Platelet count and function at high altitude and in high-altitude pulmonary edema

2006 ◽  
Vol 100 (2) ◽  
pp. 690-694 ◽  
Author(s):  
T. Lehmann ◽  
H. Mairbäurl ◽  
B. Pleisch ◽  
M. Maggiorini ◽  
P. Bärtsch ◽  
...  
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Platelet Function ◽  
Altitude Exposure ◽  
High Altitude Pulmonary Edema ◽  
Function Analyzer ◽  
History Of ◽  
Platelet Function Analyzer

Platelet aggregation is the key process in primary hemostasis. Certain conditions such as hypoxia may induce platelet aggregation and lead to platelet sequestration primarily in the pulmonary microcirculation. We investigated the influence of high-altitude exposure on platelet function as part of a larger study on 30 subjects with a history of high-altitude pulmonary edema (HAPE) and 10 healthy controls. All participants were studied in the evening and the next morning at low altitude (450 m) and after an ascent to high altitude (4,559 m). Platelet count, platelet aggregation (platelet function analyzer PFA100; using epinephrine and ADP as activators), plasma soluble P (sP)-selectin, and the coagulation parameters prothrombin fragments 1+2 and thrombin-antithrombin complex were measured. High-altitude exposure decreased the platelet count, shortened the platelet function analyzer closure time by ∼20%, indicating increased platelet aggregation, increased sP-selectin levels to ∼250%, but left plasma coagulation unaffected. The HAPE-susceptible subjects were prophylactically treated with either tadalafil (a phosphodiesterase 5 inhibitor), dexamethasone, or placebo in a double-blind way. Subgroup analyses between these different treatments and comparisons of the seven placebo-treated individuals developing HAPE and controls revealed no differences in platelet count, platelet aggregation, or sP-selectin values. We conclude that exposure to high altitude activates platelets, which leads to platelet aggregation, platelet consumption, and decreased platelet count. These effects are, however, not more pronounced in individuals with a history of HAPE or actually suffering from HAPE than in controls and therefore may not be a pathophysiological mechanism of HAPE.

scholarly journals Hypoxia-Induced Inflammatory Chemokines in Subjects with a History of High-Altitude Pulmonary Edema

2015 ◽  
Vol 31 (1) ◽  
pp. 81-86 ◽  
Author(s):  
K. P. Mishra ◽  
Navita Sharma ◽  
Poonam Soree ◽  
R. K. Gupta ◽  
Lilly Ganju ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
High Altitude Pulmonary Edema ◽  
Inflammatory Chemokines ◽  
History Of

Exercise-induced VA/Q inequality in subjects with prior high-altitude pulmonary edema

1996 ◽  
Vol 81 (2) ◽  
pp. 922-932 ◽  
Author(s):  
A. Podolsky ◽  
M. W. Eldridge ◽  
R. S. Richardson ◽  
D. R. Knight ◽  
E. C. Johnson ◽  
...  
Keyword(s):  
Standard Deviation ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Control Group ◽  
Pulmonary Capillary ◽  
High Altitude Pulmonary Edema ◽  
History Of ◽  
Capillary Pressures ◽  
Exercise Induced

Ventilation-perfusion (VA/Q) mismatch has been shown to increase during exercise, especially in hypoxia. A possible explanation is subclinical interstitial edema due to high pulmonary capillary pressures. We hypothesized that this may be pathogenetically similar to high-altitude pulmonary edema (HAPE) so that HAPE-susceptible people with higher vascular pressures would develop more exercise-induced VA/Q mismatch. To examine this, seven healthy people with a history of HAPE and nine with similar altitude exposure but no HAPE history (control) were studied at rest and during exercise at 35, 65, and 85% of maximum 1) at sea level and then 2) after 2 days at altitude (3,810 m) breathing both normoxic (inspired Po2 = 148 Torr) and hypoxic (inspired Po2 = 91 Torr) gas at both locations. We measured cardiac output and respiratory and inert gas exchange. In both groups, VA/Q mismatch (assessed by log standard deviation of the perfusion distribution) increased with exercise. At sea level, log standard deviation of the perfusion distribution was slightly higher in the HAPE-susceptible group than in the control group during heavy exercise. At altitude, these differences disappeared. Because a history of HAPE was associated with greater exercise-induced VA/Q mismatch and higher pulmonary capillary pressures, our findings are consistent with the hypothesis that exercise-induced mismatch is due to a temporary extravascular fluid accumulation.

