Contraction Of Spleen Research Articles

In vivo pharmacology of spleen contraction in rainbow trout

Rainbow trout, Oncorhynchus mykiss, were injected with an adrenergic agonist, an adrenergic antagonist, or a cholinergic antagonist, via a dorsal aorta cannula. Spleen size and haemoglobin content were measured at rest and, for antagonists, following an air exposure stress. Injection of phentolamine (an α-antagonist) blocked the spleen contraction induced by air exposure, suggesting that control is mediated by α-adrenergic receptors. Air exposure effects were unaffected by β-adrenergic blockade or muscarinic cholinergic blockade.

Relationships between spleen and respiration in the newt.

Specimens of newt, Triturus cristatus carnifex (Laurenti), anesthetized by submersion in 0.2% chlorbutol in tap water for 15 min, and then placed out of water in a damp terrarium, show hypertrophy of the spleen that in 2 hr gradually increases from 0.31 +/- 0.12%with respect to body weight to 1.56 +/- 0.26% (means and standard deviation calculated for groups of six animals). Other anesthetics either do not produce hypnosis (Veronal), do not have a prolonged enough effect (ethyl ether, chloroform), or induce vasodilatation, which prevents hypertrophy (MS-222, urethane). The spleen hypertrophy, seen histologically to be due exclusively to blood congestion, is not caused by either a pharmacological effect of the chlorbutol or by the hypnotic state, as it does not appear in submerged anesthetized animals, unless the water is constantly stirred by a magnetic agitator, and can be reversed depending on the ventilation of the animal's skin. The spleen hoards blood when oxygenation is good (in air or stirred water) and releases this supply in the bloodstream when oxygenation is insufficient (in still water). The hypoxic "diffusion boundary layer," which, in still water, forms around the immobile newts, hampers respiratory exchange and stimulates the spleen contraction. This mechanism and its relationship to oxygenation has been demonstrated statistically in unanesthetized newts as well, in both air and water, despite the interference of two contrasting factors--lung respiration and spontaneous motor activity--absent in anesthesized animals. Congestion and decongestion of the spleen are the physiological mechanisms compensating for variations in the level of oxygenation, an alternative to the "capillary recruitment" described by Poczopko and Burggren and Moalli in may amphibians that appears to be absent in newts. The newt spleen, known to play a lesser role in erythropoiesis and destruction of aged erythrocytes than that traditionally assigned to it is thus of primary importance in respiration.

Contraction of spleen in three perciformes and two tetraodontiformes during severe exercise

1. 1. The spleen of three species of Perciform fish and two species of Tetraodontiform fish contracted fully within 3–5 min of the start of severe exercise, and decreased by 52–82% in weight and by 70–87% in hemoglobin content.

Contraction of spleen in exercised freshwater teleost

1. 1. The spleens of six species of freshwater teleost fish contracted fully within 3–5 min of the start of severe exercise, and then decreased by 47–85% in weight and by 56–93% in hemoglobin content.

Effects immédiats d'une augmentation rapide de température sur certains paramètres sanguins du “loup” Dicentrarchus labrax (Linne, 1758)

A 1-h temperature increase from 20 to 26°C results in a stress response of the young European sea bass: spleen contraction, an increase in the erythrocytes count, hyperglycaemia, and hyperosmolarity. A 1-h temperature increase from 16 to 26°C is still more stressful and in addition to the above symptoms causes an increase in leucocrit and swelling of erythrocytes. The latter phenomena could signify that the fish are in a hypoxic situation.

Contraction of spleen in exercised cyprinid

The spleens of five cyprinid fish contracted fully within 3–30 min from start of severe exercise, and then decreased 63–85% in weight and 72–93% in hemoglobin content.

Splenic and renal sympathetic responses to stimulation of splenic receptors in cats.

The effect of selective stimulation of splenic receptors on reflex responses of splenic and renal efferent nerves was studied in anesthetized, vagotomized, sinoaortic denervated cats. The following substances were injected into the artery or vein of vascularly isolated spleens: warm physiological saline (congestion), capsaicin (CAPS), bradykinin (BK), and norepinephrine (NE). Splenic congestion increased efferent activity of splenic and renal nerves, splenic venous pressure, systemic arterial pressure, and heart rate. CAPS and BK elicited responses similar to those produced by congestion but caused greater excitation of splenic than renal nerves. Reflex responses were eliminated by section of splenic nerves. Injection of NE increased splenic venous pressure but did not elicit reflex responses. Finally, in contrast to a previous report light- and electron-microscopic examination of splenic nerves revealed myelinated, as well as unmyelinated, fibers. These results have demonstrated that activation of splenic receptors elicits reflex cardiovascular responses and excitation of splenic and renal efferent nerves, contraction of the spleen does not produce reflex responses, the adequate stimulus for reflex responses is stretch of vessels and possibly capsule, and splenic receptors play a role in the reflex control of circulation.

