these results is ultrasound-induced platelet activation counterbalancing its thrombolysis-accelerating effect.

Animals↗
PubMed1994

Electrical injury in the femoral artery of rabbits as a model for arterial thrombosis: a pilot study.

Electrical stimulation was delivered to the femoral artery of 20 rabbits to examine whether endothelial injury results in a consistent formation of arterial thrombosis. The arterial patency was monitored throughout the experiment by flowmeter and was visualized by femoral angiography in 5/20 cases. The arterial segments remained totally occluded in 7/20 (35%), partially occluded in 9/20 (45%), and patent in 4/20 (20%) rabbits following stimulation with 200 microA anodal current for 180 minutes. The average time of electrical stimulation needed to achieve total occlusion (n = 7) was 110 +/- 49 minutes. Alternating occlusion and recanalization of the artery (cyclic flow variation) was observed in 12 rabbits, with total occlusion ensuing in 6/12 cases. Intravenous administration of recombinant tissue-type plasminogen activator (20 micrograms/kg/min for sixty minutes) resulted in femoral reflow and subsequent reocclusion in 2/5 cases. Histopathologic examination disclosed arterial thrombi composed of platelets, fibrin, and red blood cells. Thus, according to these data this technique was found to induce arterial thrombosis following electrical stimulation of the rabbit femoral artery but was inconsistent regarding the arterial patency.

Animals↗