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Biomedical subjects

B Lisander

Publications and source records attributed to B Lisander.

At least 19 recordsLinked to original sources

Capsaicin pretreatment of rats does not prevent tissue extravasation of albumin from intra-abdominal trauma.

Intra-abdominal surgery causes a loss of plasma into tissues within and around the abdomen, predisposing to a decreased tissue viability and postoperative complications. In a rat model of intra-abdominal trauma, we investigated whether neuropeptides released from thin afferent nerve endings may contribute to this extravasation. Newborn male Wistar rats were pretreated with capsaicin 50 mg/kg s.c., leading to a lifelong degeneration of thin afferents. The same animals, when adult, were subjected to experiments under chloralose anesthesia in which tissue clearances of radiolabelled albumin were determined by a double isotope technique. Non-pretreated animals served as controls. In non-traumatized animals, pretreated rats had a higher loss of labelled albumin in calf muscle. In animals subjected to the standardized intra-abdominal trauma, the pretreatment did not decrease the trauma-induced loss of albumin. In neck skin, the loss of protein was higher in pretreated animals, possibly due to a decreased trauma-induced sympathetic activation. In conclusion, degeneration of thin afferent fibers may alter the autonomic reflex response to intra-abdominal trauma, but neuropeptide release from afferents apparently plays no role in the relocation of albumin.

Abdominal Injuries

Tissue extravasation of albumin from intraabdominal trauma in rats.

Intraabdominal surgery tends to lower circulating plasma volume by mechanisms unrelated to bleeding and evaporation. In chloralose-anesthetized rats, the tissue clearance of radiolabelled albumin was determined by a double isotope method. Animals were subjected to a standardized abdominal trauma, eliciting minimal bleeding and evaporation, and others served as controls. The trauma significantly increased tissue albumin extravasation in abdominal skin, abdominal wall, pancreas, small intestine, colon, mesentery and diaphragm. Considering the mass of the respective tissues, a substantial portion of the albumin extravasation took place in the abdominal wall. No increased albumin clearance was found in extra-abdominal tissues. It is suggested that abdominal surgery decreases plasma volume by extravasation in the operation field.

Abdominal Injuries

Anaphylatoxin and terminal complement complexes in red cell salvage.

Thirteen patients undergoing elective orthopedic surgery were studied regarding anaphylatoxin (C3a and C5a) and terminal complement complex (TCC) formation in association with red cell salvage. The auto-transfusion equipment gave a centrifuged and washed erythrocyte fraction. The concentrations of C5a and TCC were not increased but elevated C3a levels were found in the suspension. After infusion of the erythrocyte fraction to the patient, no signs of systemic complement activation were observed. Thus, plasma levels of C3a, C5a and TCC were within the normal range in all the patients before and after autotransfusion. This study indicates that the complement system is activated in the cellsaver equipment. The washing procedure, however, seems to eliminate most of the anaphylatoxins and terminal complement complexes. No extensive systemic activation of complement seems to occur in association with autotransfusion to patients undergoing elective surgery.

Aged

Gamma 2-MSH immunoreactivity in the human heart.

In patients undergoing aorto-coronary by-pass surgery, we found a 26% arterial-venous difference of immunoreactive gamma 2-melanocytostimulating hormone (MSH), a proopiomelanocortin (POMC) derived peptide known to possess profound hemodynamic effects. These results prompted an investigation of the presence of gamma 2-MSH in the human heart. Using a two-step extraction procedure, regions of human hearts were examined by sensitive and specific radioimmunoassays to determine their gamma 2-MSH content. Mean (+/- SEM) concentrations of 0.14 +/- 0.023 pmol/g and 0.12 +/- 0.017 were found in right atrium and right ventricle, respectively. High performance liquid chromatography indicated that 80-90% of the total immunoreactivity eluted in a single sharp peak in a position identical to that of synthetic gamma 2-MSH.

Chromatography, High Pressure Liquid

Decrease in plasma volume from intraabdominal trauma in rats.

