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Biomedical subjects

H N Sapru

Publications and source records attributed to H N Sapru.

At least 73 records · Page 4Linked to original sources
PubMed1983

Vasopressor and depressor areas in the rat medulla. Identification by microinjection of L-glutamate.

L-Glutamate (in 0.1 microliter of 0.9% NaCl) was injected via multibarrelled glass micropipettes into the ventrolateral medulla of urethane-anesthetized rats. This area, explored stereotaxically, extended from 2.2 mm rostral (near trapezoid bodies) to 0.4 mm caudal, with respect to the obex, 2.4 mm lateral to the mid-line on each side and 2.4 mm deep from the ventral surface of the medulla. Two types of responses were elicited by injection of L-glutamate. One type was a dose-related increase in arterial pressure and heart rate; these responses were elicited from the lateral portion of nucleus reticularis gigantocellularis, the medial aspect of nucleus reticularis parvocellularis and the dorsal-lateral reticular nucleus. The second type of response was a dose-related fall in arterial pressure with no change in heart rate; this response was localized caudal to pressure areas in the caudal ventrolateral part of nucleus reticularis gigantocellularis, ventrolateral nucleus reticularis ventralis, nucleus ambiguous and the A1 region. Glutamic acid diethylester (GDEE), an antagonist of L-glutamate, blocked all the cardiovascular effects of L-glutamate. These results indicate the presence of receptors for glutamate in the pressor and depressor areas. Glutamic acid diethylester caused a fall in blood pressure when injected on its own into pressor sites suggesting the existence of a glutaminergic input to the pressor sites. Inhibition of neuronal activity in pressor sites produced by microinjection of muscimol (a potent neuroinhibitory analogue of GABA) caused a decrease in blood pressure. On the other hand, pressor responses resulted following similar inhibition in the depressor sites. These results indicate that the pressor and depressor sites identified in the ventral medulla of the rat may have an important role to play in central cardiovascular regulation.

Animals↗
PubMed1983

Electrophrenic respiration following anastomosis of phrenic with branchial nerve in the cat.

Patients with high spinal cord injuries may be totally dependent on artificial ventilation. Prolonged use of mechanical devices requires intensive care, which restricts the mobility of these patients. Electrophrenic respiration has been used with success to overcome this difficulty. However, a prerequisite for electrophrenic respiration is a viable phrenic nerve. Patients with spinal cord injuries at the C-3 to C-5 levels do not have a viable phrenic nerve due to gradual degeneration of axons in these nerves. In the present study on cats, the authors caused degeneration in one of the phrenic nerves by sectioning it low in the neck. Then the distal end of the phrenic nerve was anastomosed to the proximal segment of a sectioned brachial nerve. Sixteen to 32 weeks were allowed for the growth of brachial axons into the anastomosed phrenic nerve. Each cat served as its own control because one of the phrenic nerves was left intact. It was observed that pacing of the anastomosed phrenic nerve produced respiration comparable to spontaneous respiration or to respiration induced by pacing the intact phrenic nerve. Lack of rhythmic bursts of electrical activity in the anastomosed phrenic nerve and electromyographic activity in the ipsilateral hemidiaphragm confirmed that the anastomosed phrenic nerve remained disconnected from the respiratory motoneurons. Abundance of collagen matrix in the electron micrographs of the anastomosed phrenic nerve indicated that degeneration of the axons of phrenic motoneurons had occurred and the brachial nerve had grown into the phrenic nerve stump. These results indicate that electrophrenic respiration may be possible in patients with spinal cord injuries at the C-3 to C-5 vertebral levels if the phrenic nerve is kept viable by anastomosing it to a branch of the brachial nerve.

Animals↗
PubMed1983

Medullary gamma-aminobutyric acid (GABA) receptors and the regulation of blood pressure in the rat.

The cardiovascular effects of a GABAergic agonist (muscimol) and antagonist (bicuculline methiodide) were determined after microinjection (100 nl) into ventrolateral vasodepressor and vasopressor neuron pools. In urethane-anesthetized rats, these neuron pools were identified bilaterally by observing pressor or depressor responses after the microinjection of L-glutamate (333 ng). The bilateral microinjection of muscimol (0.1-10 ng/site) into vasodepressor sites caused a dose-related (0.1-10.0 ng/site) increase in the blood pressure, heart rate and pulse pressure. In ventrolateral vasopressor sites, muscimol (0.1-10.0 ng/site) caused a marked fall in blood pressure, heart rate and pulse pressure. The depressor response elicited by aortic nerve stimulation (2 V, 25 HZ, 3 msec) was blocked and reversed by muscimol microinjections into vasodepressor sites. In these sites, muscimol also caused a similar reversal of the depressor response induced by stimulation of pulmonary C-fibers (J-receptors) after the right atrial administration of phenyldiguanide (30 micrograms/kg). All the effects of muscimol were blocked or reversed by the bilateral microinjection of bicuculline methiodide into the vasodepressor and vasopressor sites. These results demonstrate the importance of ventrolateral vasodepressor and vasopressor neuron pools in the maintenance and reflex regulation of blood pressure and suggest that intrinsic GABAergic systems may serve to modulate activity in these neuron pools.

