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Biomedical subjects

N Subramanian

Publications and source records attributed to N Subramanian.

At least 55 records · Page 3Linked to original sources
PubMed1986

Direct communication of a pulmonary artery with left atrium--report of a case with balloon occlusion studies and successful correction: a case report.

A 10 year old cyanotic boy had direct communication between right pulmonary artery and left atrium. During cardiac catheterization, the catheter-tip balloon occlusion of this communication resulted in restoration of arterial oxygen saturation to normal levels, predicting that surgical interruption of the communication would be curative. Successful surgical correction was achieved by interruption of the communication.

Cardiac Catheterization↗
PubMed1986

Inhibition of immunological and non-immunological histamine release from human basophils and lung mast cells by formoterol.

3-Formylamino-4-hydroxy-alpha(N-1-methyl-2-p-methoxyphenethyl-a min omethyl)benzylalcohol hemifumarate (formoterol fumarate, BD40 A, CGP 25 827 A-E) inhibited both allergic (anti-IgE) and non-allergic histamine release (calcium ionophore and human complement component C5a) from human basophils. The degree and efficacy of inhibition was comparable to that of ketotifen, equal to or better than fenoterol and ten times more potent than isoprenaline (beta 2-stimulator). Salbutamol, another beta 2-stimulator was practically ineffective in these models. Similarly the anti-IgE, calcium ionophore and complement component C5a induced release of histamine from human lung mast cells could be blocked by formoterol, its potency being again comparable to that of ketotifen. The above degranulation inhibition effect taken together with the pronounced bronchodilator property would confirm formoterol as a drug of choice in asthma with more efficient action than the other beta 2-stimulators such as fenoterol, salbutamol or isoprenaline.

Albuterol↗
PubMed1983

Type D double aortic arch. Double aortic arch with interruption of its left component proximal to the site of origin of left common carotid artery.

Type D double aortic arch in a five year old boy (with interruption of left arch proximal to left common carotid artery)--with persistent ductus arteriosus and stenosis of right and left pulmonary arteries diagnosed during life is reported. At surgery for P.D.A., the anatomy was confirmed. There was no vascular ring. Types A, B and C double aortic arches with interruption of left arch respectively distal to P.D.A., proximal to P.D.A. and proximal to left subclavian artery have already been reported. Ours happens to be the first case of type D double aortic arch diagnosed ante-mortem and confirmed at surgery.

Aorta, Thoracic↗
PubMed1982

Electrically induced release of radiolabeled histamine from rat hippocampal slices: opposing roles for H1- and H2-receptors.

Rat hippocampal slices were preloaded with 3H-histamine and superfused with physiological medium and electrically stimulated in the absence (S1) and in the presence (S2) of drugs. The electrically evoked 3H-overflow consisted mainly of histamine, was Ca++ dependent and completely blocked by tetrodotoxin, all pointing towards an impulse triggered neuronal release. Mepyramine, promethazine and diphenhydramine the H1-antagonists, inhibited the stimulation evoked histamine release in a dose dependent manner. Burimamide and cimetidine, the H2-antagonists, enhanced the stimulation induced release of histamine whereas dimaprit, the H2-antagonist, had the opposite effect. Histamine by itself did not influence its own release. The observations indicate an opposing role for H1- and H2-receptors in modulating spike induced histamine release and represents a functional consequence of the stimulation of the receptors.

Animals↗
PubMed1981

Experimental cerebral infarction in primates: regional changes in brain histamine content.

Histamine levels in different regions of the brain in the primate Macaca Radiata were studied following experimental infarction induced in the basal ganglia by coagulation of the middle cerebral artery. In the basal ganglia an elevation of histamine level was seen probably due to proliferation of mast cells. In the hypothalamus, a main constituent of the ascending histaminergic neuronal pathway, a sharp rise in histamine content occurred in infarcted as well as sham-operated animals: this probably reflects non-specific stress-related alterations. In contrast, the cortical area of the ischemic hemisphere showed a higher elevation of histamine, demonstrating that infarction in one region can cause widespread specific changes in histaminergic systems remote from the infarct. The rise in histamine level at the ischemic site could evoke an increase in microcirculation which might aggravate cerebral edema, while changes in the remote regions may be responsible for some of the neurological deficits following stroke.

