10 research outputs found
Evaluation of the genetic damage to workers in a Greek shipyard
Shipyards are industrial areas where workers are likely exposed to environmental pollutants such as welding fumes, fine organic solvent and dye dust, that render the occupational environment a high risk one. Assessing the risk that workers are exposed to is a high critical factor in improving their working conditions. The present study aims to investigate the potential genetic damage to workers exposed to a harsh environment in a Greek shipyard. It is focused on assessing the percentage of induced micronuclei, as well as on changes in the various cell types of shipyard workers’ oral mucosa epithelium by implementing the buccal micronucleus cytome assay. Exposed workers appeared with statistically significant induced micronuclei as compared to office employees. Statistically, significant cell lesions were detected and are related to workers’ exposure to environmental conditions. The workers’ smoking habit contributed as well to the observed buccal epithelial cell alterations. The observed data signify the high-risk workers are exposed; resulting in the shipyard’s management the need to implement measures improving the working environment conditions and to reevaluate the workers’ personal protective equipment requirements. ©️ 2022 National Institute of Occupational Safety and Health
TREATMENT OF HYPERTENSION WITH PERINDOPRIL PLUS INDAPAMIDE LEADS TO REVERSE CORONARY MICROVASCULAR REMODELLING AND IMPROVED BLOOD FLOW
3D.05 TREATMENT OF HYPERTENSION WITH PERINDOPRIL
PLUS INDAPAMIDE LEADS TO REVERSE CORONARY
MICROVASCULAR REMODELLING AND IMPROVED
BLOOD FLOW
P. Camici1, D. Neglia3, E. Fommei3, A. Varela-Carver1, M. Mancini2,
S. Ghione3, M. Lombardi3, H. Parker1, G. Damati2, L. Donato3. 1Imperial
College, London, United Kingdom, 2Universita’ La Sapienza, Roma, Italy, 3CNR
Institute of Clinical Physiology, Pisa, Italy
Rationale: The heart of patients with arterial hypertension (HT) is characterized
by structural and functional abnormalities of the microcirculation
which cause coronary microvascular dysfunction (CMD) and may contribute
to myocardial ischemia. Aim of the present study was to ascertain whether
treatment with a fixed combination of perindoprilþindapamide (PþI) in
patients withHTimprovesCMDas assessed by measuring myocardial blood
flow (MBF) noninvasively with positron emission tomography (PET). The
human study was complemented by further experiments in spontaneously
hypertensive rats (SHR) to ascertain whether treatment with the same drug
regimen can reverse anatomical remodelling of the coronary arterioles while
improving coronary flow (CF).
Methods and Results: In 20 HT patients with left ventricular hypertrophy,
blood pressure (BP), left ventricular mass index (LVMI) and resting and
hyperemic MBF were measured at baseline and after 6 months of therapy
with PþI. In SHR, BP was measured at baseline and after 8 weeks of
treatment with placebo or PþI. After sacrifice, baseline and hyperemic CF
(Langendorff) and histomorphometry of intramural coronary arterioles were
measured.
In patients, PþI decreased BP (16110/965 to 13612/816 mmHg;
p<0.0001) and LVMI (9316 to 8517 g/m2; p<0.01) whilst baseline
(0.690.13 to 0.880.36 ml/min/g; p<0.05) and hyperemic MBF
(1.420.32 to 1.940.99 ml/min/g; p<0.05) were increased. In SHR treated
with PþI (n¼11), BP was 9318/5518 compared to 21518/
16117 mmHg in the placebo (n¼6) group (p<0.001) whilst the ratio
of hyperemic/baseline CF was 3.971.15 and 1.910.19 respectively
(p<0.001). The medial area of intramural arterioles was 1613410 in
the PþI group and 104992152mm2 in the placebo (p<0.001).
Conclusions: In patients, treatment with PþI reduced BP and LVMI and
improved MBF, suggesting reversal of both myocardial and microvascular
remodelling. The SHR data provide translational evidence that the improvement
of CF observed after treatment with PþI is due to reverse remodelling
of intramural arterioles
Induction of mitochondrial biogenesis is a maladaptive mechanism in mitochondrial cardiomyopathies.
Defects of the mitochondrial genome cause a heterogeneous group of clinical disorders, including mitochondrial cardiomyopathies (MIC). The molecular events linking mtDNA defects to cardiac remodeling are unknown. Energy derangements and increase of mitochondrial-derived reactive oxygen species (ROS) could both play a role in the development of cardiac dysfunction in MIC. In addition, mitochondrial proliferation could interfere with sarcomere alignment and contractio