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Biomedical subjects

J R Mitchell

Publications and source records attributed to J R Mitchell.

At least 289 records · Page 16Linked to original sources
PubMed1971

Sensitive procedure for detecting residual viable virus in inactivated rabies vaccine.

A procedure for testing inactivated rabies vaccines of tissue culture origin for residual viable virus is reported in which the vaccine to be tested is passed in primary hamster kidney cell culture (PHK) before mouse inoculation. In preliminary experiments, titrations of rabies virus in which each dilution was passed in PHK before inoculating mice yielded titers 100 to 10,000 times higher than the titers obtained for the same virus by direct mouse inoculation. This rabies virus amplification procedure was evaluated by testing 18 lots of inactivated rabies vaccine of tissue culture origin. No viable virus was found in these vaccine lots when tested by direct intracerebral inoculation of mice. Eight of these 18 lots were found to contain viable virus, however, when tested by passage in PHK cell culture. The significance of low levels of viable virus in rabies vaccines is discussed. It is recommended that the amplification procedure described in this report be used in the safety testing of rabies vaccines of tissue culture origin and that it be evaluated for use in testing other rabies vaccines of low tissue content.

Animals↗
PubMed1971

Hypertension and arterial disease.

There is abundant evidence that the height of an individual's systemic arterial pressure is related, in a graded way, to his chances of developing ischaemic heart disease or cerebrovascular disease. The way in which the link operates in respect of coronary disease is not yet known, and further evidence is required before we can accept that the hypertension is necessarily a direct causal factor rather than a marker of some feature in the individual's make-up which is itself linked to the onset of arterial thrombosis (the ;series' or ;parallel' wiring dilemma). In respect of haemorrhagic stroke not only have we a link but we also have a mechanism of action plus evidence that pressure reduction can modify the risk. We have a ;series' wired circuit, and the problem now facing us is to acquire the wisdom which will allow us to decide when to seek out hypertension and what we should do when we find it.

Adult↗
PubMed1970

Guanethidine and related agents. 3. Antagonism by drugs which inhibit the norepinephrine pump in man.

Antagonism of the antihypertensive action of guanethidine by the tricyclic antidepressants, desipramine and protriptyline, has been demonstrated in controlled studies. These antidepressants also prevent the effect of the related ring-substituted guanidinium adrenergic neuron blockers, bethanidine and debrisoquin. That the rise in blood pressure when desipramine is added to guanethidine therapy is not due simply to a pressor action of the two drugs in combination was demonstrated by the lack of an increase in blood pressure when guanethidine was added to desipramine therapy. Investigations were conducted to determine whether antagonism of guanethidine's clinical effect could result from blockade by the tricyclic antidepressants of the norepinephrine pump in the adrenergic neuron membrane, thereby preventing the uptake of guanethidine into the neuron by this pump. Like guanethidine, the indirectly acting pressor amine, tyramine, enters the neuron via the norepinephrine pump. Desipramine, protriptyline, and amitriptyline in clinical doses all were found to block the pressor action of tyramine while potentiating the pressor effect of norepinephrine. The amino acid, methyldopa, does not enter the neuron via the norepinephrine pump, and its antihypertensive action is not altered by concomitant administration of tricyclic antidepressants. It is concluded from the evidence in this investigation together with the results of previous studies in experimental animals that clinical doses of desipramine-like drugs inhibit the norepinephrine pump in the peripheral adrenergic neuron in man and thereby prevent uptake of guanethidine to its site of action.

Antidepressive Agents↗