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F Espinosa

Publications and source records attributed to F Espinosa.

13 recordsLinked to original sources

Mouse sperm membrane potential: changes induced by Ca2+.

Mouse sperm resting membrane potential (Er) (-42 +/- 8.8 mV), determined with a potential sensitive dye, depended on extracellular K+ and, in the absence of extracellular Ca2+ ([Ca2+]e), on external Na+ ([Na+]e). Ca2+ addition (> 5 microM) to sperm in Ca-free media induced a transient hyperpolarization (Ca-ith) which strongly depended on [Na+]e and less on external Cl- ([Cl-]e). Cd2+ and Mn2+ (microM) mimicked the Ca2+ effect, but not Ba2+. The Ca-ith was partially inhibited by ouabain (74%, IC50 = 5.8 microM) and niflumic acid (38%, IC50 = 240 microM), indicating the participation of the Na-K ATPase and Cl- channels. In Ca-free low-Na+ media, Ca2+ addition caused a depolarization sensitive to: nimodipine (25 microM), trifluoperazine (12.5 microM) and Mg2+ (1.2 mM), suggesting the participation of Ca2+ channels. Since some inhibitors of the sperm Ca-ith block the acrosome reaction (AR), both processes may share transport systems.

Animals

Arterial wall changes in cerebral vasospasm.

A right-sided subarachnoid hemorrhage (SAH) was created in 12 monkeys. Only the right (clot-side) cerebral arteries developed angiographic vasospasm (VSP), which was maximal 7 days after SAH. Eight animals were killed at this time and the remainder at 14 days. At the time of killing the middle cerebral arteries (MCAs) were harvested, and four normal, left (non-clot-side) MCAs were vasoconstricted in vitro with prostaglandin F2 alpha. All MCAs were studied with scanning and transmission electron microscopy. Right MCAs in maximal VSP 7 days from SAH were undistinguishable on scanning electron microscopy from normal arteries vasoconstricted in vitro: both groups demonstrated a mean 57% reduction in vessel caliber and a 5-fold increase in vessel wall thickness compared to normal, nonvasoconstricted left MCAs. On transmission electron microscopy, however, arteries in SAH-induced VSP showed degenerative changes in the tunica intima and media. These changes were still evident at 14 days, despite considerable resolution of VSP. These findings, as well as those from other pathological studies of animal and human cerebral arteries in VSP, suggest that the arterial narrowing and vessel wall thickening seen within several weeks of SAH is due primarily to medial contraction, but unlike simple vasoconstriction, is associated with degenerative ultrastructural changes in the endothelium and vascular smooth muscle cells which may denote a temporarily irreversible state.

Animals

Electron microscopy of simian cerebral arteries after subarachnoid hemorrhage and after the injection of horseradish peroxidase.

A large unilateral subarachnoid hemorrhage (SAH) was created in 21 monkeys, and horseradish peroxidase (HRP) was injected into the cisterna magna or left internal carotid artery in 3 others (normals). Cerebral fixation was performed on Day 14 after SAH or 15 minutes after HRP injection. The major cerebral arteries from both the nonclot (control) and clot sides and the normal animals were examined with scanning and transmission electron microscopy (SEM and TEM). SEM of the adventitial surfaces of control and normal arteries revealed tunnel-like structures along the longitudinal axis. No vasa vasorum were seen, but adventitial rounded openings were observed, 10 to 35 micron in diameter in vessels of the anterior circulation and up to 80 micron in diameter in the basilar arteries. The stomas, numbering 5 to 10/mm of specimen, appeared to connect the subarachnoid and intraadventitial spaces or pathways. In SAH arteries, the tunica adventitia was coated with cellular remnants of hematoma or dense, well-organized blood clots, the removal of which revealed blocked stomas. TEM showed HRP in the vessel walls after injection into the cisterna magna, but not after injection into the carotid artery. TEM of control arteries revealed Virchow-Robin (intraadventitial) spaces lined by simple planar epithelium-like cells; Virchow-Robin spaces contained sparse nerve fiber bundles and connective tissue fibers. In SAH arteries, these spaces were almost filled with strands of connective tissue and fibroblasts; no nerve fibers were detected. Vasogenic substances probably reach smooth muscle cells via the adventitial stomas. SAH occluding the stomas may block the cerebrospinal fluid circulation, disturbing nutrition of the arterial wall or removal of wastes from it, thereby aggravating vasospasm.