Animals↗
PubMed1982

Opioids increase laryngeal resistance and motoneuron activity in the recurrent laryngeal nerve.

[D-Ala2,Met5]enkephalinamide (DAME), [D-Ala2,Leu5]enkephalinamide (DALE) and morphine sulfate (MS) increase activity in the recurrent laryngeal nerve (RLN) within 1 s subsequent to right atrial administration. The activation of the RLN was correlated with a large increase in the resistance to airflow in the in situ isolated larynx. Single unit recurrent laryngeal motoneuron recordings showed that the increase in laryngeal resistance was caused by the continuous activation and recruitment of expiratory motoneurons. Results obtained with opioids mimicked those of phenyldiguanide (20-40 micrograms/kg RA), an agent known to stimulate pulmonary J-receptors. Opioid-induced increases in laryngeal resistance were blocked by bilateral section of the RLN and pretreatment with naloxone (100 micrograms/kg RA). Naloxone had no effect on PDG responses. During the initial period of laryngeal motoneuron activation, the phrenic nerve (PN) was inhibited, however, the activation of the RLN was not dependent upon PN inhibition. It was concluded that stimulation of pulmonary opiate receptors, which may be associated with vagal afferents, elicit a reflex activation of expiratory recurrent laryngeal motoneurons resulting in an increase in laryngeal resistance.

Animals↗
PubMed1982

Pulmonary opiate receptor activation evokes a cardiorespiratory reflex.

The administration of [D-Ala2,Met5]enkephalinamide (D-AME) and [D-Ala2,Leu5]enkephalinamide (D-ALE) into the right atrium of decerebrate rats caused bradycardia, a slight transient biphasic blood pressure response and apnea within 1-2 sec. Apnea was followed by rapid shallow breathing. These effects were dose related (1-1000 micrograms/kg) and blocked by pretreatment with naloxone. Atropine blocked the bradycardia. Sectioning the vagi at the level of the diaphragm did not affect the responses, whereas bivagotomy below the cardiac branches abolished all responses. The triad of responses was attributed to a reflex action arising from vagal afferents within the lung. These results were confirmed in paralyzed , artificially ventilated animals. In these animals, the enkephalin analogues produced a cessation of phrenic nerve (PN) activity followed by a decrease in the duration of bursts. The recurrent laryngeal nerve (RLN) was concomitantly excited in a continuous decremental fashion. This excitation was independent of PN inhibition. Recordings of single and near single pulmonary vagal afferents demonstrated no effect of D-AME or D-ALE on stretch and irritant receptors. However, type J-receptors were stimulated.

Animals↗
PubMed1982

Peripheral versus central cardiorespiratory effects of morphine.

The administration of morphine sulfate (MS, 2 mg/kg) into the right atrium in decerebrate rats, produced a dramatic bradycardia, apnea, and a slight transient biphasic blood pressure response within 1 sec. The bradycardia was slowly restored to control levels within 8-10 min and was prevented by pretreatment with atropine. Apnea (7.3 +/- 2.2 sec) was followed by a period of rapid shallow breathing. Acute tolerance to these effects developed to subsequent doses of morphine. In paralyzed artificially ventilated animals, morphine produced: (1) cessation of phrenic nerve (PN) activity which was followed by bursts of shortened duration; and (2) concomitant excitation of the recurrent laryngeal nerve (RLN), this activity exhibited a continuous discharge which was asynchronous with that of phrenic nerve. These actions of morphine were qualitatively similar to those observed with phenyldiguanide (PDG) and were found to be reflexogenic, i.e. emanating from the lungs via stimulation of pulmonary C-fibers. Bilaterally vagotomized animals only responded to morphine with respiratory depression, characterized by a severe decrease in respiratory rate and minute ventilation. On the other hand, animals with intact vagi showed stimulation of rate and minute ventilation following a brief period of apnea. They were less sensitive than vagotomized animals to the depressant action during the first 8 min after administration of morphine. All the effects of morphine were blocked by pretreatment with naloxone (50-400 micrograms/kg, i.v.). These results indicate that the initial cardiorespiratory effects of morphine are due to a peripheral reflex action arising from the stimulation of opiate receptors associated with pulmonary C-fibers, e.g. J-fibers.

Animals↗
PubMed1982

Pulmonary vagal afferent stimulants in the conscious rat: opioids and phenyldiguanide.

