effects of hypoxic hypoxia and carbon monoxide-induced hypoxia on the cardiovascular system and regional blood flow of the anesthetized cat

the purpose of this study was to investigate the potential responses of the cardiovascular system and regional blood flow to hypoxic hypoxia (bb) and to carbon monoxide (co)-induced hypoxia (coh). ten anesthetized cats were studied under two nonnoxic (control: cont) and two hypoxic conditions. four types of radioactive micro spheres were used to measure regional blood flow during cont and two hypoxic conditions. during cont the animal was ventilated with 22% 02&apos; 5% co2 and n2 (room air). hh was induced by ventilating the cat for 15 min with 6-8% o2, and coh by adding 0.1 % co to room air and reducing blood oxygen content to the same level as hh. cardiac output and contractility significantly increased (p<0.05) during hh and coh but this increase was more pronounced during hb. there was a 22% increase in mean arterial blood pressure (pa) without a significant change in total peripheral resistance (tpr) during hh. on the other hand, despite a 47% increase in cardiac output during coh, there was a 29% reduction in pa which was due to peripheral vasodilation (tpr diminished by 45%). analysis of regional blood flow (ml/min per 100g) showed that each organ acted differently. coronary blood flow (80±7 cont) increased during hh (678±153) and coh (584±1 06). cerebral blood flow (30±4 cont) was augmented during hh (86±7) and coh (124±14). gracilis muscle, hepatic artery, renal, and small and large intestine blood flow did not change significantly during systemic hypoxia (p>o.05). gastric blood flow (14±2 cont) only increased during hh (22±4) but splenic blood flow (119±2 cont) decreased with both hh (40±9) and coh (37±9). regional blood flow of other segments measured showed a mixed response to hh and coh. in conclusion, it seems that: 1) systemic hypoxia would stimulate the heart to increase its output to maintain pa and overcome the increased demand of some organs, and 2) the different responses of regional vascular beds to hh and coh may be due to various sensitivities of each organ to arterial blood oxygen tension and autonomic neuro-hormonal controls that have originated from stimulations of aortic and carotid chemoreceptors.