To investigate the effect of nifedipine on hypercalcemic electrocardiographical alterations, steadily increasing hypercalcemia was induced in guinea-pigs by continuous calcium gluconate infusion until cardiac arrest occurred. During the experimental time the electrocardiograms were continuously recorded and compared in animals with and without pretreatment by nifedipine (Adalat). The hypercalcemia-induced electrocardiographical alterations intensified during increasing serum calcium levels. Ascending serum potassium and magnesium levels indicated increasing cell damage with a leak of these mainly intracellular ions. Pretreatment by nifedipine did not significantly influence the hypercalcemia-induced bradycardia and augmentation of the P-Q interval except a small and transient effect during relatively low calcium levels. The drug, however, exerted a distinct normalizing effect on hypercalcemic reduction of the S-T segment and the Q-T interval despite of an unaltered development of hypercalcemia. Accordingly, the cellular potassium and magnesium leaks were markedly reduced and the survival time during calcium infusion was significantly prolonged after nifedipine pretreatment. These electrophysiological data are in agreement with our previous cytochemical studies, which showed a protective effect of nifedipine against hypercalcemia-induced overloading of the cellular calcium depots in myocardial cells. Whether this cardio-protective effect of nifedipine during hypercalcemia can be used therapeutically in hypercalcemic crisis, has to be examined in clinical studies.
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http://dx.doi.org/10.1007/BF01908127 | DOI Listing |
Cureus
December 2024
Department of Intensive Care Medicine, Centro Hospitalar Universitário de São João, Porto, PRT.
This case involves a 21-year-old male healthcare student with a medical history of HIV-1 infection for two years and anxiety disorder. He presented to the emergency department with hemoptysis and dyspnea of sudden onset. A thoracic CT scan revealed multiple bilateral nodular ground-glass opacities suggestive of diffuse alveolar hemorrhage (DAH).
View Article and Find Full Text PDFHeliyon
January 2025
Department of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands.
Objective And Rationale: Small studies have shown that the QT interval follows a circadian rhythm. This finding has never been confirmed in a large real-world hospital population and the clinical meaning of disrupted rhythmicity remains unknown.
Methods: In this cohort study, all consecutive adult patients with at least one 12-lead ECG acquired between 1991 and 2021 were considered.
Physiol Rep
January 2025
Department of Cardiovascular Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan.
While autonomic dysregulation and repolarization abnormalities are observed in subarachnoid hemorrhage (SAH), their relationship remains unclear. We aimed to measure skin sympathetic nerve activity (SKNA), a novel method to estimate stellate ganglion nerve activity, and investigate its association with electrocardiogram (ECG) alterations after SAH. We recorded a total of 179 SKNA data from SAH patients at three distinct phases and compared them with 20 data from controls.
View Article and Find Full Text PDFMicrobiol Spectr
January 2025
Department of Molecular and Comparative Pathobiology, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.
Unlabelled: is a protozoan parasite that causes human and animal African trypanosomiases (HAT and AAT). Cardiac symptoms are commonly reported in HAT patients, and intracardiac parasites with accompanying myocarditis have been observed in both natural hosts and animal models of infection. Despite the importance of as a cause of cardiac dysfunction and the dramatic socioeconomic impact of African trypanosomiases in sub-Saharan Africa, there are currently no reproducible murine models of associated cardiomyopathy.
View Article and Find Full Text PDFElife
January 2025
Department of Neurosurgery, Washington University School of Medicine, Springfield, United States.
Background: Subarachnoid hemorrhage (SAH) is characterized by intense central inflammation, leading to substantial post-hemorrhagic complications such as vasospasm and delayed cerebral ischemia. Given the anti-inflammatory effect of transcutaneous auricular vagus nerve stimulation (taVNS) and its ability to promote brain plasticity, taVNS has emerged as a promising therapeutic option for SAH patients. However, the effects of taVNS on cardiovascular dynamics in critically ill patients, like those with SAH, have not yet been investigated.
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