cardiovascular-agents and Spinal-Cord-Injuries

Distributive shock is defined as circulatory insufficiency induced by excessive dilatation of the peripheral vasculature or maldistribution of cardiac output. Septicemia, systemic inflammatory response syndrome, anaphylaxis, injuries to the central nervous system, and drug intoxication are causative factors of shock. Circulatory derangements induced by bacterial infection have been divided into hyperdynamic and hypodynamic shock. Administration of inotropic drugs, vasopressors, and/or vasodilators are primary treatments in this type of shock. Continuous infusion of norepinephrine to maintain blood pressure or administration of inoptropes such as dopamine or dobutamine are recommended to improve tissue perfusion. High-dose intravenous epinephrine is required to reestablish cardiac function, followed by continuous infusion of norepinephrine in severe anaphylactic shock. Vasoconstrictors such as norepinephrine, vasopressin, or amaminone are administered to maintain vascular tone in shock caused by nerve damage or drug overdose.

Topics: Anaphylaxis; Brain Injuries; Cardiovascular Agents; Dopamine; Epinephrine; Humans; Norepinephrine; Sepsis; Shock; Spinal Cord Injuries; Vascular Resistance

Salvianolic acid A (Sal A), a bioactive compound isolated from the Chinese medicinal herb Danshen, is used for the prevention and treatment of cardiovascular diseases. However, the protective function of Sal A on preserving the role of blood-spinal cord barrier (BSCB) after spinal cord injury (SCI) is unclear. The present study investigated the effects and mechanisms of Sal A (2.5, 5, 10mg/kg, i.p.) on BSCB permeability at different time-points after compressive SCI in rats. Compared to the SCI group, treatment with Sal A decreased the content of the Evans blue in the spinal cord tissue at 24h post-SCI. The expression levels of tight junction proteins and HO-1 were remarkably increased, and that of p-caveolin-1 protein was greatly decreased after SCI Sal A. The effect of Sal A on the expression level of ZO-1, occluding, and p-caveolin-1 after SCI was blocked by the HO-1 inhibitor, zinc protoporphyrin IX (ZnPP). Also, Sal A inhibited the level of apoptosis-related proteins and improved the motor function until 21days after SCI. In addition, Sal A significantly increased the expression of microRNA-101 (miR-101) in the RBMECs under hypoxia. AntagomiR-101 markedly increased the RBMECs permeability and the expression of the Cul3 protein by targeting with 3'-UTR of its mRNA. The expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and HO-1 was significantly increased after agomiR-101 treatment. Therefore, Sal A could improve the recovery of neurological function after SCI, which could be correlated with the repair of BSCB integrity by the miR-101/Cul3/Nrf2/HO-1 signaling pathway.

Topics: Animals; Caffeic Acids; Capillary Permeability; Cardiovascular Agents; Caveolin 1; Cullin Proteins; Disease Models, Animal; Drug Evaluation, Preclinical; Heme Oxygenase (Decyclizing); Hypoxia; Lactates; Male; MicroRNAs; Motor Activity; Neuroprotective Agents; NF-E2-Related Factor 2; Random Allocation; Rats, Sprague-Dawley; Spinal Cord; Spinal Cord Injuries; Tight Junctions; Zonula Occludens-1 Protein

We report the case of a 55-year-old man who presented with acute coronary syndrome due to coronary slow flow after spinal cord injury. Data regarding the causes and clinical manifestations of coronary slow flow are inconclusive, but the autonomic nervous system is believed to be at least a contributing factor. The predominant vagal activity causes vasodilation and hemostasis, which can lead to acute coronary syndrome. We hereby call attention to hyperactive parasympathetic tonicity, which can lead to coronary slow flow and acute coronary syndrome in acute spinal cord injury patients.

Topics: Acute Coronary Syndrome; Cardiovascular Agents; Coronary Angiography; Coronary Circulation; Electrocardiography; Hemostasis; Humans; Magnetic Resonance Imaging; Male; Middle Aged; No-Reflow Phenomenon; Physical Therapy Modalities; Spinal Cord Injuries; Treatment Outcome; Vagus Nerve; Vasodilation

Acute distal aortic dissection rarely causes spinal cord ischemia presenting with paraplegia or paraparesis. Spinal cord involvement has poor outcomes, and there is no established effective treatment for this disorder. In this report we describe the acute conservative treatment of two cases of paraplegia/paraparesis due to acute type B aortic dissection. Early reversal of lower-limb dysmobility was achieved.

Topics: Aged; Antihypertensive Agents; Aortic Aneurysm; Aortic Dissection; Cardiovascular Agents; Cerebrospinal Fluid; Drainage; Humans; Male; Naloxone; Paraparesis; Spinal Cord Injuries

Topics: Adult; Airway Obstruction; Algorithms; Cardiopulmonary Resuscitation; Cardiovascular Agents; Electric Countershock; Electrocardiography; First Aid; Heart Arrest; Humans; Physical Examination; Posture; Respiration, Artificial; Spinal Cord Injuries; Tachycardia, Ventricular; Ventricular Fibrillation

Topics: Cardiovascular Agents; Methocarbamol; Muscle Relaxants, Central; Muscle Spasticity; Paraplegia; Spinal Cord Injuries