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Biomedical subjects

H F Janssen

Publications and source records attributed to H F Janssen.

31 records · Page 2Linked to original sources

Influence of central nervous system on arterial pressure during endotoxin shock.

Some investigators have suggested that the hypotensive effects of endotoxin are exerted at the level of central nervous system (CNS). Others feel the effects are exerted peripherally and that the CNS is involved in the regulation of the cardiovascular system during the shock state. Still other data suggest that endotoxin shock is entirely a peripheral phenomenon. The present study used ventriculocisternal perfusion of endotoxin, a pretrigeminal brainstem transection, two midcollicular decerebrate preparations, and Cushing's reflex to investigate the involvement of the CNS during endotoxin shock. The results suggest the following: 1) endotoxin perfused centrally at a concentration equivalent to the maximum obtainable after peripheral injection will not alter mean arterial pressure (MAP); 2) either the forebrain is not involved in the MAP response or the remaining regions can compensate for its absence; and 3) Cushing's reflex will block the initial endotoxin-induced hypotension.

Animals↗

Cardiac taurine levels during endotoxemia.

Three hours after dogs were given an intravenous injection of Escherichia coli endotoxin significant decreases in cardiac taurine levels were observed in the apex and epicardial regions of the right ventricle and in all regions sampled from the left ventricle. A decrease in taurine was seen in all regions of the heart (including the atria) by 90 min after endotoxin treatment but the results were not statistically significant. Echocardiography and left ventricular cannulation were used in a separate group to confirm that the dose of endotoxin used was adequate to produce depression of cardiac output and force of contraction.

Animals↗

Studies on a central site of action for naloxone in endotoxin shock.

A complete understanding of naloxone's role in shock has not been well established; however, it has been accepted that naloxone applied specifically to the central nervous system can improve the course of the cardiovascular response. The currently available data would suggest that these central effects are mediated via nuclei that 1) are found in both the rostral and caudal regions of the brainstem, 2) contain opiate receptors, 3) interact with the fastigial nuclei of the cerebellum, and 4) possibly receive input from peripheral thermoreceptors. Recordings of neural activity from specific nuclei during shock as well as microinjections and iontophoresis of naloxone onto specific sites is needed to improve the current understanding of this apparently complex process.

Animals↗

Cyclic sequential compression of the lower limb in prevention of deep venous thrombosis.

Patients undergoing operations on the hip for either replacement or fracture were chosen for this study. Fifty-two subjects received cyclic sequential compression as well as elevation of the lower limb while another fifty-two patients were treated with only elevation of the lower limb. No other method of prophylaxis for deep venous thrombosis was employed during the study period. Support stockings were used after removal of the compression device. Doppler ultrasound, phleborheography, and, when possible, radioiodinated fibrinogen scanning were used for identification and location of thrombi. A deep-vein thrombosis developed in ten patients (19 per cent) in the control group and in only one patient (2 per cent) in the group that was treated with compression. This difference is statistically significant (p less than 0.05).

Aged↗

An observed pressor effect of the cerebellum during endotoxin shock in the dog.

The current study investigates the possibility that the cerebellum may be involved in the regulation of mean arterial pressure (MAP) during endotoxin shock in the anesthetized dog. The effect of intravenously injected Escherichia coli endotoxin on MAP in the cerebellectomized dog was compared to that observed in the intact animal. Even though removal of the cerebellum did not significantly affect MAP in a control group, the cerebellectomized animal (unlike the intact animal) was unable to recover from the initial hypotension typically seen immediately following an intravenous endotoxin injection. Previous investigators have demonstrated that stimulation of fastigial nuclei in the cerebellum increases MAP via beta-adrenergic activation of the renin-angiotensin system. Captopril (SQ 14,225, an angiotensin I-converting enzyme inhibitor) was used to determine whether this system could be responsible for the maintenance of MAP during endotoxin shock. When continuously infused into the intact dog given endotoxin, captopril suppressed MAP to a level similar to that of the cerebellectomized group. A similar response pattern to endotoxin was also observed in animals with a spinal transection at C2.

Animals↗

Hypotensive action of parathyroid hormone preparations on rats and dogs.

