The association of ABO and Rhesus blood type with the risks of developing SARS-CoV-2 infection: A meta-analysis.

Coronavirus Disease 2019 (COVID-19) has been spreading like a wildfire everywhere in the globe. It has been challenging the global health care system ever since the end of 2019, with its virulence and pathogenicity. Recent studies have shown the association between ABO blood group, Rhesus blood type and susceptibility to COVID-19 infection. Various studies and few meta-analyses have been done and some might be inconsistent; therefore, this meta-analysis was done to assess the relationship between different ABO and Rhesus blood types on the susceptibility to COVID-19 infections. This meta-analysis assessed the odds ratio of COVID-19 infection of different ABO and Rhesus blood types. Subgroup analyses according to (1) age and gender matched; (2) different blood group antigens; (3) Rhesus positive and negative of each blood group were carried out. Publication bias and Quality Assessment of Diagnostic Accuracy Studies-2 (QUADAS-2) were also done to assess the risk of bias in these publications. It was found that blood group A showed significant difference in odds ratio of COVID-19 infection (OR, 1.16; 95% CI, 1.08-1.24). Blood group AB showed significant difference in odds ratio when studies with lower QUADAS-2 score were removed. This means that populations with blood group A and AB are more likely to be infected with COVID-19. As there is a higher tendency that blood group A and AB to be infected with COVID- 19, precautious care should be taken by these populations.

Monitoring of toxic substances in the Hong Kong marine environment.

A long-term programme for monitoring toxic substances in the marine environment was established in Hong Kong in 2004, focusing on chemicals of potential ecological and health concern. The programme ran on 3-year cycles, with the first two years monitoring marine water, sediment, biota, and the third year monitoring pollution sources. Twenty-four priority chemicals were measured, including dioxins/furans, dioxin-like PCBs, total PCBs, PAHs, DDTs, HCHs, TBTs, phenol, nonylphenol (NP), NP ethoxylates, PBDEs and metals. Results from the first three years of monitoring indicate that toxic substances in the Hong Kong marine environment were within the range reported for the coastal waters in China and other regions, but generally lower than in the Pearl River Estuary. The levels met the standards for protecting aquatic life and human consumption. Sewage effluent, stormwater and river water were possible sources of phenolic compounds; whereas air deposition or regional pollution, rather than local discharges, may contribute to the dioxins/furans, PAHs and PCBs found in the marine environment.

Nitroglycerin rebound associated with vascular, rather than platelet, hypersensitivity.

OBJECTIVES: The purpose of this study was to determine whether acute withdrawal of nitroglycerin (NTG) during hemodynamic tolerance is associated with platelet hypersensitivity. BACKGROUND: Nitroglycerin is an effective antianginal medication but its use is limited by the development of tolerance and rebound. We have previously demonstrated a sustained inhibition of platelet function during continued use of NTG, but whether cessation of NTG is associated with an increase in platelet function that may contribute to rebound is unknown. METHODS: Normal porcine aortic media were exposed to flowing arterial blood from pigs (n = 8) treated continuously with NTG patches (Nitrodur 0.8 mg/h) for 48 h. Platelet function, blood pressure and the responses to angiotensin II infusion were evaluated before, during and after NTG treatment. RESULTS: Mean arterial pressure fell by 15% after 3 h of treatment compared with control, returned to baseline by 48 h and increased significantly 2 h after drug removal. Autologous 51Cr-labelled platelet deposition on the aortic media was reduced by 30% after 48 h of continuous NTG administration compared with baseline (p = 0.02) and remained decreased 2 h after cessation of NTG therapy. Platelet aggregation to thrombin decreased in parallel to the decrease in platelet deposition. Blood pressure increase after intravenous injection of 10 microg of angiotensin II was blunted during treatment with NTG but increased significantly 2 h after cessation of nitrate therapy when compared with baseline. CONCLUSIONS: Supersensitivity of the vessel wall to vasoconstrictors such as angiotensin 11, but not platelet hyperactivity, may contribute to the rebound phenomenon after acute nitrate withdrawal.

