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Biomedical subjects

M T Khan

Publications and source records attributed to M T Khan.

At least 37 records · Page 2Linked to original sources
PubMed1991

Goat erythrocyte calmodulin is not abnormal.

Calmodulin was purified from goat erythrocyte hemolysate using heat treatment and Sephadex G-100 gel filtration chromatography. The molecular weight and Stokes, radius of the purified calmodulin was determined. The goat erythrocyte calmodulin stimulated (Ca(2+)-Mg2+)-ATPase but not (Mg2+)-ATPase and (Na(+)-K(+)-Mg2+)-ATPase. The (Ca(2+)-Mg2+)-ATPase of the erythrocyte membrane derived from human, rat, rabbit and pig were significantly stimulated.

Animals↗
PubMed1990

Serpentine aneurysm of the posterior circulation: report of two cases.

Giant serpentine aneurysms form a subgroup of giant intracranial aneurysms with specific radiological and surgical features. Previous reports have stressed the predilection of these lesions for the carotid circulation, particularly the middle cerebral artery. Two cases of serpentine aneurysm affecting the posterior circulation are reported and the problems of diagnosis and treatment of this lesion are discussed.

Cerebral Angiography↗
PubMed1988

Lack of some Ca2+-mediated processes in goat erythrocytes.

Ca2+ does not promote crosslinking of proteins nor stimulate proteolysis in goat and sheep erythrocyte membranes. Neither crosslinking nor proteolysis was observed even when the goat erythrocytes were loaded with calcium with the help of calcium ionophore A23187. Membrane-free human erythrocyte hemolysate, however, induced Ca2+-dependent crosslinking in goat erythrocyte membranes.

Animals↗
PubMed1987

Evidence for endothelium-dependent vasodilation of resistance vessels by acetylcholine.

In the perfused mesenteric arterial vasculature of the rabbit, vasodilation by acetylcholine (ACh) was almost completely blocked after a 15-min perfusion of the vasculature with 0.2% collagenase, an enzyme capable of removing endothelial cells. In the perfused mesenteric arterial vasculature of the rat, vasodilation by ACh was markedly, though not completely, inhibited by hemoglobin (10 microM), an agent which can inactivate endothelium-derived relaxing factor (EDRF). These results suggest that a major component of vasodilation of mesenteric resistance vessels in rabbit and rat by ACh is mediated by EDRF.

Acetylcholine↗
PubMed1987

Chorio angioma.

Explore the source record for details and available documents.

Adult↗
PubMed1986

Studies on the inhibitory effect of ouabain on the release of [3H]-noradrenaline from the rat heart.

In the rat Langendorff heart perfused with Krebs solution and prelabeled with [3H]-noradrenaline, ouabain caused arrhythmia as well as significant inhibition of spontaneous and electrically stimulated release of tritium. However, there is no causal relationship between the inhibition of tritium release and the occurrence of arrhythmia. Chromatographic analysis of the labeled perfusate suggests that ouabain reduced intact [3H]-noradrenaline fraction obtained during electrical stimulation. The inhibitory effect of ouabain on electrically stimulated release was completely antagonized by atropine, but not by indomethacin and phenoxybenzamine. However, none of the above agents antagonized the inhibitory effect of ouabain on spontaneous tritium release. Infusion of acetylcholine also inhibited electrically stimulated tritium release, and this effect was largely abolished by atropine. Thus it appears that in high concentrations, ouabain may release acetylcholine, which in turn activates presynaptic muscarinic inhibitory receptors leading to inhibition of noradrenaline release from the rat heart.

Animals↗
PubMed1984

Anti-hyperglycaemic effect of an extract of Myrtus communis in streptozotocin-induced diabetes in mice.

Intraperitoneal injection of streptozotocin (150 mg/kg) in mice produced an initial transient hyperglycaemia at 2 h followed by a second hyperglycaemic phase after 48-72 h which persisted throughout the 7-day observation period. An ethanol-water extract of Myrtus communis (2 g/kg) administered intragastrically 30 min before streptozotocin abolished the initial hyperglycaemic without affecting the second phase. Myrtus extract given prior to streptozotocin and repeated at 24 h and 30 h, did not allow hyperglycaemia to develop until after 48 h. Administration of Myrtus extract 48 h after streptozotocin significantly reduced the hyperglycaemia and this effect was maintained by its repeated administration. Myrtus extract had no effect on the blood glucose level of normal mice. These studies confirm the "folk-medicine" indication of Myrtus extract as potentially useful in the treatment of diabetes mellitus.

Animals↗
PubMed1982

Modulation by prostaglandins of the release of [3H] noradrenaline evoked by potassium and nerve stimulation in the isolated rat heart.

In the isolated rat heart perfused with Krebs solution and prelabeled with [3H] noradrenaline, we examined the effect of prostaglandins (PG) I2, E2, 6-keto-PGF1 alpha and their precursor, arachidonic acid, on the overflow of tritium elicited by potassium (K+) and by stimulation of cardiac sympathetic nerve plexus. Prostaglandins E2, I2 and arachidonic acid but not 6-keto-PGF1 alpha reduced K+ and nerve stimulation-induced overflow of tritium. Administration of indomethacin, an inhibitor of cyclooxygenase, increased tritium overflow elicited by either K+ or by nerve stimulation. During infusion of indomethacin, the inhibitory effect of both PGE2 and PGI2 on the K+ or nerve stimulation-induced overflow of tritium remained unaltered. In contrast, the effect of arachidonic acid to reduce K+ or nerve stimulation-induced overflow of tritium was abolished by indomethacin, indicating that the fatty acid inhibits release of tritium by its conversion to a product(s) of cyclooxygenase, presumably PGI2 and PGE2. These data suggest that prostaglandins, particularly PGI2 and PGE2 synthesized in the isolated rat heart act on prejunctional sites to modulate release of the adrenergic transmitter.

Animals↗
PubMed1980

Inhibitory effect of adenosine and adenine nucleotides on potassium-evoked efflux of [3H]-noradrenaline from the rat isolated heart: lack of relationship to prostaglandins.

1 In the isolated heart of the rat prelabelled with [3H]-noradrenaline (NA) and perfused with Krebs solution, administration of potassium (K+ 60 mumol) increased the efflux of total radioactivity and of [3H]-NA in the perfusate. 2 Adenosine triphosphate (ATP), adenosine diphosphate (ADP) and adenosine, but not inosine, dibutyryl cyclic adenosine 3',5'-monophosphate (db cyclic AMP) or db cyclic GMP reduced the K+/-evoked overflow of total radioactivity and of intact [3H]-NA, in concentrations too low to cause release of prostaglandins. ATP, ADP and adenosine did not affect tyramine-evoked overflow of tritium. 3 Blockade of prostaglandin synthesis with indomethacin did not alter the inhibitory effect of either ATP, ADP or adenosine on K+/-induced overflow of tritium, thereby indicating that these nucleotides inhibit adrenergic transmission by a mechanism unrelated to stimulation of prostaglandin synthesis. 4 Theophylline which increases entry of calcium (Ca2+) across the cell membrane and reduces its binding in the cell, enhanced K+/-evoked overflow of tritium and diminished the inhibitory effect of ATP, ADP and adenosine on K+/-evoked overflow of tritium from the heart, presumably by interfering with transneuronal Ca2+ metabolism.

Adenine Nucleotides↗
PubMed1979

Relationship between accumulation, storage and overflow of noradrenaline in the rat salivary gland after chronic treatment with guanethidine.

1 The effect of guanethidine on the endogenous noradrenaline (NA) content, accumulation and overflow of [3H]-noradrenaline ([3H]-NA) in the rat salivary gland was examined at various times after drug administration. 2 Twenty-four h after a single injection of guanethidine (1 or 10 mg/kg s.c.), the respective values for the endogenous NA content and for the accumulation and overflow of [3H]-NA were approximately 55, 85, 30%, and 15, 55, 10% of the controls. 3 Although [3H]-NA accumulation had returned to control levels within 48 h after the dose of 10 mg/kg guanethidine, the overflow of [3H]-NA evoked by electrical stimulation or excess potassium (K+) remained depressed. 4 After the low or the high dose of guanethidine, the NA content of the salivary gland was restored to about 50% of the normal value between 4 to 24 and 48 to 72 h, respectively. 5 The accumulation of [3H]-NA was inhibited by about 75% by cocaine. The same degree of inhibition was obtained 4 h after 10 mg/kg guanethidine. In these experiments phenoxybenzamine did not reduce the residual (25%) uptake. 6 The reasons for differential rates of recovery of the endogenous NA content and the storage of [3H]-NA after guanethidine are discussed.

Animals↗
PubMed1978

The local anaesthetic activity of a benzotriazinium salt.

1 The local anaesthetic properties of 2-n-propyl-4-p-tolylamino-1,2,3-benzotriazinium iodide (TnPBI) were compared with those of lignocaine hydrochloride on intact and desheathed sciatic nerves of the frog, on the phrenic nerve-hemidiaphragm preparation of the rat, and by the intradermal wheal test in the guinea-pig. 2 Both TnPBI and lignocaine were more potent on desheathed than on intact sciatic nerves. The potency of TnPBI was affected more than that of lignocaine by the presence of the sheath in intact nerves. 3 Both drugs inhibited conduction in the rat phrenic nerve, as shown by the reduction in twitch tension of the diaphragm elicited by nerve stimulation. TnPBI also caused an initial augmentation of the twitch tension of the diaphragm when applied directly to the muscle. 4 TnPBI was shown to be approximately twice as potent as lignocaine by the guinea-pig intradermal wheal test. 5 These results are discussed in view of the known effects of TnPBI on intracellular calcium storage.

Anesthetics, Local↗
PubMedDate not supplied

Vasodilation induced by acetylcholine and by glyceryl trinitrate in rat aortic and mesenteric vasculature.

In endothelium-containing rings of rat aorta which had been precontracted with phenylephrine, addition of acetylcholine (ACh) (0.010-10 microM) resulted in concentration-dependent, graded relaxation through the release of endothelium-derived relaxing factor (EDRF). Hemoglobin (3 and 10 microM) and methylene blue (10 microM) both produced marked inhibition of this EDRF-mediated relaxation. In the perfused mesenteric arterial vasculature of the rat, ACh-induced vasodilation was also inhibited by hemoglobin and by methylene blue, although to a lesser extent than was ACh-induced relaxation of aortic rings by these two agents. These findings indicate that EDRF mediates in large part ACh-induced relaxation of resistance vessels in the mesenteric vascular bed as well as large arteries. The nitrovasodilator glyceryl trinitrate (GTN) caused endothelium-independent relaxation of aortic rings as well as vasodilation of mesenteric arterial vasculature. GTN-induced relaxation of aortic rings was antagonized by hemoglobin as well as methylene blue, but to a lesser extent than was ACh-induced relaxation. However, hemoglobin did not inhibit and methylene blue actually potentiated GTN-induced vasodilation in the perfused mesenteric vasculature. Possible explanations of these paradoxical results are discussed.

Acetylcholine↗