Download The Intracellular pH and Potassium Content of

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Medical Research Society
Department of Medicine, Royal Victoria Infirmary,
Newcastte upon Tyne
A radiofibrinogen catabolism study has been performed in forty patients with glomerulonephritis.
Increased catabolism has been shown to correspond
with disease activity of immune complex disorders.
Illustrations will be made by reference to a patient
with post-streptococcal acute nephritis, a patient with
Henochs who developed recurrence of nephritis in a
renal transplant, a patient with scleroderma and a
transplant patient with cytomegalic virus infection.
significantly in left ventricular muscle. Despite the
changes that occurred in [ K + J in atria and right
ventricle, no significant change in pH1 occurred in
these tissues or left ventricle. [Na+II was significantly
increased in muscle from all chambers of the heart.
These results emphasize that differences in the
relationship of pHI to [K-t], exist between the
chambers of the heart as well as between cardiac and
skeletal muscle.
This work was supported by a grant from the British
Heart Foundation. R.J.C.H. was a British Heart
Foundation Junior Research Fellow.
14. THE INTRACELLULAR pH AND POTASSIUM CONTENT OF RABBIT CARDIAC AND
SKELETAL MUSCLE IN POTASSIUM DEPLETION
R. J. C. HALLand I. R. CAMERON
Department of Medicine, St Thomas’s Hospital Medical
School, London SEl 7EH
Potassium depletion in the rat causes skeletal muscle
to lose intracellular potassium ([K+ 11) and develop
an intracellular acidosis (Irvine rt al., 1960, Clinical
Science, 20, I ) . In contrast, in cardiac muscle from
the guinea-pig [K+Ii is not decreased during potassium depletion which is severe enough to reduce
skeletal muscle [K+I1 (Bolte et al., 1973, European
Journal of Clinical Inuest&ation, 3, 215). The effect of
K + depletion on cardiac muscle pHl is unknown.
The aim of our experiments was to compare the
changes in [K+], and pHi occurring in muscle from
the quadriceps and the various chambers of the heart
as a result of potassium depletion.
Eight New Zealand white rabbits were fed a diet
deficient only in K + ( K + < 1 mmol/kg feed): ten
control rabbits were fed a normal diet (K+ 350
mmol/kg feed). After 3 weeks of normal or K f
deficient diet, the animals were anaesthetized and pHi
of muscle from left ventricle, right ventricle, atria and
quadriceps was measured with the 14C-DM0 technique. The extracellular space was calculated from
the distribution volume of S*Cr EDTA. The equilibration time for these isotopes was 45 min; at the
end of this time tissue specimens were removed for
electrolyte analysis and counting. Differences between
group means were analysed for significance using
Student’s t test for unpaired data with Bailey’s
modification for groups of different variance.
In quadriceps, K+ depletion caused [K+], to
fall from 173.3 f 1.9 mmol/l cell water to 127.1 & 6.3
mmof/lcell water(P< 0001)and “a], rose(P< 0001).
An intracellular acidosis developed in quadriceps with
pHI falling from 6.75k0.02 to 6.50+0.08 (P<002).
[ K + Ii loss from heart muscle varied according
to the chamber; [K+ J i was reduced in right ventricular muscle from 143k2.6 mmol/l cell water to
135.8-+ 2-0 mmol/l cell water (Pc0.05), and in atrial
muscle from 156.7 4.6 mmol/l cell water to 138.7+
did not fall
2.5 mmol/l cell water (Pc0.005).[K
15. MAINTENANCE OF PULSATILE LUNG
CAPILLARY BLOOD FLOW: THE ROLE OF
THE PULMONARY VENOUS SYSTEM
B. RAJAGOPALAN,
J. FRIEND,T. STALLARD
and
G . DE J. LEE
Department of Cardiovascular Medicine, Radcliffe
Infirmary, Oxford
Even in pulmonary hypertension lung capillary blood
flow remains pulsatile (Lee & DuBois, 1955, Journal
of Clinical Investigation, 34, 1380; Karatzas & Lee,
1970, Cardiovascular Research, 4,265). The characteristics of the pulmonary arterial system responsible
for this finding have already been described (Reuben
el al., 1970, Cardiovascular Research, 4, 473, 1971,
Cardiovascular Research, 5, I ; Reuben, 1971, Circulation Research, 29, 40). We now describe studies
on the role of the left atrium and pulmonary veins
upon lung capillary blood flow. In dogs, the main
pulmonary vein from the left lower lobe was divided.
Cannulating electro-magnetic flow probes and pressure lines were inserted into the cut ends. These were
connected to a ‘shunt’ manifold, which allowed blood
flow from the lung lobe either to enter the left atrium
directly or to be diverted to a constant pressure
reservoir while a companion reservoir returned the
blood to the left atrium at an identical flow rate.
Lobar pulmonary arterial inflow was measured with
an electro-magnetic flow cuff. Lung capillary blood
flow was measured using the N20-plethysmograph
method.
The pulmonary vein flow pulse was a mirror image
of the left atrial pressure events when the lung lobe
and left atrium were in continuity. Lung inflation
produced little change in the vein flow pattern.
When lobar vein outflow was isolated from the
left atrium, using the reservoir system, its profile
resembled the pulmonary capillary flow pulse,
attenuated in amplitude and delayed in time; although
vein flow entering the left atrium from the companion
constant flow reservoir continued to be dominated
by left atrial pressure events. Lung inflation attenuated
the lobar vein outflow pulse but had little effect on the
left atrial inflow pattern.
At normal left atrial pressures the main pulmonary
veins appear to have a reservoir as well as a transmission function. The effects of elevating left atrial and
+