The pathogenesis and prevention of aortocoronary vein bypass graft occlusion and restenosis after arterial angioplasty: role of vascular injury and platelet thrombus deposition.

Vascular injury during aortocoronary vein bypass graft surgery and arterial angioplasty initiates platelet thrombus deposition and mandates antithrombotic therapy, starting before the procedures to maximize protection against occlusion. This has been shown in studies in animals and in patients undergoing aortocoronary vein bypass graft operation where dipyridamole therapy was started before the operation, heparin was given intraoperatively and combined dipyridamole and aspirin therapy was started 7 hours after operation and markedly reduced vein graft occlusion in patients with grafts at both high and low risk for occlusion without increasing bleeding. Other alternative regimens, particularly preoperative dipyridamole followed postoperatively with aspirin alone, offer a promising future. Therapy should be continued for at least 1 year and perhaps indefinitely. Control of coronary risk factors appears important for long-term therapy to try to retard the atherosclerotic and occlusive process that leads to approximately 50% vein graft attrition by 10 years after operation. The possible role of cod liver oil and internal mammary artery bypass is discussed. Arterial angioplasty appears to cause deep arterial injury that activates both platelets and the coagulation system. These potentiate each other to form macroscopic mural thrombus within 1 hour in more than 90% of arteries that manifested deep arterial injury in pigs. Acute platelet thrombus deposition was retarded but not eliminated by only certain platelet-inhibitor agents. Implications for ongoing trials, current empiric therapy and future therapy are discussed.

Exogenous prostacyclin decreases vasoconstriction but not platelet thrombus deposition after arterial injury.

OBJECTIVES: The aim of this study was to examine the in vivo effects of increasing doses of prostacyclin (PGI2) on arterial vasoconstriction, platelet deposition and their interrelation after balloon injury of porcine carotid arteries. BACKGROUND: Extensive platelet deposition and localized vasoconstriction occur acutely after arterial injury in vivo. The platelet deposition and vasoconstriction are directly correlated, and previous studies suggest that platelets may mediate the vasoconstrictive response. However, it is unclear whether vasoconstriction contributes to platelet deposition. METHODS: Seven pigs received an intravenous infusion of PGI2 at 10 ng/kg per min (PGI2 10), 8 pigs at 50 ng/kg per min (PGI2 50) and 4 pigs at 500 ng/kg per min (PGI2 500); 24 pigs with saline infusion served as a control group. RESULTS: Vasoconstriction immediately proximal and distal to the balloon-dilated carotid arterial segment where selective endothelial injury occurred was directly related to indium-111-labeled platelet deposition within the dilated segment in both control pigs and PGI2-treated pigs. However, this relation was such that for any given level of platelet deposition relative to control, PGI2 decreased vasoconstriction in a dose-related manner. None of the treatments (PGI2 10, 50 or 500) decreased quantitative 111In-labeled platelet deposition or the proportion of deeply injured arteries with mural thrombus (91%, 70% or 75%, respectively, p = NS) compared with values in control pigs (81%). Thus, vasoconstriction was directly related to platelet deposition in control and PGI2-treated animals, but vasodilation alone did not decrease platelet deposition. CONCLUSIONS: Intravenous infusion of PGI2 significantly decreases vasoconstriction but not platelet deposition or mural thrombosis after arterial injury by balloon dilation. It is therefore unlikely that vasoconstriction mediates platelet deposition in this model. At hemodynamically tolerated doses, PGI2 infusion probably will not prevent the thrombotic complications associated with angioplasty.

Deep arterial injury during experimental angioplasty: relation to a positive indium-111-labeled platelet scintigram, quantitative platelet deposition and mural thrombosis.

