Biomedical subjects

Peter Pickkers

Publications and source records attributed to Peter Pickkers.

22 records · Page 2Linked to original sources

PubMed2004

Emphysema and pneumothorax after percutaneous tracheostomy: case reports and an anatomic study.

STUDY OBJECTIVE: Part 1: To describe cases of emphysema (subcutaneous and/or mediastinal) and pneumothorax after percutaneous dilational tracheostomy (PDT) in a series of 326 patients, and to review the existing literature describing the incidence and possible mechanisms. Part 2: To analyze the potential mechanisms for the development of emphysema and pneumothorax in human cadaver models. DESIGN: A retrospective analysis of PDTs, in combination with an anatomic study in human cadavers. MATERIALS AND METHODS: Part 1: All ICU patients who underwent PDT between 1997 and 2002 were enrolled in the study. We analyzed the cases of emphysema and pneumothorax. Similar cases were retrieved from the literature and underwent a systematic review. Part 2: The relevant anatomic structures were studied. We simulated the clinical situation after PDT in a human pathologic study in order to induce subcutaneous emphysema and pneumothorax. MEASUREMENTS AND RESULTS: Part 1: Five cases of subcutaneous emphysema (1.5%) and two cases of pneumothorax (0.6%) are described. In the literature search, we found 41 cases of emphysema (1.4%) and 25 cases of pneumothorax (0.8%) in a total of 3,012 patients. Part 2: Subcutaneous emphysema could easily be induced in a human cadaver model by inflating air in the pretracheal tissues and after posterior tracheal wall laceration. Air leakage was also possible through a fenestrated cannula via the space between the inner nonfenestrated cannula and outer cannula and then through the fenestration. CONCLUSIONS: We conclude that one mechanism for the development of emphysema is an imperfect positioning of the fenestrated cannula, whereby the fenestration is extraluminal. For this reason, fenestrated cannulas should not be used immediately after placement of a PDT. Posterior tracheal wall laceration is another mechanism responsible for emphysema after PDT. After perforation of the posterior tracheal wall, the pleural space can be reached easily. This may result in a pneumothorax.

Adult↗

PubMed2003

Only weak vasorelaxant properties of loop diuretics in isolated resistance arteries from man, rat and guinea pig.

Besides their diuretic action, loop diuretics may induce a rapid vasodilator effect that contribute to their short-term therapeutic properties. We examined the effects of furosemide (10(-6)-10(-3) mol l(-1)) in comparison with bumetanide (10(-6)-10(-4) mol l(-1)) on isolated resistance arteries from rat and guinea pig mesentery and human subcutaneous fat, and investigated the mechanism of the acute direct vasorelaxant action on an isometric microvascular myograph. Both loop diuretics induced concentration-dependent relaxation of resistance vessels irrespective of membrane potential. The maximal effect of furosemide was greatest in rat and least in human arteries. Both diuretics caused a rightward shift in the concentration-response curve to extracellular Ca(2+). Incubation with indomethacin (2 x 10(-5) mol l(-1)) or mechanical removal of the endothelium did not inhibit the loop diuretic-induced relaxation. At high concentrations (10(-4)-10(-3) mol l(-1)) loop diuretics exert only weak direct relaxant effects on isolated human subcutaneous resistance arteries compared to the vasorelaxant effects in rat and guinea pig mesenteric vessels.

Animals↗

PubMed2003

Calcitonin gene-related peptide: exploring its vasodilating mechanism of action in humans.

OBJECTIVE: In vitro studies suggest that the vasodilator mechanism of action of calcitonin gene-related peptide (CGRP) involves various endothelium-dependent and endothelium-independent mechanisms. An in vivo analysis of the contribution of nitric oxide, prostaglandins, calcium-sensitive potassium channels (K(+)(Ca) channels), and adenosine triphosphate (ATP)-sensitive potassium channels (K(+)(ATP) channels) to CGRP-induced vasodilation in humans was performed. METHODS: CGRP (3, 10, and 30 ng x min(-1) x dL(-1) forearm) was infused into the brachial artery of 40 healthy subjects. Forearm vascular responses were measured by venous occlusion plethysmography. First, dose-response curves were constructed during coinfusion of CGRP with placebo (sodium chloride, 0.9%). After washout, in 5 subgroups (n = 8 each), the infusions of CGRP were repeated with placebo (time-control experiments), N(G)-monomethyl-L-arginine (L-NMMA, a nitric oxide-synthase inhibitor), indomethacin (a cyclooxygenase inhibitor), tetraethylammonium chloride (TEAC) (a K(+)(Ca)-channel blocker), and glyburide (INN, glibenclamide) (a K(+)(ATP)-channel blocker), respectively. RESULTS: CGRP induced a dose-dependent and reproducible decrease in forearm vascular resistance (P < .001). Compared with placebo, L-NMMA reduced the decrease in forearm vascular resistance induced by CGRP (P < .001) (3 and 10 ng x min(-1) x dL(-1) forearm). The absence of an inhibitory effect of L-NMMA on CGRP-induced vasodilation at the highest dose of CGRP suggests that still other mechanisms are involved. The vasodilator response to CGRP was not affected by coinfusion of indomethacin, tetraethylammonium chloride, or glyburide. CONCLUSIONS: The intrabrachial infusion of CGRP results in a dose-dependent and reproducible forearm vasodilator response. CGRP-induced vasodilation is dependent at least in part on the release of nitric oxide and does not involve the release of prostaglandins or the activation of K(+)(Ca) channels or K(+)(ATP) channels in humans.

Adult↗

PubMed2002

TNFalpha and IL-1beta exert no direct vasoactivity in human isolated resistance arteries.

The proinflammatory cytokines TNFalpha and IL-1beta are thought to play a role in the mechanism of septic vasodilatory shock. Most evidence indicate that the vascular effects these cytokines are mediated through increased expression of inducible nitric oxide synthase, whereas several animal studies report a more rapid vasorelaxant effect. We studied the direct vascular effects of TNFalpha and IL-1beta in human isolated resistance arteries (n=9) using a microvascular myograph. After precontraction with noradrenaline or a depolarising high potassium solution, TNFalpha and IL-1beta (up to 10(-8) M, alone or in combination) did not exert any relevant vasoactive effect. We conclude that, in contrast with some animal experiments, these cytokines exert no direct vasoactivity in human resistance arteries.

Arteries↗