Animals

Rupture of an experimentally induced aneurysm in a primate.

Cerebral aneurysms are extremely rare in all animals except man. We report the occurrence of a carotid-ophthalmic aneurysm in a cynomolgous monkey two months following accidental occlusion of the ipsilateral cervical internal carotid artery. This was documented angiographically. The aneurysm was deliberately ruptured by the insertion and withdrawal of fine needles. This produced a large subarachnoid hemorrhage visualized on CT scan. There was a progressive severe fall in cerebral blood flow and moderate vasospasm. The neurological status deteriorated on the tenth day and the animal was sacrificed on day 13. On electron microscopy, the aneurysm showed a fibrous wall, and the endothelium showed balloon-like endothelial cells with gaps. Corrugations occurred in the inner aspect of the anterior circulation arteries.

Animals

Effect of reserpine-kanamycin treatment on chronic vasospasm after platelet-enriched subarachnoid hemorrhage in primates.

A model of chronic cerebral vasospasm (VSP) analogous to the clinical situation was established by inducing subarachnoid hemorrhage (SAH) in monkeys. Platelets harvested from 4 ml of blood were added to autologous blood in an attempt to accentuate any effect that vasoactive substances such as serotonin, contained in platelets, might have on producing cerebral VSP. Antiserotonin medications were administered in an attempt to reduce the frequency or severity of angiographically proven VSP. Animals were divided into small (1 ml/kg) and large (1.2 to 1.5 ml/kg) hemorrhage groups and later were randomized equally to receive either saline placebo or reserpine (0.013 mg/kg i.m.) and kanamycin (50 mg/kg p.o.) administered 3 hours after SAH and daily thereafter to Day 7. In both the small and the large hemorrhage groups of treated animals, there was a significant reduction in serotonin levels (P less than 0.01 and P less than 0.05, respectively) compared to base line levels. In the groups of nontreated monkeys with small and large hemorrhages, serotonin levels were not statistically different from control values. Despite reduction of serotonin levels to 19 and 26% of the control values in the small and large hemorrhage, treated groups, there was no apparent difference in the frequency or severity of angiographically proven VSP. This study found no evidence that reserpine and kanamycin have a beneficial effect on preventing VSP when treatment is begun after SAH.

Animals

A randomized placebo-controlled double-blind trial of nimodipine after SAH in monkeys. Part 1: Clinical and radiological findings.

The authors have developed a method to induce chronic cerebral vasospasm after subarachnoid hemorrhage (SAH) in monkeys. With microsurgical techniques, 33 monkeys had a frontotemporal craniectomy and unilateral opening of the subarachnoid cisterns. Cerebrospinal fluid was drained and a fresh hematoma, obtained from an average of 7 ml of autologous blood, was carefully placed against the major arteries of the anterior circulation on one side. The 30 monkeys studied for 7 to 14 days after the SAH were allocated randomly to two treatment groups of 15: one group received placebo and the other nimodipine, 1 mg/kg every 8 hours. Indices monitored before and after SAH included neurological status, cerebral blood flow, computerized tomography, and angiographic vessel caliber. In the placebo group, delayed ischemic neurological deficit developed in one monkey 4 days after clot placement and was present at sacrifice on Day 14. No such deficit occurred in the nimodipine group. The effect of nimodipine on vessel caliber at this dosage was equivocal. Significant vasospasm (31% to 100% reduction in vessel caliber) developed in 87% (26 of 30) of the animals. Overall, vasospasm was slightly more common in the placebo group: in this group, on Days 7 and 14, the incidence of vasospasm was significantly higher (p less than 0.05) than in the nimodipine group. However, the average percentage reduction in vessel caliber of the maximally constricted vessel in each monkey was not significantly different between the two groups.

Animals

A randomized placebo-controlled double-blind trial of nimodipine after SAH in monkeys. Part 2: Pathological findings.