Intraabdominal surgery tends to lower circulating blood volume by mechanisms unrelated to bleeding. This phenomenon was investigated in chloralose anesthetized rats. Plasma volume was determined with radiolabelled albumin. Animals were subjected to a standardized abdominal trauma, eliciting minimal bleeding and evaporation, and others served as controls. The trauma decreased plasma volume and increased hematocrit significantly, whereas the plasma concentration of labelled albumin followed a similar time course in traumatized animals and in controls. It is concluded that experimental abdominal trauma may decrease blood volume by a loss of fluid with virtually the same albumin concentration as that of plasma.

Abdomen

Hypothalamic inhibition of duodenal alkaline secretion via a sympatho-adrenergic mechanism in the rat.

Experiments were performed on rats anaesthetized with chloralose. A duodenal segment was perfused with recirculating isotonic saline, and alkalinization of this perfusate (HCO3- secretion) was measured by continuous pH-stat titration. Stereotaxic electric unipolar stimulations were performed in the perifornical region of the hypothalamus. Stimulation points eliciting an increased arterial pressure were stimulated for a period of 15 min. Duodenal HCO3- secretion decreased in 19 out of 25 experiments and increased in four out of 25 experiments. Inhibitory responses to hypothalamic stimulation were blocked either by thoracic epidural anaesthesia or by the adrenolytic agent guanethidine, suggesting a spinal pathway to the duodenum, presumably in the thoracic splanchnic nerves, and involvement of adrenergic neurons.

Anesthesia, Epidural

The role of cardiac receptors in clonidine-induced vagal bradycardia.

In chloralosed, spinalized and beta-blocked cats, clonidine, 10 microgram/kg i.v. caused a vagally mediated bradycardia which was further analysed with particular attention to cardiopulmonary receptors. Cardiovascular deafferentiation, with preservation of vagal cardiac efferents, abolished the bradycardia. However, in animals with arterial baroreceptors denervated but with vagal cardiopulmonary pathways intact, clonidine decreased heart rate simultaneously with an increase in left atrial pressure to an extent known to activate cardiac receptors with unmyelinated vagal efferents. Clonidine somewhat enhanced the bradycardia to efferent vagal stimulation and also had a slight positive chronotropic effect on the non-innervated heart. The reflex bradycardia from electrical stimulation of unmyelinated cardiac afferents was augmented by the drug but not more than could be accounted for by the changed neuroeffector sensitivity. The data suggest that clonidine can reflexly augment vagal tone on the heart by an increased activity in vagal cardiac afferents, secondary to the drug's peripheral vasoconstrictor action, whereas no evidence for any central facilitation of these reflexes has been found.

Animals

Baroreceptor-induced decrease in muscle blood flow upon propranolol administration.

The acute effects of propranolol, 1 mg/kg i.v., were studied in chloralosed, vagotomized cats. The vascularly isolated but innervated calf muscles were perfused from another animal. In one group of experiments, the carotid baroreceptors were exposed to ambient arterial pressure. Here, propranolol caused a fall in heart rate and an increase in resistance of the isolated muscle bed. In other experiments, the carotid sinuses were perfused at a constant pressure. In these animals, no increase in muscle flow resistance was observed after the drug. It is concluded that the increase in total peripheral resistance, seen initially upon propranolol administration, may be reflexly induced via the baroreceptors.

Animals

The interrelation between hypothalamically induced changes in sympathetic discharge to the gastrointestinal and cardiovascular systems.

