Search PubMed⌕ Search

Biomedical subjects

V S Murthy

Publications and source records attributed to V S Murthy.

At least 73 records · Page 4Linked to original sources
PubMed1977

The spinal cord central canal in kaolin-induced hydrocephalus.

In order to study the cause of the great individual variations in kaolin-induced hydrocephalus, the lower brain stem and upper spinal cord were examined histologically in a series of young rabbits that had received injections of kaolin into the cisterna magna. Animals with complete occlusion of the outlets from the fourth ventricle into the subarachnoid space showed only a moderate ventricular dilatation, while cases with marked hydrocephalus also plugs of kaolin in the caudal part of the fourth ventricle. The intraventricular kaolin was adherent to the roof of the fourth ventricle by strands of connective tissue and it is suggested that the plugs served as valves that initially occluded the opening of the central canal and were then lifted away as the ventricle dilated and the roof moved posteriorly. The animals with marked hydrocephalus also had extensive dilatation of the central canal with cleft formation in the posterior columns. The observations support the concept that in hydrocephalus the central canal may serve as an alternative resorption route for the cerebrospinal fluid through communication with the spinal subarachnoid space.

Animals↗
PubMed1975

Hemoglobin solution: a potential oxygen transporting plasma volume expander.

The potential of a 6% stroma-free human hemoglobin solution (WXb8326) as a plasma volume expander with oxygen transport capabilities was evaluated in barbiturate-anesthetized spontaneously breathing dogs. WXb8326 compared favorably with dextran-70 and 5% albumin solution as a plasma volume expander. Serial phlebotomies to a blood pressure of 35 mm Hg and immediate replacement with the above colloid expanders showed that only WXb8326-exchanged dogs survived acute reductions in hematocrit to critical levels of smaller than or equal to 5%. After several exchanges with WXb8326 to levels as low as 1%, it was possible to demonstrate acute survival. With less drastic reductions in the hematocrit (between 5 and 10%) all dogs survived acutely regardless of the type of plasma volume expander used; however, subacute survival rates varied. Oxygen transport characteristics during isovolumic hemodilution (phlebotomy and simultaneous replacement with WXb8326) were studied in a separate series of spontaneously breathing dogs in which hematocrit was reduced to approximately 50% of control. Oxygen content of erythrocytic hemoglobin (EHb) and extraerythrocytic hemoglobin (EEHb) resulting from infusions of WXb8326 was studied in arterial and venous blood at different levels of hemodilution. WXb8326 did not interfere with the arterial oxygen saturation of EHb in the pulmonary vascular bed and EEHb was oxygenated as efficiently as EHb. Oxygen delivery to tissues differed between EHb and EEHb. Erythrocytic hemoglobin met oxygen demands under basal conditions while EEHb contributed oxygen to tissues during conditions of high oxygen extraction. It is concluded that WXb8326 is an attractive condidate as a plasma volume expander with the capacity to transport oxygen to tissues.

Anemia↗
PubMed1973

Further observations on mesenteric vasoconstriction, survival and the clotting defect after endotoxin administration.

1. The initial response after endotoxin administration (3 mg/kg) in cats involved pulmonary vasoconstriction. This was not seen when endotoxin was given by slow infusion and it could be prevented after a bolus injection of endotoxin by pretreatment of the cats with aspirin (10 mg/kg). Intense mesenteric vasoconstriction occurred in all the cats.2. The mesenteric vasoconstriction was a specific response of the mesenteric blood vessels. At the time the mesenteric bed constricted, the renal bed dilated, the hepatic arterial bed remained unchanged and the smooth muscle of the intestinal wall relaxed.3. Arterial blood from cats with a fully developed mesenteric vasoconstriction after endotoxin administration was perfused through a normal intestine. No immediate vasoconstriction developed but the perfused intestine constricted slowly over 60 minutes. This suggests that mesenteric constriction was not due to circulating vasoconstrictor factors or the intestinal innervation, but involved a slow local mechanism within the intestine. It could not be prevented or reversed by a variety of pharmacological agents.4. These observations suggest that endotoxin caused a unique type of mesenteric vasoconstriction in cats by a local mechanism which took up to 60 min to develop, was sufficiently potent to reduce mesenteric flow to <30% control, and was maintained until death of the cats. Blood from these animals did not clot when placed in a glass tube.5. The mesenteric constriction and the clotting defect could be prevented by repeated administration of aminophylline and dextran solution before and after a bolus intravenous injection of endotoxin. Arterial pressure and mesenteric flow were maintained for at least 10 h in these experiments. Inadequate treatment intensified rather than reduced the intestinal mucosal damage.6. Cats were treated with aspirin, endotoxin and the optimal regimen for prevention of the mesenteric constriction and allowed to recover from the anaesthetic agent. In this series, 63% survived indefinitely compared to 25% after aspirin and endotoxin treatment and 0% after endotoxin alone.7. The possible mechanisms of action of aspirin and aminophylline-dextran solution are discussed. Our failure to obtain 100% survival is probably due to pulmonary damage which develops 10-24 h after endotoxin administration. This delayed pulmonary action of endotoxin is not prevented by aspirin treatment and it seems unlikely that aspirin will be of any value in the treatment of the pulmonary lesion in man.