Animals↗
PubMed1981

Omega chain methylated analogs of PGF2 alpha and PGE2.

Our previously published prostaglandin (PG) synthesis route, in which the omega-chain is added in the penultimate step, provides facile access to a wide variety of omega-chain variant PG analogs. Each series requires only the synthesis of the appropriate methylated acylphosphonate for the Emmons' condensation. The syntheses of analogs bearing the following methylation patterns are detailed: 15-Me; 17,17-(Me) 2; 17, 17, 20-(Me) 3; 18, 18, 20-(Me) 3; 15, 18, 18, 20-(Me) 4; and 15-OMe-18, 18, 20- (Me) 3. The well-known 16., 16-dimethyl prostaglandins have also been prepared by this sequence. The synthesis of 16, 16-tetramethylene-PG analogs is also described.

Methods↗
PubMed1981

Synthesis of macrolide prostaglandin analogs.

Prostaglandin analogs of the E- and F2 alpha-functional type, which are constrained to conformations in which the side-chains are close in space and specifically aligned in the terminal portions by covalent bonding, have been synthesized. These analogs are 1, (omega-1)-macrolides. The syntheses proceeded from aldehyde intermediate I via the Emmon's condensation with dimethyl n-(dimethyl-t-butylsilyloxy)2-oxoalkylphosphonate anions (II a or b). The macrolide closures were performed using 2, 2'-dipyridyl disulfide. For the synthesis of 9-ketoprostaglandin macrolides, a free 9-hydroxy is available for oxidation after macrolide closure, so long as the 9-position is protected as the acetate rather than benzoate. Chiroptical data revealed that the conformations of the macrolide prostaglandins are unchanged (relative to the natural unconstrained prostaglandins) in the vicinity of the five-membered ring and the allyl alcohol unit by the formation of the macrolide linkage.

Methods↗
PubMed1981

Molecular basis for prostaglandin potency. III. Tests of the significance of the "hairpin conformation" in biorecognition phenomena.

Prostaglandin analogs of the PGF2 alpha, 15-epi-PGF2 alpha, and PGE2 type bearing the following methyl substitution patterns -- 15-Me, 16, 16-(Me)2, 17, 17-(Me)2, and 18, 18, 20-(Me)3 -- and analogs constrained to "hairpin" alignment [via 1, (omega-1)-olide formation] and to "non-hairpin" arrangements [via 1, 9- and 1, 15-olide formation] are compared in the following biological assays: contraction of uterine and gastro-intestinal smooth muscle strips, luteolytic antifertility potency in the hamster, binding affinity to two different PGF2 alpha-receptor preparations from bovine corpora lutea, binding to the PGE-specific receptors from rat kidney and liver, inhibition of ADP- induced aggregation of human platelet-rich-plasma, and the effect on rat blood blood pressure. The methylated prostaglandins were also concerted to the corresponding prostacyclins and examined as to action on the platelet and on rat blood pressure. All evidence points to topographically distinct receptors for F2 alpha-, E- and I2- type prostaglandins. Cross-reactivity is reduced in most of the analogs examined. Independent of the target organ or tissue, the receptors show common features based on the functional class of PG recognized. "Hairpin" alignment improves binding (and potency) only for the PGF2 alpha specific assays. PGE-specific binding and potency is disrupted to an increasing extent as the chain branching point is moved further from the 15-hydroxyl center. In contrast 16, 16-dimethylation is particularly disruptive for the PGI2/E1 platelet receptor interaction.

Animals↗
PubMed1981

Methyl ethers of prostaglandins F2 alpha and I2.

