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The Response of the Awake Spontaneously Hypertensive Rat (SHR) to Acute Blood Loss
Author(s) -
Wennberg E.,
Hagberg H.,
Haljamäe H.
Publication year - 1984
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1984.tb02098.x
Subject(s) - medicine , blood pressure , endocrinology , hypoxia (environmental) , glycogen , acidosis , spontaneously hypertensive rat , perfusion , metabolic acidosis , organic chemistry , oxygen , chemistry
In order to evaluate experimentally if the presence of hypertensive disease is an additional risk factor in connection with emergency situations including blood loss, awake spontaneously hypertensive rats (SHR) and normotensive Wistar‐Kyoto rats (WKY) were subjected to standardized acute haemorrhage (35% of blood volume) via an aortic catheter. Mean arterial blood pressure (MAP), blood gases, acid‐base balance, blood glucose and haematocrit values were followed and the 5‐h survival rate was determined. In the early posthaemorrhagic phase similar plasma refill, as evidenced from haematocrit readings, was seen in SHR and WKY. Hyperglycaemia occurred in both groups but the hyperglycaemic response was only moderate and transient in SHR. The inability of SHR to maintain hyperglycaemia was intimately correlated to early appearance of metabolic acidosis and short posthaemorrhagic survival times. Determination of liver glycogen content of unbled SHR and WKY indicated that the deficient hyperglycaemic response in SHR was not due to inadequate glycogen stores but rather to poor liver perfusion resulting in liver hypoxia. Since spontaneous hypertension in rats in many ways is considered to be similar to essential hypertension in man, these findings suggest that human hypertensive disease constitutes a considerable risk factor in connection with acute haemorrhage.