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Intrapartum Fetal Surveillance
Published in Gowri Dorairajan, Management of Normal and High Risk Labour During Childbirth, 2022
Catecholamine release in response to stress helps by increasing the heart rate and force of contraction of the myocardium as well as by diverting blood from the less important circulation (such as skin and gut) by triggering peripheral vasoconstriction. The vasoconstriction also increases the blood pressure, which helps to increase the force with which blood is delivered to central organs. The ability to respond to hypoxic stress seems to be greater with the fetus than the adults because of the increased amount of haemoglobin which has a higher oxygen affinity.
Cardiovascular Risk Factors
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
One of the key advances in understanding the pathophysiology, or development, of CVD and hypertension is elucidating the interaction between contributory factors of genetics and environment. This interaction is principally driven by environmental daily life exposures, such as nutritional status and exposure to nutrients, which then cause downstream disturbances of gene expression patterns involved in vascular responses. The initial vascular responses include inflammation, oxidative stress, and vascular immune dysfunction, which then propagate endothelial and vascular smooth muscle dysfunction and lead to vasoconstriction and hypertension (Houston, 2013). These responses are augmented by changes in the renal system involving renin-angiotensin-angiotensinogen-system (RAAS). The next section will cover the multiple responses and systems involved in hypertension development in order to provide a framework for understanding the role of nutrition and nutrients.
Pulmonary Circulation
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Both metabolic and respiratory acidosis augment HPV. Alveolar hypercapnia. Elevated alveolar Pco2 causes pulmonary vasoconstriction.Humoral factors. Catecholamines such as epinephrine cause, predominantly, vasoconstriction. Thromboxane and leukotrienes are all pulmonary vasoconstrictors whilst prostacyclin (PGI2) is a vasodilator. Serotonin released by activated platelets is a potent vasoconstrictor.Drugs. Inhaled nitric oxide is a potent pulmonary vasodilator. Nebulized prostacyclin is effective but its effects are due to systemic absorption. Phosphodiesterase inhibitors inhibit the breakdown of both cyclic guanosine monophosphate (cGMP) and cAMP. Milrinone, levosimendan and sildenafil are useful pulmonary vasodilators. Volatile anaesthetic agents also vasodilate the pulmonary vasculature.
The current and future status of inotropes in heart failure management
Published in Expert Review of Cardiovascular Therapy, 2023
Angelos Arfaras-Melainis, Ioannis Ventoulis, Effie Polyzogopoulou, Antonios Boultadakis, John Parissis
Norepinephrine is a naturally occurring molecule that exerts its effects by binding to alpha-1 adrenergic receptors in the vasculature. Through this mechanism, it results in vasoconstriction and thus raises mean arterial pressure via increasing both systolic and diastolic blood pressures. Additionally, norepinephrine acts on cardiac beta-1 receptors, thereby increasing cardiac contractility and chronotropy [8]. In the setting of acute HF and cardiogenic shock, norepinephrine is most commonly used in conjunction with other inotropic agents and inodilators to counteract their potential hypotensive effects [9]. Norepinephrine is also widely utilized in the management of other shock etiologies, including septic shock [43]. In clinical practice, norepinephrine is titrated to the desired blood pressure, typically infused at a rate ranging from 0.01 to 0.03 μg/kg/min, with doses up to 1 μg/kg/min used in certain cases. Despite its therapeutic benefits, norepinephrine has the potential to cause adverse events such as tachycardia, hypertension, and tachyarrhythmias [7,8]. Furthermore, norepinephrine has been reported to induce a toxic effect on cardiomyocytes, primarily due to beta-adrenergic stimulation-induced apoptosis [44].
Cardiovascular responses to hot skin at rest and during exercise
Published in Temperature, 2023
Ting-Heng Chou, Edward F. Coyle
One may notice that there is an inconsistency regarding the control of cutaneous vasoconstrictor and vasodilator pathways by exercise. The onset of exercise only increases vasoconstrictor activity, whereas the delayed initiation of active cutaneous vasodilation and the lower upper limit of skin blood flow are only controlled by inhibition of the vasodilation system. The explanation is that the classical “exercise reflexes” affect the vasoconstrictor system as in other vascular beds at the onset of exercise [5], whereas changes in plasma osmolality affect the vasodilator system and delay the initiation of cutaneous vasodilation. The lower upper limit of skin blood flow during exercise is achieved by limiting the active vasodilator system, but the specific mechanism is unknown. In addition, the effect of vasoconstrictor activity on cutaneous blood flow may be too small once the active cutaneous vasodilation is triggered to lower skin blood flow. Therefore, no effect is seen with vasoconstrictor blockage on skin blood flow during exercise except at the onset of exercise.
The inhibitory effects of pimozide, an antipsychotic drug, on voltage-gated K+ channels in rabbit coronary arterial smooth muscle cells
Published in Drug and Chemical Toxicology, 2023
Mi Seon Seo, Jin Ryeol An, Ryeon Heo, Minji Kang, Seojin Park, Seo-Yeong Mun, Hongzoo Park, Eun-Taek Han, Jin-Hee Han, Wanjoo Chun, Geehyun Song, Won Sun Park
K+ channels are mainly responsible for regulating the membrane potential in most cells, including vascular smooth muscle cells. Many types of K+ channels are expressed in vascular smooth muscle cells where they play unique roles regulating the resting membrane potential and thereby vascular tone (Werner and Ledoux 2014). Among these, Kv channels are postulated to be the main determinant of resting membrane potential by inhibiting the membrane potential, thereby maintaining vascular tone (Ko et al. 2008, Jackson 2018). Suppression of vascular Kv channels leads to vasoconstriction of small arteries and arterioles (Glover 1978, Cheong et al. 2001). Furthermore, dysfunction of Kv channels is closely related to circulatory diseases, such as hypertension (Tykocki et al. 2017) and coronary artery disease (Khanamiri et al. 2013). Thus, changes in Kv channel activity by some drugs can affect the overall function of the vasculature. Therefore, these unexpected effects of some drugs should be demonstrated to avoid misinterpretation of clinical and research results regarding the vascular system.