Regiospecific monomethyl prostaglandin f2 alpha ethers (at 0-9, 0-11, and 0-15) have been prepared by total synthesis. The 9, 15-bis-ether was also prepared. The 11- and 15-monoethers have been converted to the corresponding prostacyclins. Nuclear Magnetic Resonance (NMR) spectral comparisons indicate conformational changes associated with ether formation; nonetheless, the PGF2 alpha monoethers all retain significant biological activity: 3-420% of natural PGF2 alpha. The 9- and 15- menthyl ethers show increased selectivity for luteolytic activity as measured in the hamster antifertility (HAF) assay. In contrast the prostacyclin ethers are essentially devoid of agonist activity on both the platelet and vasculature. Prostacyclin diastereomers [5a] also lack activity and it appears that any modification at or of the C-11 or C-15 functions reduces receptor binding by at least a factor of 100.

Animals↗
PubMed1981

Blood loss and side effects in day case abortion.

Suction termination of pregnancy was performed in 276 patients as an out-patient procedure under general anaesthesia. Ergometrine, oxytocin, or sterile water were given with the induction of anaesthesia. There was no significant difference in blood loss in the three treatment groups, although blood loss in termination of pregnancy performed after eight weeks was increased in all three groups. Nausea, vomiting and abdominal pain occurred significantly more often after ergometrine compared to oxytocin or water.

Abortion, Legal↗
PubMed1981

Ontogeny of histaminergic neurotransmission in the rat brain: concomitant development of neuronal histamine, H-1 receptors, and H-1 receptor-mediated stimulation of phospholipid turnover.

The ontogeny of histaminergic neurotransmission in the rat brain was studied by assessing development of histamine levels in brain regions, along with H-1 receptor binding of [3H]mepyramine and H-1 receptor-mediated cellular events. In the hypothalamus, which is rich in histaminergic innervation, levels of the amine were low at birth, increased sharply at 8 days of age, and reached adult concentrations shortly thereafter; this pattern is typical of most neurotransmitters. In contrast, regions poor in neuronal histamine showed an initially high histamine level and a subsequent decline with development, as is known to occur during general growth of tissues. The developmental profile of H-1 receptor binding sites resembled that of the neuronal histamine pool, and the increases with age resulted from changes in the number of binding sites without alterations in Kd. Cellular responses to H-1 receptor activation were assessed by determining the stimulation of phospholipid turnover evoked by intracisternally administered histamine, a process that has been shown to involve only the neuronal compartment. Again, the developmental profile was superimposable upon that of H-1 receptor binding and that of hypothalamic histamine levels. These studies indicate that ontogeny of histaminergic neurotransmission is a coordinated process, with simultaneous development of neuronal histamine, its key biosynthetic enzyme, and H-1 receptors coupled directly to cellular events.

Animals↗
PubMed1981

Trans-synaptic modulation of histamine H-1 receptor development in rat brain.

To determine whether neuronal histamine influences development of histamine H-1 receptors in the rat brain, neonates were given diphenhydramine, an H-1 antagonist, daily for the first 21 days of postnatal life. In control rats, specific H-1 binding of [3H]mepyramine in whole brain was low at birth and increased progressively toward adult levels by the end of the 3rd week. Animals treated with diphenhydramine showed marked elevations in binding as early as 4 days postnatally and the differences persisted throughout the experimental period. The increased binding in treated rats was specific to treatment with H-1 antagonists (diphenhydramine, mepyramine) as opposed to an H-2 antagonist (cimetidine); the alteration reflected enhancement of the number of binding sites without a change in Kd, a finding indicative of H-1 receptor supersensitivity. Similar results were seen in the hypothalamus, an area rich in neuronal histaminergic projections. Levels of histamine in the hypothalamus were unaffected by diphenhydramine administration until the end of the 3rd week, at which time, increases were noted. After the loading of the hypothalamus with [3H]histamine, release of label by K+ depolarization in vitro (an indirect index of release from the neuronal histamine pool) was readily obtained at all ages and was unaffected by diphenhydramine administration. Diphenhydramine did not alter histamine levels in brain regions in which most of the histamine is non-neuronal. These studies suggest that, even early in the ontogenesis of histaminergic synapses, a sufficient proportion of releasable histamine is associated with histaminergic neurons to enable trans-synaptic modulation of development of histaminergic H-1 receptors; consequently, blockade of these receptors with diphenhydramine results in supersensitivity even at the earliest stages of development.

Animals↗