In chloralose-anesthetized, adrenalectomized cats, the sympathetically conveyed effects of topical hypothalamic stimulations on gastric volume, blood pressure and heart rate were systematically explored. The vagal nerves were cut but could be kept active by graded efferent stimulation. In the absence of such vagal activity, hypothalamic stimulation had no appreciable influence on gastric volume, even though the stomach maintained considerable myogenic tone. When, however, a vagal excitatory activity was present, hypothalamic stimulation could markedly affect gastric tone, indicating that the sympathetic fibres exert their inhibitory influence on the stomach via its cholinergic intramural neurons. Hypothalamic stimulations that induced reductions in pressure or heart rate also usually caused an enhancement of gastric tone. Similarly, pressor responses were associated with decreases in gastric volume whereas stimulation-induced tachycardia was not linked to any particular type of gastric response. Thus, the hypothalamic sympathoinhibitory influences on the cardiovascular system seem closely connected to a supression of the sympathetic outflow to the stomach. There is, on the other hand, no regular association between hypothalamic sympathoexcitatory influences on the cardiovascular and gastrointestinal systems; in fact, there is in many areas even a suppression of sympathetic discharge to the stomach in association with cardiovascular stimulation.

Adrenalectomy

Cardiac receptors activated during the hypothalamic defence reaction.

The increases of arterial blood pressure, cardiac inotropy and venous return seen during the hypothalamic defence reaction are likely to lead to concomitant excitation of left ventricular receptors with nonmedullated afferents. The integrated efferent pattern of response resulting from the central interaction between the defence reaction and influences from the mentioned cardiac receptors was recently analyzed. These two, essentially opposing influences on the circulation were then seen to interact in such a way as to produce an optimal cardiovascular response with respect to increases in cardiac output and blood supply to the skeletal muscles. However, direct electrophysiological recordings from nonmedullated cardiac efferents during defence area stimulation have hitherto been lacking. The present experiments, performed on chloralose-anesthetized cats and utilizing electrophysiological recordings, clearly demonstrate that the left ventricular receptors are activated by the cardiovascular readjustments induced by the defence reaction. Defence area stimulation increased the activity of these receptors, which work within a very narrow, low frequency range, from 1.1 +/- 0.3 imp/s to 2.7 +/- 0.7 imp/s associated with rises in systolic blood pressure (afterload) and heart rate. Normally such a receptor activation would induce considerable bradycardia and sympathetic inhibition, but particularly the reflex bradycardia is centrally supressed by a concomitant defence area activation. The marked bradycardia often seen immediately upon interruption of the defence area stimulation is, however, probably to a great extent initiated from the excited ventricular receptors.

Animals

Apnoea and bradycardia from submersion in "chronically" decerebrated cats.

In "chronically" but not in acutely decerebrated cats, submersion of the head caused apnoea and marked bradycardia, associated with a maintained or slightly raised arterial pressure. Since these reflex adjustments, though very reproducible, occurred with a varying latency and could be induced also by nasal injection of water, they appeared to be, at lest in part, elicited from the upper respiratory passages. Thus, a terrestrial mammal, reputed to shun any form of immersion, can exhibit adjustments during head submersion, similar to those in habitually diving species. This response pattern is basically organized at the lower brainstem level.

Animals

Interaction between the hypothalamic defence reaction and cardiac ventricular receptor reflexes.

The interference with regard to the cardiovascular and gastric motility responses which follows stimulation of the hypothalamic defence area (D.A.) and a simultaneous afferent input from cardiac ventricular receptors was analysed in chloralose-anesthetized cats. In spinalized animals with only the vagal efferent innervation of autonomic effectors from supraspinal structures intact, a D.A. stimulation increased the heart rate to the same level irrespective whether the cardiac receptor afferents were stimulated or not. This suggests that the vagal component of the reflex bradycardia of cardiac receptor origin was completely suppressed by the D.A. stimulation. The reflex gastric relaxation to cardiac receptor activation, mediated via vagal efferent non-adrenergic fibres, was similarly completely blocked by D.A. stimulation. In contrast, the reflex inhibition of the sympathetic outflow to the heart and vessels from cardiac receptors was still effective during a D.A. stimulation, a phenomenon which seems compatible with a simple summation of excitatory D.A. and inhibitory cardiac receptor influences on the sympathetic neurons. The modifying influence from ventricular receptors on D.A. responses closely resembles that exerted by the arterial baroreceptors. The two reflex mechanisms thus work in concert and synergistically with the hypothalamic influences to produce maximal cardiac output and skeletal muscle perfusion without undue increases of pressure load on the pump during a defence reaction.

