Left coronary blood flow (LCBF), left ventricular oxygen, extraction [(a-v)O₂ ], and myocardial oxygen consumption (MVO₂) were monitored in 10 dogs. HR was paced at 120 bpm and then increased to 180 bpm to elicit a hyperemic response (ΔLCBF). During the hyperemia, the vaso-dilatory response to exogenous adenosine (F_AD) was tested. Twenty min. after injection of aminophylline (100 mg/i.v.), HR was again increased. F_AD was again tested. The pacing-induced increase in MVO₂ (ΔMVO₂) was not affected by aminophylline (P>0.05). However, the slope ΔLCBF/ΔMVO₂ was decreased, and the slope (a-v)O₂ /ΔMVO₂ was increased. F_AD was also decreased and the magnitude of the reduction was correlated with the decrease in ΔLCBF/ΔMVO₂ (r=0.82). These results suggest that adenosine may play an role in coronary functional hyperemia induced by increases in heart rate.

In the present study alpha-receptor modulation of coronary flow and cardiac function was examined in exercising dogs, chronically instrumented to measure: circumflex blood flow velocity (CFV), heart rate (HR), global left ventricular function (LVP and dP/dt Max) and regional left ventricular function (%SL and dL/dt (s)max). During exercise, local adrenergic blockade was produced by intracoronary injection of 1.0 mg phentolamine ( anon-specific alpha-antagonist) or .5 mp prazosin. Exercise significantly increased HR, LVP, dP/dt max, CFV, %SL and dL/dt (s)max. Neither alpha-antagonist produced changes in HR, LVP or %SL; however, both phentolamine and prazosin produced significant increses in dP/dtmax, CFV and dL/dt(s)max of the alpha-blocked region, when compared to their exercise level before alpha-blockade. It is suggested that an alpha1-adrenergic vasoconstriction limits coronary vasodilation and, thereby, cardiac function during exercise.

The presence of an alpha-adrenoceptor--mediated coronary vasoconstrictor reflex during acute systemic hypoxia was examined in thirteen chloralose-anesthetized dogs. Local vasodilator effects were avoided by perfusing the left common coronary artery (LCC) with normoxic blood, while the dogs were ventilated with 5% 02-95% N2 . Left ventricular afterload was held constant and positive cardiac inotropic responses and beta two-adrenoceptor-mediated coronary vasodilation were blocked by propranolol. Parasympatheticmediated bradycardia and coronary vasodilation were blocked with atropine. Systemic hypoxia decreased LCC flow to normoxic myocardium by 19.4+2.6 %. Although myocardial oxygen extraction increased 9.7+2.9 %, myocardial oxygen consumption decreased 16.5+2.6 %. Intracoronary prazosin prevented the reflex vasoconstriction during repeated hypoxia.

A model was developed to predict the increased physiological effort of wearing a respiratory protective device. Specifically, the model was designed to predict the effects of varying ventilatory demands on eleven respiratory variables of the man-respirator system, breath frequency (f_b), tidal volume (V_t), inspiratory flow (dvi/dt), expiratory flow (dve/dt), inspiratory mask pressure (P_mi), expiratory mask pressure (P_me), inspiratory intrathoracic pressure (P_ii), expiratory intrathoracic pressure (P_ie), inspiratory mask work (W_mi), expiratory mask work (W_me), and mask leakage index (L_i). The model was tested by experiment in which three male subjects underwent maximal exercise testing with and without the "pressure-demand" respirator. The eleven variables were determined for each thirty second period utilizing on-line computer analysis. Application of the model to these experimental conditions resulted in significant (p<.001) relationships between each of the predicted and observed variables.