Increased resistance to acute anoxia of the respiratory and cardiac function in spontaneously hypertensive rats.
In spontaneously hypertensive rats NIbn (SHR) and in normotensive Wistar rats (NCR) 12-16 weeks old, anaesthetized with urethane, anoxia was produced by nitrogen administration through a tracheal cannula. Ventilation was measured by tetrapolar impedance rheography. NCR responded to anoxia with a marked increase in TV and in respiratory rate (f.), whereas in SHR a depression of TV and increase in f. was observed. In NCR respiratory arrests and alternating with spontaneous restorations of respiration were observed during anoxia. This pattern of response to anoxia never appeared in SHR. After the glossopharyngeal nerves had been cut anoxia caused a depression of TV and increase of f. in NCR. In contrast, chemodenervation in SHR did not qualitatively change the respiratory response to anoxia. Periods of spontaneous respiration under anoxic conditions were significantly longer in SHR than in NCR. Also left ventricular contractions and ECG activity were maintained for a longer time in SHR than in NCR during anoxia. EEG activity disappeared in both groups of animals at about the same time after the onset of acute anoxia. The above data point to: 1) reduced responsiveness of the arterial chemoreflex in SHR, and 2) markedly increased tolerance to anoxic conditions in SHR.
D000818:Animals; D003714:Denervation; D004198:Disease Susceptibility; D004562:Electrocardiography; D005930:Glossopharyngeal Nerve / Q000503:physiopathology; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D000860:Hypoxia / Q000150:complications*; D009200:Myocardial Contraction; D009584:Nitrogen / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains; D012119:Respiration / Q000187:drug effects; D012137:Respiratory System / Q000503:physiopathology*; D013990:Tidal Volume
D009584:Nitrogen