Coronary and systemic vascular response to inspiratory resistive breathing.
To evaluate the coronary and systemic cardiovascular response to graded inspiratory resistive breathing, seven dogs were studied 2-4 wk after chronic instrumentation to measure circumflex coronary artery and ascending aortic blood flows as well as aortic and left ventricular (LV) blood pressures. The experiments were performed under chloralose anesthesia (to exclude any confounding emotional effects by dyspnea on cardiovascular variables) and hyperoxic conditions (to prevent chemoreflex activation by hypoxemia). In a randomized fashion, the dogs were subjected to graded inspiratory resistive breathing (spontaneous breathing alone and moderate and severe resistive loading, corresponding to resistances of approximately 0, 40, and 110 cmH2O.s.l-1, respectively). Each run lasted 10 min. Compared with mechanical ventilation with the respiratory muscles at rest, spontaneous breathing alone and moderate and severe inspiratory resistive loading induced pronounced and significant increases in circumflex coronary blood flow (19, 32, and 62%, respectively), which were almost exclusively accounted for by significant decrements in coronary vascular resistance and were paralleled (r = 0.88, P less than 0.0001) by significant increments (18, 31, and 57%) in heart rate transmural-aortic pressure product, an indicator of LV myocardial O2 demand. An increase in myocardial O2 consumption during resistive breathing was confirmed by analysis of coronary sinus blood samples in additional experiments (n = 3). Cardiac output significantly increased (10, 14, and 35%) because of increases in heart rate (15, 24, and 49%), with LV stroke volume and diastolic dimensions remaining unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
Peters
J
J
Abteilungen für Experimentelle, Heinrich-Heine-Universität Düsseldorf, Federal Republic of Germany.
Ihle
P
P
D000403:Airway Resistance / Q000502:physiology*; D000818:Animals; D003326:Coronary Circulation / Q000502:physiology*; D004285:Dogs; D006439:Hemodynamics / Q000502:physiology*; D010101:Oxygen Consumption; D015656:Respiratory Mechanics / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology; D014664:Vasodilation / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology