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Biomedical subjects

A M Johri

Publications and source records attributed to A M Johri.

3 recordsLinked to original sources

Severe erectile dysfunction is a marker for hyperprolactinemia.

The need for routine prolactin (PRL) measurement in the initial evaluation of erectile dysfunction (ED) has been questioned because of the low rate of hyperprolactinemia (HP) in these men and the costs involved. In addition, it is widely thought that sexual desire problems are a good clinical marker for HP and/or low testosterone in men with ED. Within a 15-month period, 844 consecutive PRL and sexual hormone determinations were conducted in men at the Kingston General Hospital. Of these patients, 138 were comprehensively evaluated at the first visit for ED and completed the International Index of Erectile Function (IIEF). In the 138 patients, 2.2% had severe hyperprolactinemia (>35 ng/ml), within the range of 1-5% previously reported. No correlation between initial prolactin value and the sexual desire domain or the erectile function domain (EFD) of the IIEF was found for this population. However, all cases of severe HP were found to occur in men who scored less than 10 in the EFD of the IIEF. Low libido is widely accepted as a marker of HP. In this study, HP was found in patients not reporting major problems with a desire disorder. Clinically significant HP may be reliably found with routine biochemical evaluation and in this series was not detected in patients with EFD scores above 10. A routine PRL measurement is inexpensive and early detection of a serious and treatable disease may afford greater therapeutic success.

Adult↗

N-Type Ca(2+) channels trigger release of excitatory and inhibitory neurotransmitter from nerve endings in canine bronchi.

We set out to characterize the types of Ca(2+) channels that mediate release of the predominant excitatory (acetylcholine) and inhibitory (norepinephrine) neurotransmitters in canine bronchi, using electrically evoked contractions and relaxations, respectively, as indicators of this release. We found that the selective N-type Ca(2+) channel blocker (omega-conotoxin GVIA) eliminated electrically evoked contractions in a dose-dependent fashion (half-maximal inhibition in the presence of 1-5 nM) but had no significant effect on those evoked by exogenously added acetylcholine. Selective blockers of P-type Ca(2+) channels (omega-agatoxin TK; 10(-8) to 10(-7) M) or of L-type Ca(2+) channels (nifedipine; 10(-8) to 10(-6) M) had no significant effect on the responses to neurally released or exogenously added acetylcholine. Likewise, electrically evoked relaxations were blocked by omega-conotoxin GVIA (10(-7) M) but not by omega-agatoxin TK (10(-7) M) or nifedipine (10(-7) M); none of these Ca(2+) channel blockers had a significant inhibitory effect on isoproterenol-triggered relaxations. We conclude that excitatory and inhibitory neurotransmission in canine bronchi is mediated predominantly by N-type Ca(2+) channels, with little or no contribution from L-, P-, Q-, or T-type channels.

Acetylcholine↗

Diagnosis of fetal hydrocephalus by ultrasound.

An ultrasound scan of a fetus at 26 weeks gestation suggested abnormal dilatation of a lateral cerebral ventricle. Serial scans confirmed progressive dilatation of both lateral ventricles. Clinical hydrocephalus causing obstructed labour occurred and required craniotomy. Post mortem upon the fresh still born infant confirmed internal hydrocephalus.

Adolescent↗