Electrical modelling of tissue experiments confirms precise locations of resistance and compliance in systemic arterial tree-they are mutually exclusive.

This study presents electrical modelling of the arterial system to understand the effect of adrenaline on the aortae and small arteries in terms of their resistance and compliance. There is no categorical documentation in the current literature on the precise locations of arterial resistance (R) and compliance (C) in vasculature. Knowledge of their exact locations 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 changes in R and C in response to these drugs. Isolated goat aortae and small arteries were perfused with a pulsatile pump and lumen pressures were recorded before and after addition of adrenaline. Equivalent electrical models were simulated, and biological data was compared against the electrical equivalents to derive interpretations. In the aortae, systolic pressure increased, diastolic pressure decreased, pulse pressure increased (P = .018); but the mean pressure remained the same (P = .357). Whereas in small artery, vasoconstriction caused an increase in systolic, diastolic, and mean pressures (P = .028). Simulations allow us to infer that vasoconstriction in the aorta leads to a reduction in compliance, but an increase in resistance if any, is not sufficient to alter the mean aortic pressure. Whereas vasoconstriction in small arteries increases resistance, but a decrease in compliance, if any, does not affect any of the pressure parameters measured. The presented study is first of its kind to give experimental evidence that large arteries and aorta are the only compliance vessels and small arteries are the only resistance vessels.

Elusive Toxin in Cleistanthus collinus Causing Vasoconstriction and Myocardial Depression: Detailed NMR Analyses and Biological Studies of Cleistanthoside A.

Cleistanthus collinus leaf extracts are consumed for suicidal purposes in southern India. The boiled decoction is known to be more toxic than the fresh leaf juice. Although several compounds have been isolated and their toxicity tested, controversy remains as to which compounds are responsible for the high level of toxicity of C. collinus. We report herein that cleistanthoside A is the major toxin in the boiled aqueous extract of fresh leaves and causes death in rats in small doses. The toxicity of the boiled extract prepared in the manner described can be attributed entirely to cleistanthoside A. Cleistanthin A could also be isolated from the boiled extract, albeit in trace amounts. As hypotension not responding to vasoconstrictors is the cause of death in patients who have consumed the boiled extract, effects of cleistanthoside A on the determinants of blood pressure, namely, force of cardiac contraction and vascular resistance, were tested in isolated organ experiments. Cleistanthoside A has a direct vasoconstrictor effect; however, it inhibits ventricular contractility. Therefore, the notion that the shock in C. collinus poisoning is of vascular origin must be considered carefully, and the possibility of cardiogenic shock must be studied. We present the crystal structure of cleistanthin A and show the potency of fast NMR methods (NOAH4-BSCN-NUS) in the full spectral assignment of cleistanthoside A as a real-world sample of a natural product. We also compare the results of the NOAH4-BSCN-NUS NMR experiments with conventional NMR methods.