Phenyldiguanide (PDG, 40 microgram/kg), D-ala2-met5-enkephalinamide (D-AME, 250 microgram/kg) and morphine sulfate (MS, 2 mg/kg) injected into the right atrium (RA) of conscious freely moving rats produced a profound bradycardia and hypotension 1-2 sec subsequent to administration. Concomitant with the cardiovascular effects apnea occurred and lasted approximately 5 sec. Atropine methyl nitrate (2 mg/kg, RA) significantly attenuated the bradycardia and hypotension produced by all three agents. Naloxone blocked only the opioid responses. Coordinated motor activity was impaired following the administration of PDG (40 microgram/kg, RA). Fifty percent of the animals receiving PDG failed to remain on a rotor rod for a 2 min period. Only 8 percent of the saline treated group fell off during this period. It was concluded that the cardiovascular, respiratory, and motor effects caused by PDG, in the conscious freely moving rat, were the result of stimulation of pulmonary vagal afferents (J-receptors). The cardiovascular effects of opioids are also believed to arise from the stimulation of J-receptors. However, unlike PDG, these effects are mediated by pulmonary opiate receptors.

Animals↗
PubMed1982

Greater splanchnic nerve activity in the rat.

The greater splanchnic nerve trunks in the rat, unlike in other experimental animals, do not join celiac plexus directly. These nerve trunks join small ganglia, the cardiac ganglia, on either side. The cardiac ganglia are located about 1 cm rostro-lateral to unpaired celiac ganglion. The greater splanchnic nerve activity immediately proximal to celiac ganglion is predominantly post-ganglionic in the rat. On the other hand, the activity of the greater splanchnic nerve proximal to the celiac ganglion is predominantly preganglionic in other experimental animals, (e.g., cat), In the rat, preganglionic sympathetic nerve activity is predominant in the segment of the greater splanchnic nerve proximal to the cardiac ganglion.

Animals↗
PubMed1981

Aortic nerve stimulation in the rat: cardiovascular and respiratory responses.

Cardiovascular response and changes in the phrenic and recurrent laryngeal nerve activities to the electrical stimulation of the aortic nerves were studied in the decerebrate male Wistar rats. Stimulus parameters were varied over a wide range (intensities 0.1-10 volts, frequencies 2-150 pulses per sec, durations 0.01-10 msec) and stimulation was continued for 1 min to ensure that steady state was reached. Stimulation of the aortic nerves consistently produced decreases in blood pressure and heart rate (baroceptor responses) while increase in blood pressure and heart rate (chemoreceptor responses) were never obtained. Inhibition of phrenic and recurrent laryngeal nerve activities (baroceptor responses) always followed stimulation of aortic nerves while facilitation of these nerve activities (chemoreceptor responses) was never observed. These results indicate that the aortic nerves of the rat contain mainly baroceptor afferent fibers and there are few, if any, functional chemoreceptor fibers in these nerves.

Animals↗
PubMed1981

Stimulation of pulmonary J receptors by an enkephalin-analog.

Respiratory and cardiovascular actions of a stable enkephalin-analog (EA), D-met2-pro5-enkephalinamide, were studied in decerebrate male Wistar rats. Injection of a small dose of EA (10 micrograms/kg) into the right atrium produced apnea, bradycardia and hypotension within 1 to 2 sec. These effects lasted for 2 to 4 sec. Apnea was followed by a period of fast and shallow breathing which lasted for 7 to 10 min. The decrease in heart rate and mean blood pressure was 26 +/- 3% (S.E.) and 12 +/- 1.5% (S.E.), respectively. Higher doses of EA used in this study (100,500 and 1,000 micrograms/kg, right atrium) produced similar responses. However, the durations of apnea and fst and shallow breathing and magnitudes of bradycardia and hypotension were greater with the higher doses. Bilateral vagotomy (low in the neck) abolished these effects. These actions are typical of pulmonary J receptor stimulation. Nerve recording experiments in artificially ventilated rats showed that interruption of vagal innervation to the lungs abolished the EA-induced cessation of phrenic nerve activity (apnea), increased frequency of phrenic nerve bursts (fast breathing) and decreased spike activity in each burst (shallow breathing). These results suggested that EA stimulated lung sensory receptors. Of the known lung sensory receptors (stretch, irritant and J. receptors), only pulmonary J receptors are known to produce apnea, bradycardia and hypotension. Direct recordings from pulmonary J receptor fibers in thin filaments of vagus confirmed that EA stimulates these receptors.

Animals↗
PubMed1979

Cardiovascular and respiratory effects of some anesthetics in the decerebrate rat.

