Hari Prasad Sonwani* and Aakanksha Sinha
DOI: 10.37421/2167-1095.2025.14.498
Because of the elevated pulmonary vascular resistance and arterial hypoxemia caused by acute pulmonary embolism, right heart failure may result. It is imperative that pulmonary hypertension patients receive effective vasodilator therapy. Thus, using a rabbit model of acute pulmonary embolism, we examined the effects of a recently created, potent pulmonary vasodilator called organic mononitrates of 1,2-propanediol (PDNO). Blood gases, plasma nitrite content, exhaled Nitric Oxide (NO), and systemic and pulmonary hemodynamics were measured in anesthetized and ventilated rabbits. PDNO and inorganic nitrite were infused intravenously and into the left ventricle of naive animals, as well as in animals with pulmonary hypertension caused by a thromboxane A2 analogue, in doseresponse tests. Second, an acute pulmonary embolism was created, and after 20 minutes, either PDNO or a placebo was injected intravenously and assessed within after pulmonary embolization by one hour. Compared to inorganic nitrite given intravenously, PDNO showed effective NO donation by increasing exhaled NO, reducing pulmonary hypertension, and dose-dependently vasodilating the systemic circulation. Gas exchange disruptions and pulmonary hypertension were brought on by pulmonary embolization. Without causing tolerance, PDNO significantly reduced and stabilized the right ventricular rate-pressure product and pulmonary vascular resistance. It also had no notable side effects on methemoglobin generation, blood-gas values, or the systemic circulation. To sum up, in the pulmonary circulation, PDNO functions as both an effective vasodilator and a donor of NO. In the event of a life-threatening acute pulmonary embolism, intravenous treatment with this or comparable organic nitrites may be the future of treatment to prevent right heart failure.
DOI: 10.37421/2167-1095.2025.14.499
Pulmonary arterial hypertension is a rare but a rapidly increasing prevalent pulmonary disease that is characterised by vasoconstriction and inflammation of the pulmonary arteries leading to elevated pressure in the system eventually causing right heart failure and death. Cannabidiol (CBD), which is the major non-psychoactive component of cannabis, has substantial anti-inflammatory, immunomodulatory, and analgesic effects. This study investigated the therapeutic potential of cannabidiol alone, and adjunctive therapy with selexipag, used in the treatment of PAH, by investigating its effects on the expression of the inflammatory and hypoxic biomarker, TNF-α, as well as the effect on BNP levels and oxidative stress in the blood and heart in a Monocrotaline (MCT)-induced PAH rat model. Forty male Sprague-Dawley rats were divided into 5 groups of 8 animals consisting of: Control, MCT-Control, MCT-CBD, MCT-selexipag, and MCT-CBD-selexipag groups. The study ran for a total of 36 days with MCT (60 mg/kg) being injected interperitoneally on day 0 to 4 groups to induce PAH, CBD (10 mg/kg), Selexipag and a CBDselexipag combination were administered daily by oral gavage from day 21 onward to their respective groups. Post experiment, gene expression in the heart for TNF-α, BNP in the plasma, and Total Antioxidant Capacity (TAOC) in the heart and plasma were determined, as well as a full haematological profile. Study results showed that both CBD and selexipag treatment increased the expression of BNP and decreased TAOC levels in the plasma most when co-administered. The highest TNF-α and T-AOC levels were recorded in the heart in the MCT-CBD group. Haemoglobin and platelet counts were also the highest in the MCT-CBD group. This shows us that CBD show’s promise as another therapeutic option in the treatment of PAH by targeting BNP, but only when taken in combination with selexipag. CBD also shows promise by decreasing oxidative stress, increasing T-AOC, in the heart during PAH. CBD did, however, not show promise in decreasing TNF-α levels, but rather increase it.
Jubaida Akhtar*, Mohammad A Al-Mamun, Mohammad NN Sayem, Mohammad J Ahmed, Mahfuzur R Bhuiyan, Shamim Jubayer, Abdul Alim, Mohammad R Amin, Md R Karim, Megan E Henry, Matti Marklund, Laura Cobb, Dinesh Neupane, Lawrence J Appel and Sohel R Choudhury
Objectives: The high burden of blood pressure-related cardiovascular diseases in Bangladesh is potentially linked to excessive dietary sodium and insufficient potassium intake. This study assessed the dietary salt and potassium intake among rural and urban adults in Bangladesh through urinary sodium and potassium excretion. Methods: We conducted a cross-sectional study between December 2017 and June 2018, including participants aged 30-59 years from three urban and three rural sites. Data included urinary excretion of sodium and potassium estimated from one 24-hour urine collection and blood pressure measurements. Results: Among the 840 enrolled participants, complete data was available in 509 individuals. Mean age was 43.0 (SD ± 7.9) years; 20.9% had hypertension, 50.9% were women and 50.9% resided in urban areas. Mean systolic and diastolic blood pressure were 118.6 (SD ± 16.6) mmHg and 76.3 (SD ± 11.3) mmHg, respectively. Overall, mean urinary sodium excretion was 3.9 gm/day (95% CI=3.8 to 4.0), corresponding to a mean salt intake of 9.7 g/day (95% CI=9.4-10.1). Mean urinary potassium excretion was 1.4 g/day (95% CI=1.3-1.4), corresponding to an estimated mean dietary potassium intake of 2.0 g/day. Men and urban residents had slightly higher sodium and potassium excretion than women and rural residents. Conclusion: In Bangladesh, salt intake exceeded WHO's recommended <5 g/day limit, while potassium intake was substantially lower than the recommended intake of >3.5 g/day for adults. Promoting low-sodium and potassium-rich diets through nationwide campaigns and policies, including advocating for accessible low-sodium and potassium-enriched salt substitutes, is recommended to mitigate cardiovascular disease risks.
DOI: 10.37421/2167-1095.2024.14.497
DOI: 10.37421/2167-1095.2024.14.498
DOI: 10.37421/2167-1095.2024.14.499
DOI: 10.37421/2167-1095.2024.14.500
DOI: 10.37421/2167-1095.2024.14.501
DOI: 10.37421/2167-1095.2024.14.502
DOI: 10.37421/2167-1095.2024.14.503
DOI: 10.37421/2167-1095.2024.14.504
DOI: 10.37421/2167-1095.2024.14.505
DOI: 10.37421/2167-1095.2024.14.506
Journal of Hypertension: Open Access received 614 citations as per Google Scholar report