Aminophylline↗
PubMed1972

Effects of vasopressin and isoprenaline infusions on the distribution of blod flow in the intestine; criteria for the validity of microsphere studies.

1. The distribution of superior mesenteric arterial flow was investigated by radioactive microspheres. The small intestine received 83% of the flow ((85 ml/min)/100 g intestine) and flow was uniform along the length of the small intestine.2. The intestinal wall was separated into 3 layers-muscle, submucosa and mucosa. The muscle received (8 ml/min)/100 g intestine and the combined submucosa and mucosa (77 ml/min)/100 g intestine.3. The distribution of microspheres between the mucosa and submucosa depended on the size of the microspheres; the smaller the spheres, the more were found in the mucosa. It also depended on the state of the vascular bed; if microspheres were given during an infusion of vasopressin, a subsequent infusion of isoprenaline resulted in movement of some of the spheres from the submucosa into the mucosa.4. Histological studies after India ink injection showed few capillary-sized vessels but many large vessels in the submucosa. Capillary-sized vessels arose close to the junction with the mucosa and passed into the mucosa.5. These and other data suggest that the intestine consists of two parallel-coupled sections, one to the muscle and the other through the submucosa to the mucosa. The vessels in the submucosa are in series with those in the mucosa and submucosal shunts do not exist. Redistributions of flow between mucosa and submucosa cannot therefore occur during stimulation of the sympathetic nerves or infusions of drugs such as noradrenaline or adrenaline.6. When microspheres are used in pharmacological investigations on distribution of blood flow in organs, controls to validate the method for the particular areas being studied are essential. If the vessels in the areas studied are in series rather than in parallel, the method is invalid.

Animals↗
PubMed1971

Mesenteric vasoconstriction after endotoxin administration in cats pretreated with aspirin.

1. Study of the delayed responses to lethal doses of endotoxin in cats is complicated by acute pulmonary vasoconstriction which results in hypotension, cardiac failure and pulmonary oedema. This acute response is abolished if the animal is pretreated with aspirin (10-100 mg/kg). In these cats, pretreated with aspirin, arterial pressure and right atrial pressure remain unchanged in the first 2 h after administration of endotoxin. Later, arterial pressure falls and the animals die but no haemorrhagic lung lesions are visible.2. These results confirm our previous conclusion that the delayed lethal response to endotoxin is an independent action and not a secondary consequence of the acute response. The mechanism of the action of aspirin is discussed and it is suggested that it prevents the release by endotoxin of vasoactive substances, possibly from platelets.3. In cats pretreated with aspirin, administration of endotoxin results in a marked mesenteric vasoconstriction. Although arterial pressure does not decrease significantly, superior mesenteric arterial flow decreases to 20% of control in the first hour after endotoxin and remains at this low level until the animal dies. Mesenteric ischaemia may contribute to the cat's death.4. The mesenteric vasoconstriction is not reduced by prior administration of phenoxybenzamine and is only slightly reduced after phenoxybenzamine, hypophysectomy and nephrectomy. It is concluded that catecholamines, vasopressin and angiotensin play at most a minor role in the mechanism of this vasoconstriction and that other unknown factors are predominant.

Angiotensin II↗
PubMedDate not supplied

Cardiovascular and neuromuscular effects of esmolol during induction of anesthesia.

Sixteen subjects scheduled for surgical procedures under general anesthesia participated in an investigation of the effects of esmolol on the transient hypertension and tachycardia that was observed during endotracheal intubation and on the duration of succinylcholine-induced neuromuscular blockade. In eight subjects, infusion of esmolol was begun five minutes before induction of anesthesia and continued for 12 minutes after induction. In the remaining subjects, an equivalent volume of solvent (D5W) was infused for 12 minutes. Infusion of esmolol significantly attenuated the cardioacceleration observed during intubation without any significant effect on the pressor effects of the procedure. Esmolol delayed the recovery from succinylcholine-induced neuromuscular blockade by less than three minutes. The mechanism of this delay remains to be investigated, although such a delay does not have clinical significance. Esmolol-induced attenuation of the tachycardia seen during intubation may offer a protective effect on the myocardium, especially in elderly subjects and patients with coronary artery disease.

Adrenergic beta-Antagonists↗