Synthetic Vasopressin and Oxytocin Analogs and Their Potential Use in Hemorrhagic, Traumatic and Septic Shock: A Personal Perspective SciDoc Publishers | Open Access | Science Journals | Media Partners

As one of us has stated many years ago, “shock is a significant and sustained loss of effective circulating blood volume [1]. It will eventuate in hypoperfusion of critical peripheral tissues, thus leading to a deficit in transcapillary exchange function in critical organ regions [1-3]. Clinically, there are five major types of circulatory shock: cardiogenic; septic; distributive; anaphylactic; and hypovolemic [1-3]. Hypovolemic shock (HS) is, primarily, due to a marked decrease in venous return, falling arterial blood pressure, and ventricular preload, and usually is caused by hemorrhage, dehydration, excessive diarrhea, trauma, excessive fluid loss from severe burns, increased positive intrathoracic pressure, excessive urinary fluid loss resulting from diuretics, side effects of many chemotherapeutic agents and radiation in cancer patients, or depressed vasomotor tone in the microcirculation [1- 3]. Septic shock is often termed “a vasodilatory shock” and is a leading cause of morbidity and mortality in the USA and Europe [1-4]. Septic shock and traumatic shock both involve substantial fluid loss, and often are treated with catecholamines, inotropic agents and corticosteroids in an attempt to maintain arterial blood pressure, venous return and distribution to key peripheral tissues and organs [1-5]. However, this often results in decreased cardiac output, intense ischemia in multiple organ regions and/or tachyphylaxis to the drugs and worsening of the patient, increased morbidity and mortality. Whatever circumstances initiate the “low-flow state”(hemorrhage, trauma, sepsis, etc.) and whatever the effects these initiating circumstances may have on circulating blood volume and cardiac output, the overall vasomotor response results in a functional decrease in transcapillary exchange in the peripheral tissues [6, 7]. This is the all-important trigger mechanism that sets in motion the chain of events which, if not promptly corrected, will generate the refractory and ultimately irreversible characteristics of the shock syndrome, that is, inadequate tissue blood flow and the attendant ischemia resulting in multiple microcirculatory organ-tissue failure. The strategic role of microcirculatory failure in “low-flow states” is firmly supported by voluminous studies which demonstrate that any therapy which directly or indirectly improves local tissue blood flow is beneficial [1-9]. But most of these studies do not emphasize drugs or techniques that are either suitable or reliable for clinical use in a “tried-and-true-manner”. Many different drugs are commonly used