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Biomedical subjects

R Shukla

Publications and source records attributed to R Shukla.

At least 163 records · Page 9Linked to original sources
PubMed1985

The mechanism of opening of the blood-brain barrier by hypertonic saline.

The permeability of the blood-brain barrier was assessed in the cat, using Evan's blue as circulant. Regional blood flow and vascular resistance in various areas of brain were measured using radioactive microspheres. Cardiac output (CO), blood pressure (BP), heart rate (HR), pH, pO2 and pCO2 were also measured. Hypertonic saline (5 M, 0.5 ml/kg), administered intravenously, increased the staining of the brain substance. It also produced a marked increase in cerebral blood flow after 5 min and a marked decrease in blood flow to all the regions of the brain after 20 min. The flow returned to normal after 40 min. The vascular resistance decreased at 5 min, increased at 20 min and returned to normal at 40 min. Cardiac output increased significantly at 5 min and decreased at 20 min, while at 40 min it returned to normal. Blood pressure decreased at 5 min, increased at 20 min, while heart rate steadily decreased. A complete recovery of cardiac output, blood pressure and heart rate occurred in 1 hr. No change was observed in pH, pCO2 and pO2. It is concluded that intravenous administration of hypertonic saline causes marked haemodynamic changes and increases the permeability of the blood-brain barrier due to transient impairment of autoregulation.

Animals↗
PubMed1985

Evidence for the involvement of histamine in the regulation of blood-brain barrier permeability.

Role of histaminergic mechanisms in the regulation of blood-brain barrier (BBB) was assessed in dog. Histamine increased the entry of sodium fluorescein from the blood to the cerebrospinal fluid (CSF) in a dose-dependent manner. Histamine receptor antagonists, mepyramine (H1) and metiamide (H2) per se did not affect the entry of dye in the CSF. Mepyramine failed to affect the change induced by histamine whereas metiamide completely blocked the histamine-induced entry of sodium fluorescein in CSF. 2-Methyl histamine, a specific H1-agonist, did not affect the barrier permeability. However, 4-methyl histamine, a specific H2 receptor agonist significantly increased the permeability of BBB. This increase was blocked by metiamide. Forskolin, a stimulant of adenylate cyclase, also increased the entry of dye in the CSF which could be significantly blocked by metiamide. It is concluded that histamine increases the permeability of BBB by affecting H2-receptors linked to adenylate cyclase.

Animals↗
PubMed1985

Intensification of the base deficit induced by vagotomy after atropine treatment in dogs.

The effects of atropine treatment on the heart rate, the arterial blood pressure, the respiratory rate, the acid-base profile and the oxygenation of arterial blood were investigated in chloralose anaesthetized dogs. As the I.V. atropine sulphate (1mg/kg) in saline (9% w/v) did not induce base deficit or alter the acid-base profile, the section of vagal parasympathetic (motor) fibres in normal (untreated) ones could not be held responsible for the observed base deficit after their vagotomy. Such observed base deficit was most likely engendered reflexively due to the section of vagal sensory fibres; as only general activation, not the withdrawal (section) of vagal sympathetic fibres might induce such an effect. Moreover, the bilateral vagotomy in these atropinized dogs induced a larger base deficit, which mostly contributed to the increase of H+ion concentration therein. This comparative enhancement of base deficit suggests that the opening of the negative feed back loop of the (aortic chemoreceptor) sensory fibres points to the blocking effect of atropine on the cholinergic link in the central (medulla) chemosensitive mechanism. The base excess observed after vagotomy in propranolol treated animals suggested that the base deficit vagal sensory fibres was mediated through reflexive activation of sympatho-adrenal axis.

Acid-Base Equilibrium↗
PubMed1985

An increase in metabolic acidosis induced by chloralose anaesthesia in dogs after sino-vagal denervation.

Chloralose anaesthesia in dogs increased the H+ ion concentration significantly from its reference values. The findings favoured that it was most probably engendered through anaesthetic depression of neural centre regulating H+ ion concentration of blood. Such increase was largely contributed by a significant increase in its metabolic fraction. A further increase of metabolic fraction after separate and joint section of carotid sinus nerves and vagi indicated their holding effect. The section of carotid sinus nerve induced greater increase in this fraction than that of vagi. It indicated differences between the two nerves in their metabolic fraction controlling influence. Hyperpnoea after vagi section decreased the carbonic acid fraction, whereas marginally reduced ventilation after carotid sinus nerve section increased the carbonic acid fraction. Moreover, the overall changes in H+ ion concentration followed the changes in carbonic acid fraction. The present study suggested that the depressive effect of chloralose anaesthesia on H+ ion controlling neural mechanism could be largely determined by degree of increase in its metabolic fraction.

Acidosis↗
PubMed1984

Evidence for the lack of serotonergic mechanism in the regulation of blood-brain barrier.

Role of serotonergic mechanism in the regulation of blood-brain barrier in anaesthetised cats and dogs has been investigated. In cats, the circulant used was Evans blue. The drugs as well as the circulant were administered through the left carotid artery. The staining of the brain substance was scored at autopsy. 5-Hydroxy-tryptamine (5-HT), 5-hydroxytryptophan (5-HTP), 5-HT uptake-inhibitors, citalopram and fluvoxamine, as well as normal saline produced no staining whereas hypertonic sodium chloride solution produced significant staining of the brain substance. In experiments on dogs, sodium fluorescein was injected intravenously and the cerebrospinal fluid (CSF) was collected through a needle put in the cisterna magna for estimation of the dye. Normal saline, 5-HT, citalopram, fluvoxamine and methysergide failed to affect the entry of sodium fluorescein in the CSF while hypertonic sodium chloride solution increased it significantly. Furthermore, 5-HT did not affect the increased entry of sodium fluorescein induced by hypertonic sodium chloride. It is concluded that serotonergic mechanism does not play a significant role in the regulation of blood-brain barrier.