Blunted hypoxic ventilatory drive in subjects susceptible to high-altitude pulmonary edema

1989 ◽  
Vol 66 (3) ◽  
pp. 1152-1157 ◽  
Author(s):  
Y. Matsuzawa ◽  
K. Fujimoto ◽  
T. Kobayashi ◽  
N. R. Namushi ◽  
K. Harada ◽  
...  
Keyword(s):  
Pulmonary Function ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Pulmonary Function Test ◽  
Ventilatory Response ◽  
Hypoxic Ventilatory Response ◽  
High Altitude Pulmonary Edema ◽  
Function Test ◽  
History Of ◽  
Low Altitude

It has been proposed that subjects susceptible to high-altitude pulmonary edema (HAPE) show exaggerated hypoxemia with relative hypoventilation during the early period of high-altitude exposure. Some previous studies suggest the relationship between the blunted hypoxic ventilatory response (HVR) and HAPE. To examine whether all the HAPE-susceptible subjects consistently show blunted HVR at low altitude, we evaluated the conventional pulmonary function test, hypoxic ventilatory response (HVR), and hypercapnic ventilatory response (HCVR) in ten lowlanders who had a previous history of HAPE and compared these results with those of eight control lowlanders who had no history of HAPE. HVR was measured by the progressive isocapnic hypoxic method and was evaluated by the slope relating minute ventilation to arterial O2 saturation (delta VE/delta SaO2). HCVR was measured by the rebreathing method of Read. All measurements were done at Matsumoto, Japan (610 m). All the HAPE-susceptible subjects showed normal values in the pulmonary function test. In HCVR, HAPE-susceptible subjects showed relatively lower S value, but there was no significant difference between the two groups (1.74 +/- 1.16 vs. 2.19 +/- 0.4, P = NS). On the other hand, HAPE-susceptible subjects showed significantly lower HVR than control subjects (-0.42 +/- 0.23 vs. -0.87 +/- 0.29, P less than 0.01). These results suggest that HAPE-susceptible subjects more frequently show low HVR at low altitude. However, values for HVR were within the normal range in 2 of 10 HAPE-susceptible subjects. It would seem therefore that low HVR alone need not be a critical factor for HAPE. This could be one of several contributing factors.

scholarly journals Poor Platelet Function on Sonoclot Signature Is Associated with High Incidence of Bleeding in Severe Immune Thrombocytopenia

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 4991-4991 ◽  
Author(s):  
Kundan Mishra ◽  
Aditya Jandial ◽  
Rajeev Sandal ◽  
Pradakshna Porchezhian ◽  
Samson Charan ◽  
...  
Keyword(s):  
Platelet Count ◽  
Platelet Function ◽  
Immune Thrombocytopenia ◽  
Blood Samples ◽  
Risk Of Bleeding ◽  
Normal Platelet ◽  
Function Analyzer ◽  
Clinically Significant ◽  
Platelet Function Analyzer

Abstract Introduction: Patients of immune thrombocytopenia (ITP) are at an high risk of bleeding, and the risk of bleeding is maximum when platelet counts fall below 30,000/μL (severe ITP). Though it is not known not all patients have a similar risk of bleeding at a given platelet count. In 59th ASH annual meeting, 2017 (poster 2320) Mishra K et al showed that the platelet function measured by 'Sonoclot coagulation and platelet function analyzer' is significantly different in bleeders as compared to non-bleeders severe ITP patients. We aimed to investigate and follow up the non-bleeder severe ITP patients, whose platelet count remains <30,000 with or without treatment, and find out the incidence of bleed. Method: The study was conducted at the department of internal medicine, postgraduate institute of medical education and research, Chandigarh, India. In this prospective observational study, severe ITP (newly diagnosed) and without active bleeding (WHO bleeding grade <2) were included. All these patient were clinically evaluated, and blood samples were collected as per unit protocol for ITP including Sonoclot analysis. For Sonoclot analysis, fresh blood samples were drawn in citrated vacutainer and analyzed by Sonoclot coagulation and platelet function analyzer made by Sienco, Inc, model SCP1 (USA). The sonoclot signature assessment gives activated clotting time (ACT), clot rate (R1) and platelet function (PF). The samples for sonoclot analysis were monthly drawn for six months in patients who continued to have severe ITP. Results: A total of 50 patients with severe ITP were included. Twenty patients were not included in the final analysis as their platelet remained above 30,000/μL during follow up. The remaining 30 patients were divided into two groups based on normal platelet function (PF) (>1.5) and low PF (<1.5) as measured by the Sonoclot analyzer. The normal PF group (n= 17) had only one patient who had clinically significant bleeding (WHO grade > 2), while low PF group had four patients with clinically significant bleeding (Figure 1). Though the statistical significance level could not be achieved, likely due to a small cohort of patients, the results look promising and shows the potential of sonoclot to give valuable input regarding the risk of bleeding in severe ITP. Conclusion: The patients with poor platelet function as measured by 'Sonoclot coagulation and platelet function analyzer' had more bleeding episodes as compared to patients with normal platelet function. Therefore, Sonoclot may work as a point of care investigation to predict the risk of bleeding in severe ITP patients. This will help the clinician in being more conservative in the management of severe ITP patients with low risk of bleeding and avoid unnecessary therapy. We conclude that the use of Sonoclot during follow-up in severe ITP patients has prognostic significance. Disclosures No relevant conflicts of interest to declare.

scholarly journals Comparison of farmacodynamic properties of three different aspirin formualtions in patients with stable coronary disease