Although it is not clear why coronary occlusion and restenosis occur after successful coronary angioplasty, factors related to the procedure may influence early and late results. The possible adverse effects of a medial tear documented histologically and produced during balloon angioplasty of the common carotid arteries were studied in 30 fully heparinized (100 U/kg body weight) normal pigs. Scanning electron microscopy showed endothelial denudation and extensive platelet deposition in all dilated arterial segments. Visible macroscopic mural thrombus was present within an hour of the procedure in 29 (91%) of the 32 arteries that had a medial tear documented by histologic study; the tear produced an indium-111-labeled platelet deposition of 116.4 +/- 26.5 X 10(6)/cm2 (mean +/- SE) and total thrombotic occlusion in 2 arteries (4%). None of the 24 arteries without a medial tear had a thrombus, and the mean platelet deposition in that group was 7.0 +/- 0.5 X 10(6)/cm2 (p less than 0.0008). In 12 pigs scanned with a gamma camera, visible thrombus was associated with platelet deposition in excess of 20 X 10(6)/cm2 in 12 arteries, 9 of which had a positive indium-111-labeled platelet scintigram. Thus, arterial angioplasty causes deep arterial injury, which appears to be a major cause of mural thrombosis, heavy platelet deposition, a positive indium-111-labeled platelet scintigram and acute arterial occlusion. A positive indium-111-labeled platelet scintigram was always associated with macroscopic thrombus of at least 20 > 10(6) platelets/cm2 and underlying deep arterial injury.

Methylene blue inhibits the antithrombotic effect of nitroglycerin.

OBJECTIVES: The aim of this study was to examine whether cyclic guanosine monophosphate (GMP) may be involved in the antithrombotic action of nitroglycerin. BACKGROUND: Nitroglycerin has been shown to inhibit platelet function in vitro by stimulating prostacyclin or inhibiting thromboxane A2 production, or both. Nitroglycerin has also been shown to possess potent antithrombotic properties in vivo. However, the mechanism of this antithrombotic effect is unclear. METHODS: Nitroglycerin was infused to produce a 10% decrease in mean arterial pressure in 27 normal pigs by exposing their circulating arterial blood to porcine aortic media in an ex vivo perfusion chamber. Eight pigs received an infusion of nitroglycerin alone; eight received an infusion of methylene blue, a guanylate cyclase inhibitor, followed by nitroglycerin infusion and five pigs received an infusion of nitroglycerin followed by methylene blue and subsequent infusion of cyclic GMP. RESULTS: With nitroglycerin alone, quantitative autologous indium-111-labeled platelet deposition (x10(6) on the aortic media was decreased to 63.9 +/- 10.4% (p = 0.01) of the baseline control platelet deposition. Methylene blue given before nitroglycerin tended to increase platelet deposition relative to baseline and platelet deposition after nitroglycerin was 142 +/- 35% (p = NS) of baseline value. In pigs that received all three agents, nitroglycerin reduced platelet deposition to 42.3 +/- 12.2% of baseline value; this decrease was then attenuated by subsequent methylene blue infusion but was enhanced by cyclic GMP infusion to 16.4 +/- 3.8% of baseline value (p = 0.006 vs. baseline control and p = 0.02 versus methylene blue infusion). CONCLUSIONS: Guanylate cyclase inhibition with methylene blue abolishes the antithrombotic effect of nitroglycerin, which can be enhanced by cyclic GMP.

Safety and diagnostic accuracy of dipyridamole-thallium imaging in the elderly.