Animals

CNS site of antiarrhythmic action of diphenylhydantoin (DPH) in the cat.

Diphenylhydantoin (DPH) is known to be a potent anticonvulsant agent, useful in treating and preventing grand mal seizures. More recently, DPH was reported also to be a potent antiarrhythmic agent acting by means of a depressant action on the heart. The present experiments demonstrated that DPH has also a potent antiarrhythmic action when administered to the CNS. The posterolateral hypothalamus was stimulated in cats to evoke cardiac arrhythmias of varying severity both during and after stimulation. In general, it was found that the post-stimulus arrhythmias were obtained more readily than those during stimulation. The mean effective dose of DPH required to prevent the arrhythmias via the i.v. route was 11.9 mg/kg, and that via the vertebral artery route and via the fourth ventricular route was only 1.9--1.4 and 1.4 mg/kg, respectively. These results suggest that though DPH has identifiable antiarrhythmic action on the heart itself it has a strong antiarrhythmic effect via the central nervous system as well.

Animals

The hypothalamus and vagally mediated gastric relaxation.

Experiments, with recording of gastric volume, were performed in chloralosed cats. Topical hypothalamic stimulations produced vagally mediated increases in volume by two mechanisms. One type of response, due to central inhibition of vagal excitatory tone was induced from the defence area and eliminated by atropine or vagotomy. The other type of response, far less commonly encountered, remained after atropine and spinal cord section, but was abolished by vagotomy. The latter type was not induced from any well defined hypothalamic region, and had a high stimulation threshold. While sham feeding in conscious cats with esophagostomy and gastrostomy induced prompt, marked and longlasting gastric volume increases in connection with swallowing, such responses were not evoked as "anticipatory" reaction to food intake;The relaxations could be prevented by vagotomy but not by guanethidine nor atropine. It is concluded that the vagally mediated relaxation in connection with sham feeding occurs mainly from activation of mechanoreceptors and that the hypothalamic control over the vagal relaxatory fibres is probably minor.

Animals

Integrated somatomotor, cardiovascular and gastrointestinal adjustments induced from the cerebellar fastigial nucleus.

Behavioural, cardiovascular and gastric responses induced by fastigial stimulation were observed in conscious cats with gastric fistulas, indwelling fastigial electrodes and arterial catheters. Fastigial stimulation elicited oral behaviours, e.g. grooming and chewing, together with tachycardia and pressor responses, while gastric motility was unaffected in most cases as was gastric hydrochloric secretion. In subsequent experiments on the anesthetized animals it was found that the same fastigial area could suppress the intestino-gastric inhibitory reflex. Fastigial influences on small intestinal motility were investigated in anesthetized cats, well recovered from surgical isolation of intestinal loops whose motility could therefore be recorded without laparotomy. Fastigial stimulation either depressed or did not influence ileal motility before laparotomy but after this procedure excitatory responses were uniformly recorded. This reversal is explained by a fastigial suppression of inhibitory intestinal reflexes, elicited by the laparotomy.

Animals

Effects on gastric motility from the cerebellar fastigial nucleus.

In acute experiments on chloralosed cats gastric motility, blood pressure and heart rate were investigated for influences exerted by the fastigial nucleus. Besides pressor responses, fastigial stimulation could produce either gastric excitation or relaxation and the background of these responses was analysed by selective nerve sectioning and administration of suitable autonomic blocking agents. Suppression of prevailing gastric motility was found to be mediated mainly by increased discharge in adrenergic nerve fibres but also by adrenal catecholamine release. -- Gastric excitation could be induced in three different ways, first via increased activity in vagal cholinergic fibres, second, by fastigial suppression of the vago-vagal non-adrenergic relaxatory reflex. In addition, when laparotomy or other noxious abdominal stimuli had induced inhibitory gastric reflexes, the consequent sympathetic discharge could be suppressed by fastigial stimulation resulting in enhanced gastric motility. -- The importance of background activity in the various nervous pathways for the fastigially induced gastric responses is discussed.

Animals