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PubMed1987

Neurogenic mediation of serum-induced microvascular constriction.

We have used the rat hippocampal slice preparation as a model system for the study of microvascular vasospasm. Penetrating cerebral microvessels in the slice constrict in response to a variety of stimuli, including serum from coagulated blood. Microvascular responses to many stimuli are associated with changes in the activity of nearby neurons, and in some cases can be shown to be neurogenically mediated. Here we use the selective neurotoxin, tetrodotoxin (TTX), to show that serum-induced constriction is also neurogenically mediated. This neural regulation of microvessel caliber may participate in pathological vasoconstriction mechanisms in the whole animal.

Action Potentials↗
PubMed1987

Blood-borne factors regulating microvascular constriction in the rat hippocampal slice.

Previous work shows that blood serum contains a factor that elicits constriction of large cerebral arteries and may be responsible for cerebral vasospasm in subarachnoid hemorrhage patients. However, few studies have considered the action of potential spasmogens on intraparenchymal resistance vessels. We used a common preparation for neurophysiology, the rat hippocampal slice, to study penetrating arterioles and their response to a variety of potential vasoconstrictors. Dilute serum from clotted rat blood evoked profound microvascular constriction when applied to the slice, but plasma incubated with heparin to prevent coagulation was unable to do so. A variety of potential vasoconstrictor substances were tested to see if they could duplicate the effects of serum. Norepinephrine (10 microM), serotonin (one microM) and prostaglandin E2 (one nM) were ineffective in this regard. However, when a stable eicosanoid, thromboxane B2, was applied at a concentration achieved in the cerebrospinal fluid of subarachnoid hemorrhage patients, it duplicated a portion of the vasoconstriction produced by serum. It is concluded that thromboxane B2 may account for part of the spasmogenic property of serum and that unidentified molecules in the coagulation pathway may also play a role.

Animals↗
PubMed1991

Staining of glial fibrillary acidic protein (GFAP) in lumbar spinal cord increases following a sciatic nerve constriction injury.

The change in staining density of glial fibrillary acidic protein (GFAP) was analyzed in rats that sustained a chronic constriction injury produced by sutures tied loosely around one sciatic nerve. This injury model of peripheral neuropathy resulted in a behavioral hyperalgesia evidenced by a decrease in mean foot withdrawal latency to radiant heat. Increased GFAP immunostaining was observed in the gray matter of the spinal cord ipsilateral to the lesion and specific to spinal segments in which the sciatic nerve is distributed. Elevated GFAP staining density was attributed primarily to hypertrophy of astrocytes rather than their proliferation or migration since counts of astrocyte profiles demonstrated no significant difference when comparing the lesioned to the control side. The magnitude of the increase in GFAP staining correlated with the degree of hyperalgesia. Thus, these data suggest that astrocytes participate in the sequelae occurring in the dorsal horn following constriction injury of a peripheral nerve.

Animals↗
PubMed1992

Pial arteriolar constriction following cortical spreading depression is mediated by prostanoids.

The mechanism of pial arteriolar constriction during post-cortical spreading depression (CSD) was examined in anesthetized adult rabbits. Using a closed cranial window and intravital microscopy, the diameter of a pial arteriole was determined. A single CSD was induced by KCl micro-injection and its propagation was monitored by recording slow potential changes accompanying CSD. Prostanoid levels in cortical cerebrospinal fluid (CSF) were determined by radioimmunoassay. Pial arteriolar diameter increased significantly from 76 +/- 6 to a maximum of 119 +/- 5 microns (57%, n = 8) for 1.6 +/- 0.1 min when CSD (velocity, 2.8 +/- 0.1 mm/min) reached the cortex just beneath the vessel irrespective of its location. Shortly after CSD expiration from the cortex, pial arteriolar diameter decreased from the pre-CSD level to a minimum of 67 +/- 5 microns (12%, n = 8) for 19.5 +/- 2.1 min. CSD was elicited again in the same animal while the cortical surface under the window was continuously superfused with artificial CSF at a flow rate of 3.2-4.5 ml/min. Pial arteriolar dilation (from 75 +/- 6 to 115 +/- 3 microns, 53 +/- 9%, for 1.6 +/- 0.1 min, n = 8) was observed again during CSD (velocity, 2.7 +/- 0.2 mm/min), however, no constriction of the vessel was seen after CSD expiration. Indomethacin pretreatment (n = 11) to inhibit prostanoid production enhanced the magnitude of CSD-induced vasodilation from the pretreatment levels of 59 +/- 9% (from 82 +/- 5 to 130 +/- 8 microns for 1.7 min) to the post-treatment levels of 82 +/- 13% (from 78 +/- 5 to 142 +/- 12 microns for 1.8 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Formation of primary constriction and heterochromatin in mouse does not require minor satellite DNA.