The noninvasive diagnosis of coronary artery disease in the elderly can occasionally be difficult. Intravenous dipyridamole-thallium imaging is a potentially useful diagnostic test to determine presence and severity of coronary disease; however, the safety of the procedure has not been determined in an older population. The side effect profile and frequency of severe ischemic responses after 0.56 mg/kg of intravenous dipyridamole were compared in 101 patients greater than or equal to 70 years old and 236 patients less than 70 years old. There were no side effects in 64% and 62% of patients greater than or equal to 70 and less than 70 years old, respectively (p = NS). Among the 337 patients tested, there were no complications of myocardial infarction or death. The most common cardiac side effect was chest pain, which occurred in 21 (21%) of the 101 patients aged greater than or equal to 70 years and in 64 (27%) of the 236 patients less than 70 years (p = NS). Aminophylline was required to reverse cardiac or noncardiac side effects in 15 (15%) and 36 (15%) of the patients greater than or equal to 70 and less than 70 years old, respectively (p = NS). A severe ischemic response occurred in 2% and 2.5% of patients greater than or equal to 70 and less than 70 years old, respectively (p = NS). The sensitivity of intravenous dipyridamole-thallium imaging for obstructive coronary artery disease was 86% (25 of 29) and 83% (68 of 82) in older and younger patients, respectively (p = NS); the specificity was 75% (6 of 8) and 70% (16 of 23), respectively (p = NS). Thus, intravenous dipyridamole-thallium imaging is a safe noninvasive method for assessment of older patients with obstructive coronary disease; its side effect profile and diagnostic accuracy are similar to those seen in younger patients. The technique is associated with severe ischemic responses in only a small minority of patients.

Acute and delayed antithrombotic effects of alcohol in humans.

Alcohol intake, especially in the form of red wine, has been shown to inhibit platelet function. However, whether alcohol in spirits may inhibit platelet-dependent thrombosis in humans up to 6 hours after ingestion is unknown and was assessed in this study. Platelet thrombus that is formed on exposure of an aortic media (simulating deep arterial injury or plaque rupture) to flowing blood was assessed in an ex vivo Badimon's superfusion chamber at shear rates of 754 or 2,546 seconds(-1) (simulating flow in normal or stenosed arteries). Twelve healthy subjects were studied before and at 20 minutes and 6 hours after consumption of 2 ounces of 40% alcohol. Blood alcohol level was 1.1+/-0. 1, 8.2+/-0.7, and 1.3+/-0.2 mmol/L at baseline, 20 minutes and 6 hours, respectively, after alcohol consumption (analysis of variance [ANOVA] p = 0.0001). Compared with baseline, platelet thrombus formation at the low shear rate flow was significantly decreased by 57% and 61% at 20 minutes and 6 hours, respectively, after alcohol intake (ANOVA p = 0.0001). Platelet thrombus deposition at the high shear rate was similarly inhibited to 68% and 64% of baseline values at 20 minutes and 6 hours, respectively (ANOVA p = 0.003). Men and women showed equal benefit. Thus, moderate alcohol intake in humans significantly inhibited platelet thrombus deposition under low and high shear rates of arterial flow conditions. This antithrombotic effect of a single alcohol drink, persisting for 6 hours and even after blood alcohol level has returned to baseline, may be clinically relevant to the cardioprotective effects of alcohol in men and women.

Platelet aggregation, coronary artery disease progression and future coronary events.

The platelet-aggregatory response, platelet-release factors and markers of thrombin generation in vivo were studied prospectively in 53 patients participating in a randomized clinical trial evaluating the influence of nicardipine on the progression of coronary atherosclerosis. Coronary lesions were measured quantitatively and progression was defined as a decrease in minimum diameter by > or = 0.4 mm. At repeat angiography 24 months after study entry, 20 of the 53 patients had progression of 28 coronary narrowings. Only thrombin-induced enhanced platelet aggregation differentiated patients with from those without coronary disease progression, with an estimated odds ratio of 2.49 (95% confidence interval 1.10 to 5.66). The aggregatory response to adenosine diphosphate, collagen, epinephrine and platelet-activating factor were not different in the 2 groups of patients, nor were measurements of platelet factor 4, beta-thromboglobulin, thromboxane B2, 6-keto-prostaglandin F1 alpha and fibrinopeptide A. During 46.8 months of follow-up after repeat angiography, coronary events occurred in 11 of the 20 with and 6 of the 33 without progression (difference 37%, p = 0.013, confidence interval 11 to 63%). Those with coronary disease progression and an enhanced thrombin-induced platelet aggregation had a worse prognosis than those with no disease progression and a low thrombin-induced platelet aggregation. Thus, patients with coronary disease progression and future coronary events have an enhanced thrombin-induced platelet aggregation. This platelet abnormality may be a marker of increased risk and may play a causative role in the development of coronary events.