Animals↗
PubMed1983

Analysis of hypothermic response to centrally administered histamine in pigeons.

The effect of intracerebroventricular (i.c.v.) administration of histamine (H), H1- and H2-receptor agonists and their antagonists, on the cloacal temperature of pigeon has been investigated. Histamine produced a dose-dependent hypothermia at an ambient temperature of 24 degrees C which was significantly blocked by a combination of mepyramine and cimetidine but was only partially antagonized by either of them alone. H1-receptor as well as H2-receptor agonists also produced hypothermic response with a time-course similar to that of H. Their effects were also significantly antagonized by mepyramine and cimetidine respectively. The histamine response was not modified by pretreatment with alpha- or beta-adrenoceptor antagonists. Histamine produced an insignificant hyperthermia at 10 degrees C but the hypothermic effect increased as the ambient temperature was raised up to 40 degrees C. It is concluded that both H1- and H2-histamine receptors are present in the brain of pigeon and are responsible for H-induced hypothermia.

Animals↗
PubMed1983

Intensification of the metabolic acidosis induced under alpha-chloralose anaesthesia with graded increase in the dose.

Surgical anaesthesia between planes 2-3 with alpha-chloralose in dogs induced simultaneous depression of ventilation viz., low oxygen (PaO2) tension, high carbon dioxide (PaCO2) tension and H+ion homeostasis (high base deficit). The anaesthesia on the aforesaid planes could be achieved only by doses not below 100 mg/kg. The progressive increase in the administered dose between 100 and 200 mg/kg did not alter the acid-base profile. Further increase beyond 200 mg/kg dose was followed by a steep increase in the base deficit enhancing H+ion (cH+) concentration. However, the steep fall in PaO2 accompanied by steep rise in PaCO2 was observed only when the dose was above 250 mg/kg. The findings in the present study indicated that depression of H+ion homeostasis under chloralose anaesthesia was induced by neural mechanism independent of respiratory centres.

Acidosis↗
PubMed1983

Acid-base profile of healthy mongrel Indian familaris canis determined by different techniques under two non-volatile anaesthetics.

The acid-base status of healthy mongrel Indian dogs was compared under pentobarbital sodium and alpha-chloralose anaesthesia. The findings showed similarity of canine acid-base profile under the two types of anaesthesia. Comparison among various techniques of determination of acid-base profile indicated accuracy of findings. However, a slight metabolic acidosis was persistently observed in the majority of dogs under both types of anaesthesia.

Acid-Base Equilibrium↗
PubMed1983

The effect of polyethylene glycol-200 on metabolic acidosis induced by chloralose anaesthesia.

Chloralose may be used in a 10% solution as an anaesthetic in dogs. The solubility of chloralose was found to be much higher in polyethylene glycol-200 (PEG-200) than in either warm (body temperature) or cold saline (0.9% NaCl). The intravenous (i.v.) administration of chloralose in warm saline solution induced acidosis as a result of the increase in the level of metabolic acids. The acidity generated by chloralose in almost neutral saline was probably the result of increase in the base deficit in the animal. The infusion of PEG-200 (almost neutral) significantly reduced the base deficit without disturbing the PaO2 or PaCO2 in the arterial blood. The base deficit value was significantly lower after administration of chloralose solution in PEG-200 (almost neutral) than after administration in saline. The use of PEG-200 as a solvent for chloralose was advantageous in two ways. Firstly, it prevented the production of acids in anaesthetic solution and neutralized the blood metabolic acids generated by chloralose administration in saline. Secondly, the solubility of chloralose (10% w/v solution) in PEG-200 was very much higher than in warm or cold saline.

Acidosis↗
PubMed1982

Analysis of histamine receptors in the central thermoregulatory mechanism of Mastomys natalensis.

1 The effect of intracerebroventricular (i.c.v.) injection of histamine on the rectal temperature of Mastomys natalensis at ambient temperatures of 10, 24 and 33 degrees C has been studied. 2 Low doses (0.1-1.0 microgram) of histamine produced hypothermia while larger doses (5-20 micrograms) produced dose-dependent hyperthermia. The hypothermic effect was significantly antagonized by mepyramine while the hyperthermia was blocked by cimetidine. 3 Histamine H1-receptor agonists, 2-methyl-histamine and 2-pyridyl-ethylamine, also produced hypothermia which could be blocked by mepyramine. 4 Histamine H2-receptor agonists, impromidine and dimaprit, produced hyperthermia which was antagonized by cimetidine. 5 Pretreatment of the animals with a beta-adrenoceptor antagonist, MJ1999, did not affect the response to histamine. 6 The hyperthermic effect of histamine (10 micrograms) was most marked at 10 degrees C and was attenuated at 33 degrees C. 7 It is concluded that both H1 and H2-histamine receptors are present in the brain of Mastomys. The H1-receptors mediate hypothermia and H2-receptors hyperthermia.

Animals↗