Whereas the major satellite fraction in mouse extends its domain from the centromere to the distal end of the pericentric heterochromatin, the minor satellite DNA is present specifically in the centromere or primary constriction. We hybridized the biotinylated minor satellite sequence to L929 cells of mouse origin. The sequence hybridized to all chromosomes. Whereas hybridization was detected on all active centromeres, the inactive centromeres in certain dicentrics did not show any signal. This satellite, however, was detected in all inactive centromeres in a heptacentric chromosome. The intensity of fluorescence on the inactive centromeres of the heptacentric was similar to that present on the active centromeres. Several heterochromatin blocks, which were not associated with any centromere, were also found to lack hybridization with the minor satellite. The inactive centromeres, whether carrying the minor satellite DNA fraction or not, generally do not react with the antikinetochore antibodies present in the scleroderma serum. These studies are interpreted to show that (1) the primary constriction in mouse can be formed without the participation of minor satellite, (2) heterochromatin in mouse may constitute without this fraction, (3) the major and minor satellite may not be interspersed but are joined at some defined boundary, and (4) the binding of CENP-B does not depend upon the quantity of minor satellite or the number of CENP boxes present in the inactive centromeres.

Animals↗
PubMed1991

A ring of uncharged polar amino acids as a component of channel constriction in the nicotinic acetylcholine receptor.

The channel pore of the nicotinic acetylcholine receptor (AChR) has been investigated by analysing single-channel conductances of systematically mutated Torpedo receptors expressed in Xenopus oocytes. The mutations mainly alter the size and polarity of uncharged polar amino acid residues of the acetylcholine receptor subunits positioned between the cytoplasmic ring and the extracellular ring. From the results obtained, we conclude that a ring of uncharged polar residues comprising threonine 244 of the alpha-subunit (alpha T244), beta S250, gamma T253 and delta S258 (referred to as the central ring) and the anionic intermediate ring, which are adjacent to each other in the assumed alpha-helical configuration of the M2-containing transmembrane segment, together form a narrow channel constriction of short length, located close to the cytoplasmic side of the membrane. Our results also suggest that individual subunits, particularly the gamma-subunit, are asymmetrically positioned at the channel constriction.

Amino Acid Sequence↗
PubMed1986

Effects of vascular constriction on occlusive thrombus formation of rat mesenteric artery.

Effects of vascular constriction on thrombotic occlusion was evaluated using rat mesenteric arteries and video-recording system attached to the microscope. Topical application of norepinephrine of 1, 10 and 100 micrograms/ml reduced the arterial diameter dose dependently from 297 +/- 41 mu to 166 +/- 50, 87 +/- 18 and 84 +/- 11 mu (mean +/- SD, n = 7), respectively. The diameter reduction by the higher 2 doses persisted for more than 30 minutes until the wash out of the agent. But, no thrombus formation was observed. A reproducible thrombus formation was induced by inserting a glass micropipette into the vascular lumen. The maximal percent occlusion by the thrombus was 80 +/- 11% (range; 67 to 95%, n = 7). The topical application of 10 micrograms/ml norepinephrine induced vasoconstriction and increased the percent occlusion significantly to 97 +/- 8% (p less than 0.05). Complete occlusion of the lumen developed in 6 of 7 rats after the agent and in 2 rats it was not released until the wash out of the agent for more than 30 minutes. Thrombus formation itself did not change the arterial diameter at the site of thrombus formation as well as at sites of 300 and 600 mu down stream. It is suggested that the vascular constriction alone does not necessarily cause thrombus formation but may aggravate the arterial flow reduction induced by thrombosis.

Administration, Topical↗
PubMed1991

Vacuum constriction devices and the clinical urologist: an informed selection.

The U.S. Food and Drug Administration (FDA) lists vacuum constriction devices (VCD) as safe, nonsurgical therapy for erectile dysfunction. Our study compared the responses of 30 male (10 novice and 20 regular) VCD users of seven commercially available systems (Mentor Response, Mentor-Touch, Mentor-Piston, Dacomed Catalyst, Mission VED, Osbon ErecAid, and Pos-T-Vac). Variables evaluated included simplicity of instruction, ease of use, cost, instructional value of videotape, company follow-up, presence of a pressure-limitation gauge, and length of warranty. The results from our study show (1) 100 percent reported an additional cost to be of minor importance in determining choice of device, (2) 80 percent of novice and 95 percent of regular users stated the instructional videotape was essential, (3) 95 percent of the participants desired a twenty-four-hour hot-line, (4) 40 percent of novice users but only 25 percent of regular users wanted personalized company follow-up, (5) 100 percent of novice users preferred single-handed devices, while regulars showed no preference. (6) Regular users scored Mentor Response, Osbon ErecAid, and Mentor-Piston highest regarding ease of use. While the vacuum constriction devices are conceptually similar, there are subtle operational distinctions between the different brands. The clinical urologist should be aware of these nuances.

