We estimated the influence of acute glucagon applications on 3H-histamine uptake by the isolated guinea-pig heart, during a single 3H-histamine passage through the coronary circulation, before and during anaphylaxis, and the influence of glucagon on level of histamine, NO, O2 −, and H2O2 in the venous effluent during anaphylaxis. Before anaphylaxis, glucagon pretreatment does not change 3H-histamine Umax and the level of endogenous histamine. At the same time, in the presence of glucagon, 3H-histamine Unet is increased and backflux is decreased when compared to the corresponding values in the absence of glucagon. During anaphylaxis, in the presence of glucagon, the values of 3H-histamine Umax and Unet are significantly higher and backflux is significantly lower in the presence of glucagon when compared to the corresponding values in the absence of glucagon. The level of endogenous histamine during anaphylaxis in the presence of glucagon (6.9–7.38 × 10−8  μM) is significantly lower than the histamine level in the absence of glucagon (10.35–10.45 × 10−8  μM). Glucagon pretreatment leads to a significant increase in NO release (5.69 nmol/mL) in comparison with the period before glucagon administration (2.49 nmol/mL). Then, in the presence of glucagon, O2 − level fails to increase during anaphylaxis. Also, our results show no significant differences in H2O2 levels before, during, and after anaphylaxis in the presence of glucagon, but these values are significantly lower than the corresponding values in the absence of glucagon. In conclusion, our results show that glucagon increases NO release and prevents the increased release of free radicals during anaphylaxis, and decreases histamine level in the venous effluent during cardiac anaphylaxis, which may be a consequence of decreased histamine release and/or intensified histamine capturing by the heart during anaphylaxis.

In our paper we aimed to increase the awareness among physicians, concerning coronavirus disease 2019 (COVID-19) severity, especially in patients with specific underlying comorbidities. Obesity is the second most common condition in hospitalized COVID-19 patients. Furthermore it has a major role in the development of obstructive sleep apnoea (OSA), which is highly involved in a severe COVID-19 development and its serious outcomes. Even though obese OSA patients had an increased pulmonary embolism (PE) risk, there is no enough evidence to support the interaction between obesity and OSA regarding PE development in the setting of COVID-19. Our patient is a 45-year-old obese male with COVID-19, who was admitted to the intensive care unit (ICU) with acute respiratory failure requiring high-flow nasal oxygenation. Clinical, laboratory and diagnostic findings pointed on severe COVID-19 form, complicated with PE. After recovery, the diagnosis of OSA was established. With this case, we wanted to alert the physicians on comorbidities, such as obesity and OSA, while those conditions, to some extent, may contribute to worse COVID-19 clinical presentation.

1846COLIC M et al. Circulation JournalOfficial Journal of the Japanese Circulation Society http://www. j-circ.or.jp stress may be involved in the transport of atherogenic substances and their subsequent redistribution within the vessel wall. 9-13 Compared to other mechanical forces, shear stress acts on a surface of the blood vessel wall (endothelium) 14 and appears to be particularly important. Studies showed endothelial cell dysfunction in areas of low shear stress, which also demonstrate increased uptake of lipoproteins. 9,15-19 The goal of this work was to examine LDL uptake by the blood vessel wall in a very short period of time, taking into account shear stress variation and possible influence of cholesterol exposure to the blood vessel wall. All previous studies that examined LDL transport and accumulation into the blood vessel wall were performed either on isolated blood vessel strips 20 or segments. 21 These were done either without perfusion flow or in vitro, using cultured endothelial cell monolayers 22 or they were performed by using mathematical and computational models of blood vessels 18,23,24 based on experimental results, especially those of Meyer et al. 21 This study t is known that the leading cause of death worldwide is coronary artery disease (CAD), and special attention is given to atherosclerosis, mainly dyslipidemia, as an important risk factor for CAD. 1 Atherosclerosis, a chronic fibroproliferative disease of the arterial wall, occurs principally in large-and medium-sized elastic and muscular arteries and may induce ischemia of the heart, brain or extremities, resulting in infarction. 2-4 Because high plasma concentrations of cholesterol, particularly low-density lipoprotein (LDL) cholesterol, represent one of the principal risk factors for atherosclerosis, 5 the process of atherogenesis has been considered by many to consist largely of the accumulation of lipids within the artery wall. 6 By providing cholesterol to peripheral tissues, LDL is the key component in physiological cholesterol metabolism. 7, 8 Furthermore, blood vessels are constantly exposed to various types of hemodynamic forces induced by the pulsatile blood flow and pressure, and the spatial distribution of these hemodynamic factors such as wall pressure, fluid velocity or wall shear I

