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Hepatic sinus

The liver is a large and distensible organ. As such, large quantities of blood may be stored in its blood vessels providing a blood reservoir function. Under normal physiological conditions, the hepatic veins and hepatic sinuses contain approximately 450 ml of blood, or almost 10% of blood volume. When needed, this blood may be mobilized to increase venous return and cardiac output. [Pg.295]

Figure 4.3. Representative set of spleen and hepatic sinus volumes, measured in vivo with MRI, during an 8 min simulated dive in a young elephant seal. The MRI images indicated that spleen emptying requires only two or so minutes. The contents are initially tranferred into the hepatic sinus and then RBCs are metered out into the blood more slowly, apparently through phrenic nerve control of the caval sphincter. Data from Thornton (2000). Figure 4.3. Representative set of spleen and hepatic sinus volumes, measured in vivo with MRI, during an 8 min simulated dive in a young elephant seal. The MRI images indicated that spleen emptying requires only two or so minutes. The contents are initially tranferred into the hepatic sinus and then RBCs are metered out into the blood more slowly, apparently through phrenic nerve control of the caval sphincter. Data from Thornton (2000).
The liver is the first organ to receive blood that contains glucose absorbed from the intestine. The portal vein drains from the small intestine into the hepatic sinuses that are surrounded in a neat columnar fashion by hepatocytes. The arrival of glucose in the blood is detected by the p-cells in the pancreas, and they respond by secreting the peptide hormone insulin. Insulin facilitates glucose uptake by many cell types, from skeletal muscle to white blood cells (Fig. 11-4), but it has no effect on glucose uptake by the brain or red blood cells that rely on GLUT-1. [Pg.343]

The hydantoins are contraindicated in patients widi known hypersensitivity to die drug s. Phenytoin is contraindicated in patients widi sinus bradycardia, sinoatrial block, second and diird degree AV block, and Adams-Stokes syndrome it also is contraindicated during pregnancy (ediotoin and phenytoin are Pregnancy Category D) and lactation. Ediotoin is contraindicated in patients widi hepatic abnormalities. [Pg.258]

These drug are used cautiously in patients with renal or hepatic disease, bladder obstruction, seizure disorders, sick sinus syndrome, gastrointestinal bleeding, and asthma Individuals with a history of ulcer disease may have a recurrence of the bleeding. [Pg.305]

Blood flowing from the intestines to the liver through the hepatic portal vein often contains bacteria. Filtration of this blood is a protective function provided by the liver. Large phagocytic macrophages, referred to as Kupffer cells, line the hepatic venous sinuses. As the blood flows through these sinuses, bacteria are rapidly taken up and digested by the Kupffer cells. This system is very efficient and removes more than 99% of the bacteria from the hepatic portal blood. [Pg.295]

Drug molecules that have traversed the physieal and enzymatic barriers of the colonic mucosa may enter the blood-eapillary bed or the lymphatic sinuses. Intact drug that reaches the venous capillaries from the submucosa is transported to the liver via the hepatic-portal system where they may undergo significant metabolism. On the other hand, uptake into the lymphatie sinuses of the colon results in direct delivery into the systemic circulation that causes less metabolic breakdown of the absorbed drug [3]. [Pg.42]

Patients with decompensated cardiac failure requiring the use of IV inotropic therapy (such patients should first be weaned from IV therapy before initiating carvedilol) bronchial asthma (see Warninas) or related bronchospastic conditions second- or third-degree AV block sick sinus syndrome or severe bradycardia (unless a permanent pacemaker is in place) cardiogenic shock clinically manifest hepatic impairment hypersensitivity to the drug. [Pg.535]

Propafenone is contraindicated in the presence of severe or uncontrolled congestive heart failure cardiogenic shock sinoatrial, A-V, and intraventricular disorders of conduction and sinus node dysfunction, such as sick sinus syndrome. Other contraindications include severe bradycardia, hypotension, obstructive pulmonary disease, and hepatic and renal failure. Because of its weak (3-blocking action, propafenone may cause possible dose-related bronchospasm. This problem is greatest in patients who are slow metaboUzers. [Pg.181]

Contraindications Bradycardia-induced syncope (except in the presence of a pacemaker), second-and third-degree AVblock, severe hepatic disease, severe sinus-node dysfunction... [Pg.57]

Use with caution in older patients with Hepatic impairment Patients taking diuretics, NSAIDs or with nephropathy Sinus node dysfunction or Heart block, Osteoporosis, Unsteady gait, Urinary incontinence... [Pg.189]

Villa, R.B., E.P Osuna, and M.H.P. Cortes. 1993. Concentraciones de metales pesados en el tejida cardiaco, hepatic y renal de la vaquita Phocoena sinus (mammalia phocoenidae). Anales Inst. Biol., Univ. Nac. Auto. Mexico, Ser. Zool. 64 61-72. [Pg.529]

Serious adverse events occur in up to 6% of patients with anti-TNF therapy. The most important adverse effect of these drugs is infection due to suppression of the ThI inflammatory response. This may lead to serious infections such as bacterial sepsis, tuberculosis, invasive fungal organisms, reactivation of hepatitis B, listeriosis, and other opportunistic infections. Reactivation of latent tuberculosis, with dissemination, has occurred. Before administering anti-TNF therapy, all patients must undergo purified protein derivative (PPD) testing prophylactic therapy for tuberculosis is warranted for patients with positive test results. More common but usually less serious infections include upper respiratory infections (sinusitis, bronchitis, and pneumonia) and cellulitis. The risk of serious infections is increased markedly in patients taking concomitant corticosteroids. [Pg.1329]

Surprisingly, alcoholic fatty infiltration of the liver and alcoholic hepatitis often display ascites as well, mostly only discernible when applying ultrasonic methods of examination. This might suggest that certain pathogenic mechanisms in the formation of ascites (such as increase in portal pressure, structural sinus changes, and stimulation of biochemical or sympathoadrenergic factors) are favoured or become more intense as a result of alcohol (and possibly also its chemical additives). Ascites can also occur in severe acute viral hepatitis, in which case the course of disease deteriorates considerably. (28,46,64)... [Pg.297]


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See also in sourсe #XX -- [ Pg.328 ]




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