Restenosis after arterial angioplasty: a hemorrheologic response to injury.

Restenosis after arterial angioplasty appears to be a response to deep arterial injury, which is much more thrombogenic than superficial injury (endothelial denudation). Deep arterial injury exposes collagen, elastin and smooth muscle cells to circulating blood, releases tissue thromboplastin and causes immediate platelet-thrombus deposition as a result of activation of platelets and the clotting system, both of which mutually facilitate activation of the other. Regrowth of endothelium also is protective against platelet deposition. Platelet adherence to collagen, and thus to the arterial wall that is deeply injured, increases with shear rate (related inversely to the fourth power of luminal cross-sectional area and directly to blood flow); thus, the effect of shear rate increases the importance of adequate dilatation at the time of the procedure. Therapy that will reduce acute platelet-thrombus deposition appears to be an important factor for reduction of restenosis. Vasoconstriction occurs experimentally after arterial angioplasty in arterial segments proximal and distal to the dilated segment where there has been no necrosis of smooth muscle cells. The vasoconstriction is directly related to the severity of platelet deposition, can be reduced by reducing platelet deposition with low dose aspirin (1 mg/kg daily) and is probably mediated by vasoconstrictor substances from platelets (thromboxane A2, serotonin and other substances). Platelet-membrane receptor inhibitors to these substances reduce the vasoconstriction but do not reduce platelet deposition. Therapeutic intervention should probably involve both anticoagulation and platelet inhibition. Platelet-membrane receptor inhibition to the fibrinogen receptor, factor VIII-von Willebrand factor or both may be necessary acutely to sufficiently reduce acute platelet-thrombus deposition.

Antithrombotic properties of transdermal nitroglycerin in stable angina pectoris.

Nitroglycerin provides an external source of nitric oxide which stimulates guanylate cyclase and produces vasodilatation and inhibition of platelet function. The antithrombotic effects of intravenous nitroglycerin were recently documented in various experimental models and in patients with unstable angina. This protocol was designed to evaluate whether these effects could also be detected with transdermal nitroglycerin in patients with stable angina. In a randomized, double-blind, controlled parallel trial, 22 patients received transdermal nitroglycerin, 0.6 mg/hour (11 patients), or placebo (11 patients). Platelet aggregation to adenosine diphosphate (ADP) and to thrombin was measured in whole blood. Thrombus formation was assessed on porcine aortic media exposed to the patient's venous blood for 3 minutes at shear rates of 2,546 and 754 s-1. Platelet aggregation to ADP decreased from 7.7 +/- 0.8 to 5.3 +/- 0.8 ohms (p < 0.05) with nitroglycerin, and to thrombin from 15.6 +/- 1.2 to 12 +/- 1.2 ohms (p < 0.05). Thrombus size at the high-shear rate decreased from 2.8 +/- 0.7 to 1.0 +/- 0.3 microns 2 (p < 0.05), and at the low-shear rate from 2.5 +/- 0.5 to 1.0 +/- 0.2 microns 2 (p < 0.05). Placebo had no significant effect on platelet aggregation and platelet thrombus deposition. These parameters were all reduced by > or = 20% in 8 patients taking nitroglycerin but only in 3 patients taking placebo (p < 0.05). Transdermal nitroglycerin significantly inhibits platelet aggregation and mural thrombus formation in patients with angina pectoris.

Effects of nitroglycerin at therapeutic doses on platelet aggregation in unstable angina pectoris and acute myocardial infarction.