Chronic cerebral vasospasm was induced in monkeys by placement of an autologous blood clot after the basal cisterns had been opened over the arteries of the circle of Willis on one side. The experimental protocol was detailed in Part 1 of this paper. Twenty of the 30 monkeys studied from both groups (one receiving placebo and the other nimodipine) underwent cerebral fixation (Day 14) at controlled pressure by intra-arterial perfusion. The arteries at the base of the brain were studied by light microscopy and scanning (SEM) and transmission electron microscopy (TEM). Cerebral angiography on Day 7 showed that vasospasm was significantly more common (p less than 0.0001) and more severe (p less than 0.01) on the clot side compared to the control or non-clot side. Vasospasm was less severe on Day 14, just before sacrifice. On SEM, 80% of the 20 middle cerebral artery (MCA) specimens that had been in spasm (Day 7) showed marked corrugation , and in some the endothelium had a fish-scale appearance. All of the 10 MCA's on the clot side examined by TEM that had been in spasm (Day 7) showed marked changes such as endothelial swelling, subendothelial proliferation, corrugation of the elastic lamina, and myonecrosis. With few exceptions, none of the basilar arteries or MCA's on the non-clot (control) side showed any abnormalities. The pathological findings of vessels in spasm were considered to be slightly less severe in the nimodipine group; however, the trial drug (1 mg/kg/8 hrs) did not prevent such abnormalities from occurring. The ultrastructural changes in the arterial walls of specimens from both placebo and nimodipine groups in vasospasm are described. Since dramatic changes are present in the vessel walls even after radiologically visible vasospasm has almost completely abated, we believe that vasospasm is due to long-lasting smooth-muscle constriction and not to vessel wall thickening caused by a cellular or subcellular infiltrate.

Animals

Chronic cerebral vasospasm after large subarachnoid hemorrhage in monkeys.

The authors have developed a model of chronic cerebral vasospasm analogous to the clinical situation, by inducing a large subarachnoid hemorrhage (SAH) in monkeys. With this model, the size of the SAH apparent on the first computerized tomography (CT) scan was correlated with the incidence and severity of cerebral vasospasm that developed. Indices monitored for up to 21 days after SAH included cranial CT scan, cerebral blood flow, vessel caliber, and neurological status. The 18 monkeys studied for 48 hours or more were divided into two groups according to the size of the SAH on CT scan. Vasospasm was more common in the group with large SAH. In this group, on Days 0, 7, and 14, the incidence of vasospasm was significantly higher than at other times (p less than 0.001, p less than 0.01, and p less than 0.05, respectively), and the percentage reduction in vessel caliber was significantly greater than in the group with small/medium SAH (Day 7, p less than 0.02; Days 0 and 14, p less than 0.05). Delayed neurological deficit developed in two monkeys with large SHA. Apathy was noted from Day 17 to Day 21 in one, and unsteadiness and drowsiness were noted on Days 4 and 5 in the other. Overall, the incidence, degree, and time course of vasospasm reflected the size of the hemorrhage.

Animals

New contribution on the oesophageal mucous innervation in certain monkeys (Cercopithecidae).

Spindle-shaped, barrel-like, or bush-like corpuscular neural structures situated in the mucous epithelium of the upper third of the oesophagus are described. These structures are not homogeneously distributed in this area. Some are very close to the pharyngooesophageal sphincter, spanning the thickness of the epithelium and communicating with the basal membrane by means of a thin pedicle and with the lumen by a small hilus or pore, their morphology being that of a taste bud. The others are situated deeper in the mucous epithelium of the upper third, communicating with the basal membrane only by means of either a thin pedicle or a thicker one, and separated from the lumen by a thick layer of epithelial cells. The bush-like apparatuses lie closely adjacent to the basal membrane of the epithelium.

Animals

Spinous leafy nerve endings in the feline stomach wall.

The Champy-Maillet ZIO technique has been applied to the study of the muscular tunic of the stomach. In the corpus and antrum pyloricum some nerve fibres end in non-capsulated expansions owning thorn-like protrusions. Their morphology is studied and a possibly functional sensory significance is proposed, on the basis of previous experimental results.

Animals

[Leukocyte migration inhibitory factor and basophil degranulation in drug reactions].

We performed a prospective study in patients with a medical history of adverse reaction to drugs with the purpose of rule out allergy. We included 31 patients who were attended in the Allergy Service. We compared the sensibility and specificity of the test of inhibition factor of leucocytes migration and degranulation basophil against the exposition. After the statistical analysis, we concluded: the laboratory test, we have already mentioned, have little sensibility and specificity so the exposition test in the quickest, useful, and more simple method to determine drugs allergy, but more dangerous.

Adolescent