Splenic afferents and some of their reflex responses.

Afferent nerve activity was recorded from the distal ends of cut splenic nerves in pentobarbital- (35 mg/kg) anesthetized mongrel dogs (15-20 kg). Increases in splenic venous pressure (SVP) produced either by manual compression of discrete portions of the spleen or splenic contraction produced by injection of epinephrine (100 micrograms) into the splenic artery or vein of an occluded spleen produced significant increases in SVP and splenic afferent nerve activity. Increases in splenic afferent nerve activity were linearly related to increases in SVP. Histological sections of nerves from which afferent recordings were obtained demonstrated that all afferents were unmyelinated C-fibers. Electrical stimulation of the cut central end of splenic nerves resulted in marked reflex increases in both renal and cardiopulmonary sympathetic efferent nerve activity that remained elevated throughout the stimulation period. Reflex increase in cardiopulmonary sympathetic efferent nerve activity was associated with increases in right (22-45%) and left (11-19%) ventricular contractile force measured with Brodie-Walton strain gauge transducers, in heart rate (5-15 beats/min), and in blood pressure (5-10 mmHg). This study is the first to demonstrate both the existence of low-pressure baroreceptors in the spleen and that these splenic afferents can reflexly alter cardiopulmonary and renal sympathetic efferent nerve activity, heart rate, ventricular contractile force, and systemic blood pressure.

Free fatty acids (FFA)--blood clotting, fibrinolysis and platelet function.

The effect of an increase in the free fatty acid (FFA) concentration on platelets, blood clotting and fibrinolysis has been studied in 5 volunteers. Increased FFA‐concentration was achieved by infusion of nor‐adrenaline (NA). As a control a second NA infusion was given after pretreatment with nicotinic acid which blocks the release of FFA.There were no changes in the number of platelets or platelet stickness, in activated partial thromboplastin time (APTT), ‘stypven’ time, factor V, factor VIII, factor II‐VII‐X or antithrombin III or fibrinolytic activity, plasminogen or plasmin inhibitors which could be correlated to the fluctuations in FFA. During the first NA infusion an increase in the number of circulating platelets was observed ‐ probably due to spleen contraction. An insignificant increase in factor VIII was seen during both NA infusions. The nicotinic acid infusion caused an increased fibrinolytic activity. Notably this did not influence platelet function or clotting.

Contraction of the Spleen Following Needle Puncture: Significance in Studies of Portal Hypertension

Rapidity of the passage of contrast material to the hilar portal vein during splenoportography is a curious and unexplained phenomenon. As accumulated evidence indicates that splenic pulp puncture increases the velocity of flow from spleen to liver, and as splenic contraction is known to effect such an alteration, an attempt was made to determine whether the spleen contracts significantly following needle pulp puncture. After X-ray opacification of the spleen by intravenous injection of powdered tantalum, splenic size was compared before and after insertion of a needle into its pulp. The results demonstrate that the spleen contracts to approximately 70% of its control size almost immediately after puncture. Aspects of this response which bear on studies of patients with portal hypertension are considered.

Prostaglandins: their disappearance from and release into the circulation.

Prostaglandins are released into the splenic venous blood when the spleen contracts. Whatever the significance of this release, the liver and lungs provide an efficient protective mechanism to remove almost all the prostaglandin before it reaches the arterial circulation.

Cardiovascular effects of face immersion and factors affecting diving reflex in man.

Cardiovascular effects of face immersion and factors affecting diving reflex in man.

Insulin effects on gastric secretion and blood electrolytes modified by injected potassium.

In the intact gastric fistula dog, insulin has been shown to have several, probably independent, actions: 1. Hypoglycemia occurs, resulting in stimulation via the vagus of gastric electrolyte and pepsin secretion. 2. Plasma K+ levels fall and there is a transfer of Na from cells to plasma which is mainly K-dependent. 3. Another, and less clearly defined, effect on K+ results in inhibition of gastric electrolyte secretion and is rapidly reversed by injected K. This latter action is best explained by postulating an insulin-induced redistribution of K+ in cells with resulting depletion of cation site essential for electrolyte secretion. 4. The smooth muscle of the spleen contracts; this contraction can be only partly prevented by K injectin.