The platelet aggregation response to adenosine diphosphate (ADP) and to thrombin was quantified in 10 patients, 5 with unstable angina pectoris and 5 with acute myocardial infarction, before, during and after a 45-minute infusion of nitroglycerin. An impedance aggregometer allowing rapid bedside studies in whole blood was used. The reproducibility of the methods was documented to be within 10%. Doses of nitroglycerin were titrated for a 10 mm Hg decrease in mean arterial blood pressure with mean doses being 1.2 +/- 0.2 (standard error of the mean) micrograms/kg/min. Nitroglycerin decreased the area under the aggregation curve induced by ADP from 43 +/- 3.6 to 30 +/- 6.3 cm2 (p = 0.007) and by thrombin from 8.9 +/- 1.7 to 4.1 +/- 0.9 cm2 (p = 0.003). Peak responses to ADP were decreased from 13.3 +/- 1 to 9.1 +/- 1.7 ohms (p = 0.005) and to thrombin from 9.3 +/- 2 to 5.0 +/- 1.2 ohms (p = 0.003). All patients had greater than or equal to 50% inhibition with 1 agent or the other and the inhibition was greater than 50% with each of the 2 aggregating agents in 6 patients. Analyses performed on blood withdrawn 15 minutes after the discontinuation of nitroglycerin showed a return to baseline before nitroglycerin results. When analyses were delayed and performed on blood preserved at room temperature for 30 minutes, no effect of nitroglycerin could be detected. Thus, bedside platelet aggregation studies document a significant and reversible effect of nitroglycerin at therapeutic doses on platelet function.

A pilot trial of non-invasive home ventilation after acidotic respiratory failure in chronic obstructive pulmonary disease.

BACKGROUND: Patients with chronic obstructive pulmonary disease (COPD) who survive an episode of acute hypercapnic respiratory failure (AHRF) after treatment with non-invasive ventilation (NIV) have a high risk of recurrent AHRF. We hypothesised that continuation of NIV at home in these patients would reduce the likelihood of recurrent AHRF. METHODS: A pilot prospective randomised controlled study was designed to compare continuation of active home NIV and continuous positive airway pressure (CPAP) 5 cm H(2)O (controls) in COPD patients who had survived an episode of AHRF treated with acute NIV. Patients with significant obstructive sleep apnoea, non-COPD causes of AHRF, adverse psychosocial circumstances and serious comorbidities were excluded. The primary end-point was recurrent AHRF requiring acute NIV, intubation or resulting in death in the first year. RESULTS: Twenty-three patients were randomised to receive home NIV and 24 received CPAP. There was no significant difference in the baseline characteristics between the two study groups. The proportion of patients developing recurrent AHRF in the NIV and the CPAP groups was 38.5% vs. 60.2% at 1 year (P = 0.039). Four and eight patients, respectively, were withdrawn from the CPAP and NIV groups before the end of the pre-defined study duration. CONCLUSIONS: In selected COPD patients with AHRF treated with acute NIV, continuation with home NIV is associated with a lower risk of recurrent severe COPD exacerbation with AHRF when compared with CPAP.

Major haemoptysis in Hong Kong: aetiologies, angiographic findings and outcomes of bronchial artery embolisation.

SETTING: Tertiary referral centres. OBJECTIVE: To provide comprehensive updates on the aetiologies, angiographic findings and outcomes of bronchial artery embolisation (BAE) for life-threatening haemoptysis in Hong Kong. DESIGN: Retrospective review of clinical records of consecutive patients presenting with life-threatening haemoptysis from 2000 to 2006. RESULTS: There were 3006 admissions due to haemoptysis involving 2260 patients during the study period; of these, 251 patients had life-threatening haemoptysis. Pulmonary tuberculosis (PTB) (active or inactive) and bronchiectasis were the main underlying causes. BAE was attempted in 167 patients. There was a high prevalence of bilateral bronchial arterial abnormalities (31.7%), presence of abnormal non-bronchial arteries (41.3%) and presence of broncho-pulmonary shunt (38.9%). BAE had a high immediate success rate of 95.7%, with a 5-year recurrence rate of 45.0%. Recurrent life-threatening haemoptysis was independently associated with past history of haemoptysis (P = 0.024), presence of broncho-pulmonary shunt (P = 0.013), and incomplete embolisation (P = 0.002). Complications were uncommon (<5%) and self-limiting. CONCLUSIONS: In Hong Kong, about one tenth of admissions due to haemoptysis were life-threatening. PTB and bronchiectasis were the major causes. Complications due to BAE were uncommon and self-limiting, with super-selective catheters.