2019 ◽  
Vol 76 (6) ◽  
pp. 628-634
Author(s):  
Ana Antic ◽  
Zoran Stanojkovic ◽  
Miodrag Vucic ◽  
Milan Lazarevic ◽  
Nebojsa Vacic
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Dual Therapy ◽  
Impedance Aggregometry ◽  
Measured Time ◽  
Function Analyzer ◽  
Group 3 ◽  
Group 2 ◽  
Platelet Function Analyzer ◽  
Group 1

Background/Aim. The platelet aggregation, as a laboratory test for assessment of platelet function, is very efficient for optimal antiplatelet treatment and also to identify individuals who have suboptimal response to antiplatelet drugs, such as aspirin and clopidogrel. The aim of this study was to determine the level of inhibition of platelet aggregation using impedance aggregometry in the patients receiving different preparations of acetylsalicylic acid (ASA) in a dose of 100 mg per day. Methods. The examination included 215 patients (110 men and 105 women), treated with one of three different ASA preparations after acute myocardial infarction, as a single therapy or with clopidogrel. Among them, 89 patients were on Aspirin protect? (Bayer, Germany) ? Group 1 and 66 patients were on Cardiopirin? (GL Pharma GMBH, Austria) ? Group 2, while 60 patients were taking Andol? (Pliva, Croatia) ? Group 3. The groups were equal in the presence of factors that can influence platelet aggregation (age, gender, smoking, diabetes, taking other drugs). The platelet function was measured using the impedance aggregometer Multiplate (Multiplate Platelet Function Analyzer, Roche) in the blood samples with heparin for the platelet aggregation activated by the arachidonic acid (ASPI) and by thrombin (TRAP) tests [the area under the aggregation curve (AUC) was used to express the aggregation response over the measured time (AU*min)]. Results. Efficacy of ASA preparations showed statistically significant differences among the three investigated groups (?KW2 = 46.279; p < 0.001), and it was also observed separately in the patients undergoing single therapy (?KW2 = 26.344; p < 0.001) and dual therapy (?KW2 = 23.498; p < 0.001). It was found that the patients who were taking Aspirin protect? obtained significantly better antiplatelet efficiency compared to the patients receiving Cardiopirin? (Z = 5.472; p < 0.001) and Andol? (Z = 5.387; p = 0.022). There is reduced efficiency of all ASA preparations in smokers, while patients receiving Aspirin protect? were 10.5 times more likely to be responders. Conclusion. Different ASA preparations observed in this study showed different efficiency on the platelet function as measured by the method of impedance aggregometry.

Platelet function in cats with hyperthyroidism

2020 ◽  
Vol 22 (12) ◽  
pp. 1214-1218
Author(s):  
Elizabeth C Hiebert ◽  
David L Panciera ◽  
Katie M Boes ◽  
Lara Bartl
Keyword(s):  
Platelet Count ◽  
Platelet Function ◽  
Adenosine Diphosphate ◽  
Control Group ◽  
Closure Time ◽  
Function Analyzer ◽  
The Mean ◽  
Platelet Function Analyzer ◽  
Von Willebrand ◽  
Willebrand Factor

Objectives Cats with hyperthyroidism have been reported to develop thromboembolism, with and without echocardiographic abnormalities consistent with hyperthyroidism. The objective of this study was to compare platelet function in cats with hyperthyroidism with euthyroid age-matched cats. We hypothesized that cats with hyperthyroidism have shortened collagen and adenosine diphosphate (C-ADP) closure times as measured with the platelet function analyzer (PFA-100) in comparison with healthy, age-matched controls. Methods Sixteen hyperthyroid and nine euthyroid healthy cats >7 years of age were recruited from the hospital population. Platelet function, measured using the C-ADP closure times by the PFA-100, and platelet count were measured in healthy euthyroid cats and cats with hyperthyroidism. Results Mean ± SD closure times were not significantly different between control (66.3 ± 9.6 s) and hyperthyroid cats (65.9 ± 11.5 s; P = 0.75). The mean ± SD closure times of hyperthyroid cats that either were untreated or received methimazole for ⩽3 weeks (n = 6; mean 68.5 ± 15.4 s) was not different than that of cats treated for >3 weeks (n = 10; mean 64.3 ± 8.9 s; P = 0.57). The mean automated platelet count was higher in the hyperthyroid group than in the control group ( P = 0.023). Conclusions and relevance Platelet function, as measured by closure time under high shear conditions using C-ADP as an agonist, was not affected by hyperthyroidism in this group of cats. Further research is needed to determine if a hypercoagulable state exists in hyperthyroid cats and the potential roles platelets and von Willebrand factor may have.

scholarly journals Excessive Gas Exchange Impairment during Exercise in A Subject with A History of Bronchopulmonary Dysplasia And High Altitude Pulmonary Edema

2007 ◽  
Vol 8 (1) ◽  
pp. 62-67 ◽  
Author(s):  
Andrew T. Lovering ◽  
Lee M. Romer ◽  
Hans C. Haverkamp ◽  
John S. Hokanson ◽  
Marlowe W. Eldridge
Keyword(s):  
Gas Exchange ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Bronchopulmonary Dysplasia ◽  
High Altitude Pulmonary Edema ◽  
History Of
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