Introduction

The survival of higher organisms is dependent on an adequate supply of 02 and substrates. A variety of 02 sensors underlie the various adaptive mechanisms (changes in regional blood flow, hormone release and ventilation) that ensure optimal 02 supply. One such mechanism is hypoxic pulmonary vasoconstriction (HPV). This chapter will discuss evidence for a comprehensive vascular 02 sensor mechanism which involves redox signaling between smooth muscle cell (SMC) mitochondria and plasmalemmalK+ channels (Fig. 1). In adult mammals, under physiological conditions, the pulmonary vessels deliver deoxygenated blood to the lung's capillary bed where gas exchange takes place. In response to airway hypoxia, whether it is focal (e.g., pneumonia or atelectasis) or global (e.g., high altitude), the pulmonary artery (PA) supplying the hypoxic lung segment(s) constricts. If the airway hypoxia is localized, HPV redistributes perfusion to better oxygenated areas and optimizes systemic 02 delivery (22) while minimally elevating net pulmonary vascular resistance (PVR). Regional blood flow is also determined by gravity (38). However, with global hypoxia less benefit is derived from HPV and the elevated PVR results in right ventricular hypertrophy. Inhibition of HPV, by sepsis (68) or drugs, results in ventilation perfusion mismatch and systemic hypoxemia. HPV can be exploited in single lung anesthesia to minimize blood flow to a lung that is intentionally made hypoxic to create a dry operative field (25, 127).

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