The cardiovascular and respiratory effects of pentobarbital, ketamine, chloralose and urethane were studied in decerebrate rats. All the anesthetics reduced blood pressure and heart rate. Pentobarbital, chloralose and ketamine, but not urethane, reduced respiratory rate. None of these agents had a significant effect on tidal volume. All these anesthetics significantly attenuated the carotid occlusion, tilt and sodium cyanide chemo-receptor response. These results suggest that the decerebrate rat may be a more suitable preparation, compared to the anesthetized one, for studying cardiovascular and respiratory responses in this species.

Anesthetics↗
PubMed1979

Role of receptor elements in baroceptor resetting.

Spontaneously hypertensive rats (SHR), 4 wk of age, were treated with antihypertensive agents for 40 wk. The treatment was withdrawn for 2 wk so that the animals experienced hypertension for about 1 wk. The aortic arch was then perfused and aortic nerve activity was recorded. The threshold pressure was 140 mmHg in these SHR. This threshold pressure was less than that observed in age-matched untreated SHR (160--180 mmHg) but greater than that observed in age-matched Kyoto-Wistar rats (80--120 mmHg), indicating partial baroceptor resetting. No significant changes were observed in the vascular wall in these SHR, and partial baroceptor resetting was completely reversed when short duration of hypertension was reversed. On the other hand, baroceptor resetting in untreated SHR was always accompanied by significant changes in vascular wall, and reversal of baroceptor resetting was contingent upon regression of vascular wall hypertrophy. Partial baroceptor resetting in absence of significant changes in vascular wall may be explained by adaptation of baroceptors to persistent high blood pressure.

Animals↗
PubMed1977

Carotid and aortic chemoreceptor function in the rat.

Carotid and aortic chemoreceptor function was studied in normal Wistar rats. Sodium cyanide, lobeline HCl, and doxapram HCl in the doses of 2-400 mug/kg injected into the external carotid artery stimulated respiration significantly. Injections of the drugs into the ascending aorta produced less effects which were abolished after section of the carotid sinus nerves. The drugs produced a significant increase in the carotid sinus nerve activity but failed to do so in the aortic depressor or recurrent laryngeal nerves. These results indicate that the carotid chemoreceptor function in Wistar rats in normal while functional aortic chemoreceptors are absent in them.

Action Potentials↗
PubMed1977

Vasopressin release in the spontaneously hypertensive rat.

Vasopressin (antidiuretic hormone, ADH), release in response to hemorrhage was studied in spontaneously hypertensive rats (SHR), Kyoto-Wistar rats (KWR), and Wistar rats (WR). The rats were anesthetized with pentobarbital sodium and ADH concentration was measured before and after three successive hemorrhages at 15 min intervals. The blood samples for radioimmunoassay (RIA) of ADH were collected from the external jugular vein. The ADH release in response to hemorrhage was significantly reduced in debuffered WR (carotid and aortic baroceptors and atrioventricular receptors deafferented), intact KWR and intact SHR when compared to the intact WR.

Animals↗
PubMed1977

Effect of 5-hydroxytryptamine on the peripheral chemoreceptors in the rat.

5-Hydroxytryptamine (5-HT), in the doses of 2-5 mug/kg injected into the carotid body area, produced a significant increase in the respiratory rate and carotid sinus nerve activity. Selective ablation of the ipsilateral carotid sinus nerve abolished the respiratory stimulation produced by the drug. On the other hand, the same doses of 5-HT injected into the ascending aorta did not produce stimulation of respiration when the carotid sinus nerves were sectioned. The activity of the aortic nerves did not increase after injecting the drug into the ascending aorta or at the root of the right subclavian artery. These results indicate that 5-HT stimulates the chemoreceptors in the carotid body of the rat. The lack of responses to the injections of the drug in the aortic or subclavian region was due to the absence of chemoreceptors in these regions of the rat.

Animals↗
PubMed1977

Ventilatory responses to threshold loaded respiration in man.

In postoperative patients one frequently observes respiratory difficulty in excess of what is indicated by physical alterations in respiratory mechanics. This would suggest that some patients lack normal compensatory mechanisms which respond to mechanical changes in the lung. It is entirely possible that inadequacy of compensatory mechanisms is present before surgery and predisposes patients to respiratory distress. In the clinical environment elaborate testing is precluded by the physical status of the patients. Thus, a noninvasive procedure has been designed to apply stress to the respiratory system in order to study the effect of stress at increasing levels of CO2. In this test a subject's respiration is measured as he rebreathes a mixture of 7% CO2 and 93% O2 from a closed system. On successive trials, fixed pressure inspiratory threshold loads are applied in sequence. With this type of load the increased work required to inspire a given volume depends only on the increased inspiratory pressure. In most normal subjects CO2 response was incrementally depressed when threshold loads were introduced. Patients with brain stem lesions showed a greater depression at higher loads. This may indicate a reduced ability to tolerate increased loads to breathing.

Carbon Dioxide↗