Costs and Cost Analysis↗
PubMed1983

Constriction of fetal ductus arteriosus by non-steroidal anti-inflammatory drugs.

Transplacental effects of 24 non-steroidal anti-inflammatory drugs (NSAIDs) on the fetal ductus arteriosus were studied in full-term pregnant rats using the whole-body freezing technique. All sixteen acidic NSAIDs constricted the fetal ductus in a dose-dependent relationship, but considerable differences in the intensity of effect was noticed with the clinical dose of each drug. Six of the eight basic NSAIDs did not constrict the fetal ductus at 50 to 100 times the usual clinical dose. It is concluded that acidic NSAIDs probably should not be administered to pregnant women. However, it may be established in the future that some basic NSAIDs can be administered safely to pregnant women without hazardous effect on the fetus.

Age Factors↗
PubMed1987

Constriction of cat coronary arteries by synthetic thromboxane A2 and its antagonism.

Synthetic thromboxane A2 (TxA2S) induced rapid, concentration-dependent constriction of isolated perfused cat coronary arteries. Its potency was approximately 30 times that of the prostaglandin endoperoxide, PGH2. Pinane thromboxane A2 (PTA2), BM-13.505 and SQ-29,548, compounds previously shown to antagonize the effects of stable prostaglandin endoperoxide analogs, inhibited the constriction induced by TxA2S in a concentration-dependent fashion. These experiments provide further evidence that the oxetane structure proposed for TxA2 is correct and show that compounds that inhibit the effects of prostaglandin endoperoxides also antagonize the effects of TxA2.

Animals↗
PubMed1992

Pupillary constriction during haloperidol treatment as a predictor of relapse following drug withdrawal in schizophrenic patients.

It has been proposed that the autonomic nervous system is dysregulated in schizophrenia. We hypothesized that measures of autonomic function, even during neuroleptic stabilization, might predict relapse following withdrawal of medication. Previously, shorter latencies to maximum pupillary constriction have been reported to differentiate acutely hospitalized schizophrenic patients from control subjects. Pupillary light reactions were recorded weekly from 19 chronic schizophrenic inpatients who were initially maintained on haloperidol and subsequently were withdrawn from medication under double-blind, placebo-controlled conditions. Patients were then classified as either relapsed or nonrelapsed (clinically stable) during the drug-free period. During the treatment phase, a shorter latency to maximum pupillary constriction significantly distinguished patients who were later to relapse from the nonrelapsers. The potential use of autonomic activity as an indicator of prodromal sensitivity was supported. In addition, these findings emphasize the need for classification of drug-free patients according to clinical status.

Adult↗
PubMedDate not supplied

Neuropeptide Y-induced constriction in small resistance vessels of skeletal muscle.

The in vivo responsiveness of small arterioles and venules in the rat cremaster muscle to topical administration of neuropeptide Y was assessed using closed-circuit television microscopy. Male Sprague-Dawley rats were anesthetized with sodium pentobarbital (50 mg/kg) and the cremaster muscle was exposed to increasing bath concentrations of neuropeptide Y (10(-10)-10(-7) M). Neuropeptide Y produced dose-dependent constrictions in first (90 +/- 8 microns), second (50 +/- 6 microns) and third (21 +/- 4 microns) order arterioles. Arteriolar reactivity to the peptide was inversely related to vessel diameters. Venules were relatively unresponsive to neuropeptide Y. Exposure to the alpha-adrenergic receptor antagonist, phentolamine (10(-6) M), failed to modify the arteriolar constrictor responses to neuropeptide Y, while pretreatment with the sympathetic neuronal blocking agent, guanethidine (10(-5) M), produced a small, but significant, reduction in sensitivity. These data suggest that neuropeptide Y causes constriction of arterioles of skeletal muscle, primarily by acting directly on vascular smooth muscle to induce contraction, and not via release of endogenous norepinephrine.

Animals↗
PubMed1991

Peripheral nerve palsy associated with congenital constriction band syndrome.

Of 21 patients with congenital constriction band syndrome treated in our clinic from 1967 to 1988, four had constriction bands proximal to the wrist. Three of these also had a peripheral nerve palsy. Late surgical decompression does not help but early diagnosis, using electrodiagnosis methods, and neurolysis or nerve grafting as soon as possible may improve nerve function.

Amniotic Band Syndrome↗
PubMed1995

Contribution of the sciatic and saphenous nerve to the ventrobasal thalamic neuronal responses to pinch in rats with a chronic sciatic nerve constriction: a study using anesthetic blocks and nerve section.

