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Biomedical subjects

F Follis

Publications and source records attributed to F Follis.

24 records · Page 2Linked to original sources
PubMed1987

The normal pericardium does not affect left ventricular function.

Whether the normal pericardium exerts a constraining effect on left ventricular (LV) diastolic compliance and/or systolic function is controversial. Left ventricular filling and performance were studied in 15 patients by two-dimensional transesophageal echocardiography (2D-TEE) measuring end-diastolic area (EDa), end-systolic area (ESa), ejection fraction area (EFa), and hemodynamics immediately pre- and post-pericardiotomy. To diminish the influences of other variables such as surgical stimulation, chest wall constraint, and autoregulation, measurements were performed in deeply anesthetized patients with the chest fully opened immediately before and after pericardiotomy (PC). No significant echocardiographic or hemodynamic changes were observed after PC. Although alterations in compliance cannot be excluded, no significant changes in LV diastolic filling (EDa, pulmonary capillary wedge pressure [PCWP]) or systolic performance (EFa, cardiac output [CO]) were found. Therefore, it is concluded that the normal pericardium does not exert a measurable constraining effect on LV performance.

Coronary Artery Bypass↗
PubMed1977

[Primary thrombosis of the axillary and subclavian veins].

A case of effort thrombosis of the axillary vein caused by violent abduction of the arm in the act of raising a 40 kg weight over the head is reported. The patients was treated conservatively with anti-coagulants, antibiotics and rest. A slight functional deficiency remains one year later while control phlebography has shown good recanalization of the clot. It is personally considered that a particularly close relationship between vessels and surrounding anatomic structures may, during violent effort and in a particular position of the extremity, trigger compression of the venous wall with lesion of the intima and clot formation.

Adult↗
PubMedDate not supplied

Competitive NMDA receptor antagonists and spinal-cord ischemia.

Ischemic neuronal death is associated with excitatory amino acid (EAA) release. Their action is mediated by N-methyl-D-aspartate (NMDA) receptors. Blockade of the receptors before the ischemic insult can decrease neuronal damage. Accordingly, we investigated the protective effect during spinal cord ischemia of two competitive antagonists, 4-(3-phosphonopropyl)-2-piperazine-carboxylic acid (CPP) and cis-4-(phosphonomethyl)-2-piperidine-carboxylic acid (CGS). Male Sprague-Dawley rats underwent intrathecal administration of 10 microL saline, CGS, and CPP 10 mM solutions, in a randomized blinded fashion, and were subjected to balloon occlusion of the thoracic aorta. Proximal aortic pressure was lowered to a mean of 40 mm Hg by partial exsanguination. In the acute protocol, 21 rats divided in 3 groups of 7 (saline, CPP, and CGS) were used to calculate the aortic occlusion time (AOT) resulting in paraplegia in 50% of animals (P50). In the chronic study, 24 rats divided in 4 groups of 6 (saline, CPP, CGS, sham) underwent 12-min occlusion. The chronic animals were scored daily for 28 days and submitted to histology of the cord. In the acute study, the P50 of CGS (10 min 48 s) and CPP (11 min 11 s) was longer than saline (10 min 27 s). In the chronic groups, analysis of variance of neurologic (p = .66) and histologic (p = .66) scores did not disclose differences between CGS, CPP, and saline. In conclusion, blockade of NMDA receptors with CPP or CGS may afford some protection for durations of occlusion around the P50, but it is not beneficial when ischemic injury is more protracted.

Acute Disease↗
PubMedDate not supplied

Posterior ventricular septal rupture: an anatomical reconstruction.

Rupture of the ventricular septum following posterior myocardial infarction is an uncommon, but lethal, injury that requires prompt repair. Surgical reconstruction can be complex, demanding, and unfamiliar. Conventional techniques, as described in the literature, are associated with a variety of potential pitfalls. An alternative method we have successfully used in our last four patients is presented in detail. The procedure uses two composite (felt/pericardium) patches: an internal patch to reconstruct the left ventricular geometry and an external patch to repair the subtotal infarctectomy. For maximal security, all suture lines sandwich myocardium between two continuous felt surfaces. Specific transition stitches are described, which reliably anchor the entire repair at the critical, but poorly visualized, areas where the ventricular septum makes its transition to left and right ventricular free walls. This technique offers immediate hemostasis and a more anatomical left ventricular geometry. The method also reduces the risk of systemic thromboembolism, residual VSD, and repair disruption.

Aged↗
PubMedDate not supplied

Role of poloxamer 188 during recovery from ischemic spinal cord injury: a preliminary study.

Paraplegia following aortic surgery is not a common event. When it does occur it significantly alters the patient's outcome. Poloxamer 188 (P188) has been shown in the experimental animal to increase regional blood flow to ischemic areas. In order to investigate its protective effect during aortic cross-clamping, 23 animals were randomized to two groups (placebo n = 11, P188n = 12) and received an intravenous injection of placebo or P188 (200 mg/kg), and underwent occlusion of the thoracic aorta and both subclavian arteries for a period of 13 minutes. They were then connected to an intravenous pump delivering either placebo or P188 (250 mg/kg/hr at a rate of 0.942 ml/hour) for 48 hours. Hindlimb function was appraised, daily for 30 days, by a lesion score (0-15). Spinal cord injury was assessed by a histologic score (0-3) based on the degree of gray and white matter gliosis, number of motor neurons, and white matter myelination. Analysis of variance for repeated measures did not reveal significant difference between P188 and placebo groups (P = 0.66). Similarly, the mean histologic scores (placebo = 1.54 +/- 0.41 SE, P188 = 1.08 +/- 0.33 SE) did not differ (Wilcoxon, P = 0.43). We conclude that intravenous administration of P188 before, during, and for 48 hours after aortic cross-clamping does not prevent paraplegia or improve the long term neurologic outcome.

Animals↗