Bovine parathyroid extract and two commercial preparations containing the first 34 amino acids of synthetic bovine parathyroid hormone [bPTH-(1-34)]produced dose-related hypotension in anesthetized rats. Dogs were 10 times more sensitive to the two bPTH-(1-34) preparations than were rats. Propranolol, phentolamine, atropine, and promethazine did not affect the hypotensive action of bPTH-(1-34) in rats and dogs. bPTH-(1-34) decreased perfusion pressure in rat hindlimbs perfused in situ with Ringer's solution and was a vasodilator in dog kidneys perfused in vitro with Ringer's solution. Helical strips of rabbit aorta were also relaxed by bPTH-(1-34). We conclude that the direct vasodilatory action of bPTH preparations represents an intrinsic property of parathyroid hormone and that the hypotensive effect of this hormone is produced by part or all of the first NH2-terminal 34 amino acids.

Adrenergic alpha-Antagonists↗

Effects of synthetic parathyroid hormone on vascular beds of dogs.

Blood flow rates and vascular resistance in dogs were determined in 14 tissues with 15 +/- 2 microns radioactive microspheres (141Ce, 51Cr, 85Sr). Intravenous injections of synthetic bovine parathyroid hormone containing the NH2-terminal 1--34 amino acids [bPTH-(1--34)] at the dose of 10 USP units/kg body weight produced hypotension and increases in blood flow rate and decreases in resistance in kidney cortex, kidney medulla, heart, liver, stomach and pancreas at 1/2 and 2 min after injection. 4 U bPTH-(1--34)/kg body weight produced less vasodilation. Saline injection had no effect on the tissues studied.

Animals↗

Cerebrovasculature permeability changes following experimental cerebral angiography. A light- and electron-microscopic study.

Morphological alterations of the cerebral vasculature as related to the permeability of plasma proteins and angiographic contrast media following unilateral cerebral angiography were studied. Both Evans blue albumin and horseradish peroxidase were employed as protein tracers for light and electron microscopy investigation respectively. Grey matter regions of the cerebral cortex, cerebellum corpus striatum, hippocampus and midbrain showed the most extensive and consistent leakage of these protein tracers. The most extensive penetration of EBA was noted at 1 hr following cerebral angiography as compared to the 5 or 30 min sample times. Permeability changes were noted in small venules and arterioles as well as capillaries. The extent of permeability, however, was appreciably greater in the capillaires as evidences by rapid extravasation of HRP into the surrounding neuropil extracellular spaces. The glial basement membrane surrounding the perivascular spaces of small venules and arterioles precluded rapid penetration of HRP into the neuropil interstitium. Opening of the tight junctions between the endothelial cells was primarily responsible for the extravasation of HRP in all vessel types. Furthermore, it is out opinion that the hyperosmolar nature of the contrast medium is responsible for opening of these tight junctions.

Animals↗

Experimental studies of the effects of abnormal venous valves on fluid flow.

The effects of variations in the venous valve anatomy are studied experimentally using an artificial system that mimics the bicuspid valves normally found in veins in the lower extremities. The artificial valves are constructed from thin-walled, latex tubing and polyurethane film. The experimental variables in the study are the gap width between the leaflet attachments at the vein wall and the ratio of the sinus depth to vein diameter. The results show that the antegrade mass flow rate is not affected to the same degree when compared to retrograde flow by the various valve configurations examined in this study. The results also indicate that increases in the gap width, which serve to increase the degree of imperfect wall attachment, have less effect on retrograde mass flow rate in valves with deeper sinuses.

Blood Flow Velocity↗

Infection in patients after implantation of an orthopedic device.

During the last several decades, the use of appropriate antibiotics has significantly improved our ability to prevent and treat infection that occurs after implantation of an orthopedic device. Despite improved prevention and treatment of this condition, patients who develop an infection secondary to implantation of an orthopedic device face increased mortality, morbidity, and/or delayed recovery. The presence of an orthopedic device significantly reduces the number of bacteria required to produce colonization and decreases the ability of the body's own defense mechanism and antibiotics to resolve this condition. Efforts devoted to prevention of infection are much more effective than those spent treating the condition once it has developed. Pretreatment of patients with antibiotics and the use of ultra clean surgical rooms have been shown effective. Prevention will become increasingly important as antibiotic resistant strains of bacteria become more prevalent and the number of arthroplasty procedures performed also increases.

Anti-Bacterial Agents↗