From the foregoing results one can conclude that the
superfused rat stomach fundic strip provides a sensitive
method for continuously recording the release of cate¬
cholamines into the circulation. Injection of the animal
with oestrogen subcutaneously 18 hours before the experi¬
ment gave a reliable and sensitive preparation for the
assay of catecholamines released from the adrenal medulla
during haemorrhage. Rat ascending colon soaked in a
propranolol, (1G~^i) for half an hour before use provided
a sensitive assay preparation for angiotensin generated
during haemorrhage.The rabbit catecholamine released from the adrenal
medulla increased at the end of the period of haetaorrhage
which took 5 minutes to complete, at which time the blood
pressure was lowered to about 50 - 60 cuaHg. The release
of catecholamine is not continuous and decreased after the
haemorrhage stopped. In some experiments catecholamine
level had returned to control levels before the retransfusion of the shed blood commenced, although some
intrinsic compensation and rise of arterial blood pressure
had occurred. The blood pressure recovered slightly
during the 30 minutes resting after the bleed, partly due
to sympathetic influence, but also due to the rapid
entrance of tissue fluid into the circulation as shown by
decrease in both packed cell volume and haemoglobin con¬
centration. Heart rate did not increase significantly
in this species during haemorrhage and fell below control
levels 30 minutes after haemorrhage. This might be
related to the increase of plasma volume due to entry
of extra-cell liar fluid. This small rise in heart rate
at the beginning of haemorrhage is probably related to
the high resting heart rates in these anaesthetized
animals.The release of catecholamine during haemorrhage in
the rabbit was not reduced by muscarinic blockade but
was abolished by nicotinic blockade which Indicates most
of the receptor population are nicotinic, a finding
supported by the experiments with carbachol.No evidence of increase in angiotensin generation
luring or after haemorrhage suggests that no significant
of the rabbit
release of renin from the kidney occurs during or 30
minutes after the haemorrhage procedures, during which
arterial blood pressure was reduced to 50 - 80 amHg.
Angiotensin infusions into the aorta in 200, 400 and
even 800 ng/kg/min did not give any evidence of releasing
catecholamines from the adrenal medulla nor did discrete
injections of angiotensin. This was taken as evidence
that in the rabbit angiotensin does not act as a catecholamine releaser from the adrenal medulla.The above findings suggest that angiotensin neither
releases catecholamine in significant amounts during
haemorrhage, nor does it play any part in catecholamine
release during haemorrhage in the rabbit .In dogs, catecholamine rele s« from the adrenal
medulla commences as blood pressure falls and before the
end of haemorrhage In most experiments when blood pressure
was 50 - 80 mralig. Low levels of blood pressure did not
have to be sustained for the increase in catecholamines
to occur. Release was continuous over the whole period
(30 minutes) after the bleed, in spite of the compensatory
increase in arterial blood pressure. It returned to
normal level when retransfusion of the shed blood began.The heart rate of the dog increased during haemorrhage especially
towards the end and returned to control level within
30 minutes after haemorrhage. The increase in catecholamines released daring haemorrhage was not affected
by muscarinic blockade. In animals treated with hexamethonium however, catecholamine release Increased during
haemorrhage but not to the same level as during a bleed
prior to blockade. Moreover, the output of catecholamine
was a transient one persisting for only a few minutes
in most of the animals studied and returning back to
control levels before retransfusion started. Ligation
of the renal veins together with prior administration
of hexamethonlum totally abolished the release of catecholamine after haemorrhage.Angiotensin blood level in the dog increased markedly after
haemorrhage and only returned to control levels after
retransfusion of the shed blood. Infusion of angiotensin
in 200 ng/kg/min significantly increased the release of
catecholamine from the adrenal medulla In a transient
burst which persisted for only 2-3 minutes and not for
the whole period of the infusion. It resembled the
responses noted during haemorrhage after ganglionic
blockade with hexamethonluw.The above results suggest that the adrenal medulla
of the dog Is very sensitive to angiotensin and that
angiotension liberation during haemorrhage precedes
the release of catecholamine in the dog and could play
an important role in the initial release of catecholamine
into the circulation during haemorrhage in this animal.The species differences noted are discussed in the
context of the cardio vascular control in hypotensive
states