Duration of RT-PCR positivity in severe acute respiratory syndrome.

Severe acute respiratory syndrome (SARS) is a highly infectious respiratory infection with a high mortality. The duration of infectivity is unknown. The RT-PCR positivity for SARS-associated coronavirus (SARS-CoV) was followed in 45 virologically confirmed SARS patients. Serial RT-PCRs for SARS-CoV were performed in the nasopharyngeal aspirate, stool and urine of 45 SARS patients who survived until discharge. All patients had at least one site that was positive for SARS-CoV on presentation. Time to RT-PCR conversion was studied in all patients. There were 15 males (33.3%) and 30 females (66.7%), with a mean+/- SD age of 40.7+/-14.7 yrs. The median (range) time of RT-PCR conversion was 30 days (2-81). On discharge from the hospital, 18 (40%) remained RT-PCR positive in at least one site. For patients with positive RT-PCR on discharge, the median (range) time to RT-PCR conversion after discharge was 13 days (2-60). A significant proportion of severe acute respiratory syndrome patients remained RT-PCR positive for severe acute respiratory syndrome-associated coronavirus for a substantial duration after discharge. The clinical significance is unknown and this finding merits further study. It is prudent to advise patients to adhere to strict personal hygiene on discharge until RT-PCR becomes negative.

[Not Available]. / Le rôle de l'aspirine dans la maladie coronarienne.

Antiplatelet agents are effective in reducing mortality and the incidence of infarction in patients with unstable angina and in reducing cardiovascular mortality and reinfarction in cases of acute myocardial infarction. Individuals with multiple risk factors who are likely to develop coronary disease could benefit from prophylactic treatment with these agents.

Neutrophil implications in platelet deposition and vasoconstriction after deep arterial injury by angioplasty in pigs.

BACKGROUND: Experimental studies in vitro suggest that neutrophils can modulate platelet function and vasomotor responses. In the present study, the interactions among neutrophils, platelets, and arterial responses to injury in vivo were assessed. METHODS AND RESULTS: The acute thrombotic and vasomotor responses of porcine carotid arteries to balloon injury in vivo were evaluated in three groups of animals: neutropenic pigs treated (n = 11) or not treated (n = 12) with aspirin and healthy untreated control pigs (n = 15). Neutropenia was achieved by treatment with cyclophosphamide (50 mg/kg, 4 days before the experiment), which decreased circulating leukocyte count by 92% and almost abolished neutrophil aggregation to N-formyl-methionyl-leucyl-phenylalanine without affecting blood platelet count, hematocrit, hemoglobin concentration, or whole blood platelet aggregation to ADP. 51Cr platelet deposition on deeply injured and uninjured arterial segments was not statistically influenced by neutrophil depletion, whereas the angiographic vasoconstrictive response at the site of endothelial injury distally was significantly reduced by 41% from 46.3 +/- 2.9% in the control group to 27.2 +/- 4.1% in the neutropenic group (P < .05). Aspirin treatment in combination with neutropenia produced a 50% reduction in whole blood platelet aggregation, resulted in a significant inhibition of platelet deposition to deeply injured arteries, and decreased vasoconstriction by 66% to 15.6 +/- 3.0% (P < .05 versus control and neutropenic). CONCLUSIONS: Neutrophils can influence the vasoconstrictive response at the site of endothelial injury in vivo. In addition to platelets, neutrophil interaction with the injured vessel wall may be implicated in the pathophysiological response to arterial injury in vivo.