Abstract
Vasoconstriction in small arteries and arterioles is known to increase resistance to flow, while vasoconstriction in large arteries and aorta is known to decrease their compliance. Besides this general understanding, there is no systematic documentation on what happens to small artery compliance and large artery resistance during vasoconstriction and the corresponding alterations in vascular pressure. The aim of the study is to assess the effect of adrenaline on goat aortae and small arteries in terms of resistance and compliance.
Isolated goat aortae and small arteries were perfused with a pulsatile pump and lumen pressure was recorded before and after addition of adrenaline. In the aortae, systolic pressure increased, diastolic pressure decreased, pulse pressure increased (p = 0.018, WSR); but the mean pressure remained the same (p = 0.357, WSR). Small artery vasoconstriction caused an increase in systolic, diastolic and mean pressures (p = 0.028, WSR). Using length, radius, and thickness data from the tissues and the tubes of the experimental set-up, electrical models were simulated to understand the biological data. The simulations allow us to infer that vasoconstriction in aorta leads to a reduction in compliance, but an increase in resistance if any, is not sufficient to change the mean aortic pressure. On the other hand, vasoconstriction in small arteries increases resistance, but a decrease in compliance if any, does not affect any of the four pressure parameters measured. Vasoconstriction in aorta decreases compliance and therefore increases pulse pressure but does not change resistance significantly enough to alter mean pressure.
Key Points Summary
The main aim of the study is to understand where exactly resistance (R) and compliance (C) components of the vasculature occur. There is no definitive evidence for the effect of large artery vasoconstriction on resistance and hence the mean arterial pressure.
The manuscript presents biological experiments studying the pressure response of goat aorta and small arteries to adrenaline (invitro) and the interpretations using equivalent electrical models.
The study shows that in aorta and large arteries, vasoconstriction does not lead to a reduction in lumen diameter sufficient to cause a rise in resistance and mean pressure as compared to small arteries.
Knowledge of exact location of R and C in the arterial tree enables re-assessment of the differential action of vasoactive drugs on resistance versus compliance vessels once we resolve beat-to-beat R and C changes in response to a drug. This way antihypertensive therapy can be tailored to address the specific cause of the type of hypertension.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
↵a MS Bioengineering; Ph. D Scholar (current)- Department of Engineering Design, Indian Institute of Technology (IIT) Madras, Christian Medical College (CMC) Vellore and Sree Chitra Tirunal Institute for Medical Sciences & Technology Trivandrum.
↵b MD Physiology; Civil Assistant Surgeon (current), Government Hospital, Anaicut, Vellore, Tamil Nadu, India.
↵c MD Physiology; Senior Resident (current), Dept. of Forensic Medicine, Kanyakumari Government Medical College, Tamil Nadu, India.
↵d MBBS, MD Physiology (current), Dept. of Physiology, CMC Vellore.
↵e Ph. D; Professor & Head, Department of Bioengineering, CMC Vellore.
↵f Ph. D; Professor, Department of Engineering Design, IIT Madras.
↵g Ph. D; Professor, Department of Physiology, CMC Vellore.