To extend the study on the respective contribution of the sciatic and saphenous nerve in abnormal nociceptive responses observed in rats with a loose constriction of one sciatic nerve, neuronal responses to pinch applied to the territory of the injured nerve, recorded in the ventrobasal complex of the thalamus have been studied. Eleven neurones recorded in 11 rats with a nerve constriction since 15-19 days and clear abnormal pain-related behaviour to mechanical stimulus, were tested before and during an anesthetic block of the saphenous and/or of the sciatic nerve, and/or after the saphenous nerve section. Only the sciatic nerve block depressed significantly the pinch responses.

Anesthetics↗
PubMed1995

Axonal constriction at Ranvier's node increases during development.

We have studied the ratio between the nodal and the internodal diameter (the dn/d(in) ratio) of large myelinated axons in the L7 ventral spinal root of the cat during pre- and postnatal development using light and electron microscopy. A substantial nodal constriction, dn/d(in) = 0.6, was found at the beginning of myelination, about 2 weeks before birth. The ratio decreased during the subsequent 10 weeks and approached the adult value of 0.47 (SE 0.01, N = 45) in the 8 weeks old kitten. The observations are discussed with respect to the maturation of the nodal region and to our earlier idea that the constricted nodal axon segments of large peripheral myelinated nerve fibres of adult cats and kittens 2 months and more of age are sites capable of interacting with and perhaps even controlling the passage of axonally transported materials.

Age Factors↗
PubMed1992

Evaluation of constricted affect in chronic pain: an attempt using the Toronto Alexythymia Scale.

The Toronto Alexythymia Scale (TAS) was applied as a potential measure of constricted affect among a sample of patients with chronic, non-malignant pain (n = 195). As previously demonstrated with non-clinical samples, the scale was found to possess moderate reliability with two principal internal factors. These factors seemed to reflect social introversion and a lack of proneness to fantasy. There was a moderate, negative association between them. The domain sampled by the TAS was apparently heterogeneous, with total scores showing no relationship to reported disability or pain intensity and a low relationship to reported distress. These results suggest potential limitations of the TAS and the alexythymia construct as means for evaluating constricted affect that accompanies chronic pain.

Adult↗
PubMed1992

Effects of intrathecal capsaicin and an NK-1 antagonist, CP,96-345, on the thermal hyperalgesia observed following unilateral constriction of the sciatic nerve in the rat.

We evaluated the effect of intrathecal (i.t.) capsaicin (CAP) and the NK-1 selective non-peptidic antagonist, CP,96-345, on the thermal hyperalgesia ordinarily observed after unilateral partial ligation of the sciatic nerve in rats. CAP was injected i.t. 2 days after constriction injury. Seven days after partial ligation, the levels of substance P (sP), calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) were the same in the left and right dorsal horns of the lesioned rats which were injected with vehicle (VEH). CAP (75 micrograms/15 microliters of 20% 2-hydroxypropyl-beta-cyclodextrin) resulted in an equal reduction (40-50%) in the dorsal horn levels of sP and CGRP, but not VIP. After 7 days, i.t. CAP increased the paw withdrawal latency (PWL) of the non-injured hind paw. In contrast, there was no change in the PWL of the injured paw when compared to that of VEH-treated animals. Thus, CAP did not abolish the hyperalgesic state. We concluded that the thermal hyperalgesia after sciatic nerve constriction injury is not mediated by CAP-sensitive C fibers. CP,96-345 given i.t. at a dose which is physiologically active (400 micrograms) had little effect on the thermal response latency of either the normal or hyperesthetic paw. This provides further evidence that neither the normal pain response nor hyperalgesic state is dependent upon a dorsal horn action of sP.

Animals↗
PubMed1993

Effects of colchicine applied to the peripheral nerve on the thermal hyperalgesia evoked with chronic nerve constriction.

Loose ligatures placed unilaterally on the sciatic nerve results in a thermal hyperalgesia. We applied 5 or 50 mM colchicine (COL, blocker of the fast axonal transport) to the sciatic nerve and examined the effects of COL on thermal hyperalgesia and the levels of substance P (sP), calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) in the spinal cord and the sciatic nerve. These data showed that the application of 50 mM COL to the sciatic nerve in this study functioned as an axonal transport blocker. COL abolished the hyperalgesic state in a concentration-dependent manner when applied proximal to the constriction injury. COL (50 mM), when applied distal to the injury, had no effect on the hyperalgesia. COL did not alter motor function or paw withdrawal response in the non-lesioned animal. Examination of peptide levels in nerve shows that COL resulted in an accumulation of sP, CGRP and VIP in the nerve. In the dorsal horn, COL resulted in a modest reduction in levels of sP and CGRP as compared to the non-lesioned side while VIP levels were elevated. These data suggest that active factors generated by the focal nerve compression and carried by fast axonal transport from the lesioned site to the spinal cord and/or dorsal ganglion are important in the development of thermal hyperalgesia after constriction injury in rats.

Animals↗