Autoantigens and autoantibodies in the pathogenesis of disease with special reference to blackwater fever

A hypothesis of the pathogenesis of blackwater fever, suggested by the observation that liver emulsion from a rhesus monkey dead of yellow fever, stimulates the formation of antiliver antibodies when injected into another rhesus monkey, is put forward and discussed. This hypothesis may be formulated thus:— ▪ ▪ It is noted that, in cases of blackwater fever, the red cells show auto-agglutination and spherocytosis and that erythrophagocytosis is commonly seen in smears of the spleen, and, occasionally, in films of peripheral blood: Further, it has been observed, red cells from healthy donors haemolyze as rapidly in a case of blackwater fever as the patient's own cells and, on the other hand, red cells from a case of blackwater fever, transfused into a healthy recipient, haemolyze as rapidly as the red cells remaining in the patient. There is usually a considerable interval between the first attack of malaria and the onset of blackwater fever, during which the patient suffers from repeated attacks of malaria, often inadequately treated with quinine. It is noted, too, that blackwater fever is closely simulated by the effects of an incompatible blood transfusion by paroxysmal haemoglobinuria and by the effects of the injection of an artificially produced haemolytic serum into experimental animals. All these observations are readily explained on the assumption that a biological autohaemolysin is concerned in the pathogenesis of blackwater fever. Other hypotheses put forward cannot satisfactorily account for them, especially for the specific association of blackwater fever with malaria. It is concluded, therefore, that an autohaemolysin is almost certainly concerned in the production of blackwater fever. The site of formation of this autohaemolysin is discussed, and it is considered that it is mostly produced in the spleen. The boosting of the titre of the autohaemolysin resulting from repeated attacks of malaria often inadequately treated, and factors producing a sudden contraction of a congested spleen, in which autohaemolysin has accumulated, are considered likely to precipitate an attack and to account for the sudden dramatic onset of blackwater fever. The treatment of the condition in the light of this hypothesis is discussed, and it is considered important to prevent such sudden contractions of the spleen. It is also important, in order to avoid the development of a state of sensitivity, to treat malarial infections adequately. Other conditions characterized by intravascular haemolysis are briefly discussed. It is noted that apart from incompatible blood transfusion, and paroxysmal haemoglobinuria which are known to be caused by biological antibodies, such conditions as the acute haemolytic anaemias following certain drugs and of favism can also be reasonably explained. Cases of aplastic anaemia, of agranulocytosis, and of thrombocytopenia, are briefly described, and it is noted that an explanation for their development is possibly to be found in the hypothesis here enunciated.

Response of the Exteriorized Spleen to Ephedrine, Acetyl Choline, Pilocarpine and Pituitrin

ConclusionsInjection of acetyl choline, pilocarpine, ephedrine, and pituitrin (S) into the saphenous vein causes significant contraction of the exteriorized spleen in conscious dogs. In 2 single observations, chloroform inhalation caused contraction and sodium amytal (intravenously) caused relaxation of the exteriorized spleen.

Sobre o mechanismo de formação das hyperglobulias de origem toxica

Tendo verificado uma acção hyperglobulinogena do tetrachloreto de carbono, thynol e essencia de chenopodio, quando administrados ao homem como vermifugos, procuramos averiguar qual o mechanismo destas hyperglobulias. Para isso tomamos duas substancias tambem hyperglobulinogenas (chloroformio e chloretona) e escolhemos o cão para animal de experiencia. Observamos que, com anesthesias prolongadas pelo chloroformio e pela chloretona, tal como naquellas substancias applicadas ao homem como vermicidas, apparecem intensas hyperglobulias no sangue circulante. constatamos ainda uma rapidez extraordinaria no augmento de hematias (1 a 2 horas após o inicio da anesthesia), e a existencia de um nivel maximo para este augmento, que não é ultrapassado apezar de novas anesthesias prolongadas. Entretanto, em cães esplenectomisados este effeito das anesthesias prolongadas desapparece inteiramente em sua acção sobre o sangue. em todos os casos, tanto em homem como em cães (esplenectomisados ou não), ao par da hyperglobulia, notou-se sempre estados hypotensivos as vezes bastantes accentuados. Estes resultados nos levaram a concluir que no mechanismo das hyperglobulias de origem toxica, o factor principal está em uma contracção esplenica, (provocada provavelmente pela hypotensão observada), contracção está, que resulta em um lançamento na corrente circulatoria do sangue concentrado (lama esplenica) que normalmente se acha em reserva no baço.