No abstract

Med. čas. 2012; 46(1): 7-13. hypertension enhances LDL entry into the intima by changing the permeability of the endothelium (9, 10). Previous in vitro studies indicated that stretching of the arterial wall induced by pressure is the major factor of LDL accumulation in atherosclerotic disease and the other mass transport into the arterial wall, especially in the inner section of the vessel (4,11,12). It has also been suggested ABSTRACTObjective. The aim of this study is to present the experimental model which can be used to determine LDL transport into the blood vessel wall.Method. We used isolated rabbit carotid arteries under physiologically relevant constant pressure and perfusion flow in conditions more similar to in vivo. We used Rapid dual-isotope dilution method, Steady -state method, testing of transport of LDL-before and after removal of the endothelium, in conditions with intact endothelium and after its removal.Results. First we used Rapid dual-isotope dilution method and the data obtained showed that the transport of LDL could not be precisely determined in this way because it was in the range of standard error. Then we used Steadystate method and uptake (Us) was 3.52 ± 1.07% at higher pressure (140±10 mmHg) than at lower pressure (p<0.05). Also, LDL uptake was evaluated before and after the endothelium removal. The results after endothelial removal showed that Us of LDL was almost 3 times higher (9.2%) than with intact endothelium (p<0.05) and that the accumulation of LDL in the blood vessel wall was 0.1% (0.06% in intact endothelium) indicating that intact endothelium was a strong barrier.Conclusion. Our experimental model and applied mathematical procedures can provide a precise description of the LDL uptake by the blood vessel wall. SAŽETAKCilj. Cilj ove studije bio je da predstavi eksperimentalni model kojim se može utvrditi transport LDL-a u zid krvnog suda.Metod. Izolovane karotidne arterije zečeva tretirali smo u uslovima fizioloških vrednosti pritiska i pri perfuzionom protoku koji je najsličniji in vivo uslovima. Korišćeni su "Rapid dual-isotope" dilucioni metod, "Steady-state" metod, ispitivanje transporta LDL-a pre i posle uklanjanja endotela, u uslovima intaktnog i posle uklanjanja endotela.Rezultati. Prvo smo koristili "Rapid dual-isotope" dilucioni metod i dobijeni podaci pokazali su da se transport LDL-a ne može na ovaj način precizno utvrditi, jer je u granicama standardne greške. Zatim smo koristili "Steadystate" metod i na višem pritisku (140 ± 10 mmHg) preuzimanje LDL-a je bilo 3,52 ± 1,07% u odnosu na niži pritisak (p < 0,05). Takođe smo ispitivali transport LDL-a pre i posle uklanjanja endotela. U uslovima posle uklanjanja endotela rezultati su pokazali da je preuzeto skoro 3 puta više LDL-a (9,2%) u odnosu na intaktni endotel (p < 0,05) i da je nakupljanje LDL-a u zidu krvnog suda bilo 0,1% (dok je u intaktnom endotelu bilo 0,06%) što ukazuje na to da je intaktni endotel snažna barijera.Zaključak. Dobijeni rezultati ukazuju na to da primenjen eksperimentalni i matematički model ...