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Biomedical subjects

J C Torner

Publications and source records attributed to J C Torner.

At least 73 records · Page 4Linked to original sources
PubMed1989

Effects of subarachnoid hemorrhage on platelet-derived vasoconstriction of rabbit basilar artery.

The effects of subarachnoid hemorrhage on platelet-derived vasoconstriction of the isolated rabbit basilar artery were examined using an isometric tension recording method. The subarachnoid hemorrhage was induced by injecting arterial blood in the cisterna magna. The following points were confirmed: (1) the maximal contraction produced by the platelets (10(7)/mL) treated with indomethacin or dazoxiben (thromboxane synthetase inhibitor) were suppressed (65% or 70% of the control); (2) the contraction of the arteries treated with ONO-3708 (thromboxane A2 antagonist) or ketanserin was inhibited (73% or 8.4%), as was contraction after subarachnoid hemorrhage (67% or 14%); (3) platelet-induced contraction was potentiated after subarachnoid hemorrhage; and (4) serotonin-induced contraction was potentiated after subarachnoid hemorrhage. However, synthetic thromboxane A2-induced contraction was not potentiated. The present experiments suggest that both serotonin and thromboxane A2 contribute to vasoconstrictions induced by the platelets, before and after subarachnoid hemorrhage. The platelet-derived contraction response is potentiated after subarachnoid hemorrhage and serotonin is responsible for the increased reactivity.

Animals↗
PubMed1989

Neurologic assessment of subarachnoid hemorrhage in a large patient series.

Data from the International Cooperative Aneurysm Study including 3521 cases of aneurysmal subarachnoid hemorrhage were used to statistically derive a simple scoring method for assessing neurologic status of subarachnoid hemorrhage patients. Discriminant analysis was used to identify the best combination and weighting of seven neurologic assessment variables to classify outcomes at 6 months post-subarachnoid hemorrhage. The sum of eye opening response and worst motor response classified patient outcomes nearly as well as all variables combined. The validity of this summary score was tested using good recovery and mortality endpoints. The result is a useful scale for classifying subarachnoid hemorrhage patients.

Discriminant Analysis↗
PubMed1989

Sensitivity and specificity of transcranial Doppler ultrasonography in the diagnosis of vasospasm following subarachnoid hemorrhage.

Vasospasm is the leading cause of death and disability in patients with aneurysmal subarachnoid hemorrhage (SAH). Transcranial Doppler ultrasonography (TCD) can detect the arterial narrowing noninvasively, but the sensitivity and specificity of this technique have not been reported in a population of patients with a high frequency of angiographic vasospasm. In this study, 34 consecutive patients with SAH undergoing angiography during the period of risk for vasospasm had technically adequate TCD examinations within 24 hours of the angiogram. Using a mean flow velocity of 120 cm/sec and above as indicative of vasospasm, TCD correctly detected angiographic vasospasm in 17 patients; there were no false positives. It correctly determined that 5 patients did not have vasospasm, whereas there were 12 false negatives. False negatives were frequently due to angiographic vasospasm involving vessels not assessable by TCD. The correlation between mean flow velocity and the angiographic residual lumen diameter of the middle cerebral artery was statistically significant. These data suggest that TCD is a highly specific (100%), but less sensitive (58.6%) test for the detection of angiographic vasospasm following SAH. Confirmatory angiography may be avoided if the TCD study is positive, but additional studies may be necessary if the clinical picture is suspicious and the TCD study is negative.

Cerebral Angiography↗
PubMed1989

Head injury mortality in two centers with different emergency medical services and intensive care.

The authors report data collected prospectively on 551 cases of head injury in New Delhi, India, and 822 cases in Charlottesville, Virginia. The mortality rate, adjusted for initial severity of injury, was 11.0% in New Delhi versus 7.2% in Charlottesville (p less than 0.02). There was a striking similarity in mortality rates at both centers when comparing patients with the least severe head injuries and those with the most severe injuries according to the motor score of the Glasgow Coma Scale (GCS M). However, in the group with an abnormal but purposeful motor response (GCS M = 5), the mortality rate was 12.5% in New Delhi versus 4.8% in Charlottesville (p less than 0.01). The relative absence of prehospital emergency care and the delay in admission after head injury in New Delhi are cited as two possible causes for the differences in mortality rates in this subgroup of patients with "moderate" head injuries.

Adult↗
PubMed1988

Intracranial operation within seven days of aneurysmal subarachnoid hemorrhage. Results in 150 patients.

We evaluated the results of intracranial operation in 150 consecutive patients surgically treated within seven calendar days of aneurysmal subarachnoid hemorrhage (SAH). Patients in all clinical grades, except those who were moribund, were treated. Those with either anterior or posterior circulation aneurysms were included. On follow-up assessment, favorable outcomes were noted in 107 patients (71%), 17 had major disabilities (11%), and 26 had died (17%). During hospitalization, vasospasm was diagnosed in 63 patients (42%) and rebleeding occurred in 39 (25%). Operations were performed throughout the first week after SAH; results of operation were similar on each day. A lower rate of good recovery was observed among patients operatively treated four to seven days after SAH than among those operated on earlier. The admitting neurologic condition influenced outcome after early operation, but age did not have a major impact. We find that aneurysm surgery can be performed within one week of SAH with acceptable results, although there is room for improvement.

Female↗
PubMed1988

Immunohistochemically demonstrated increase of prostaglandin F2-alpha in neurons after reoxygenation in anoxic rats.

Immunohistochemical staining for prostaglandin F2-alpha (PG F2 alpha) was conducted to identify PG F2 alpha synthesizing or binding sites in anoxic rat brains. Anoxia was produced in 22 rats to lower the arterial oxygen tension (PaO2) to 21 +/- 4 mmHg by ventilation with a 95% nitrogen and 5% carbon dioxide gas mixture. In 8 animals anoxia was continued for 30 sec, and in 14 rats for 3 min. Prior to decapitation, 5 animals in the 30-sec anoxia group and 8 rats in the 3-min anoxia group were reoxygenated for 5 min, while the remaining 9 were not. Five-min reoxygenation returned the PaO2 to 106 +/- 7. Three non-reoxygenated and 3 reoxygenated rats, all pretreated with indomethacin, and 5 normal rats served as controls. The brains were snap-frozen. The cryosections were stained by the indirect immunofluorescence method. PG F2 alpha was noted mainly in pial vessels in all normal rats. All reoxygenated rats showed a positive reaction not only in blood vessels, but also in neurons, particularly hippocampal neurons and Purkinje cells. The staining of the above neurons was noted to be less in non-reoxygenated rats. The stronger staining was observed in rats reoxygenated after 3-min anoxia than 30-sec anoxia. The indomethacin-pretreated rats showed almost no increase in staining intensity. The above results indicate that reoxygenation after anoxia results in an increase of PG F2 alpha in neurons of both cerebrum and cerebellum.

Animals↗
PubMed1988

Primary cytomegalovirus infection in pediatric nurses: a meta-analysis.

A meta-analysis of six controlled studies was performed to evaluate the risk of cytomegalovirus (CMV) infection among pediatric nurses. The pooled risk ratio for CMV infection in pediatric nurses using cumulative incidence data was statistically significant (risk ratio [RR] 2.7; 95% confidence interval [CI] 1.33 - 5.52), but person-year analysis taking account of follow-up periods demonstrated a trend toward increased risk that failed to reach statistical significance (RR 1.8; 95% CI 0.88 - 3.55). Despite pooling, there was low statistical power for comparing person-year rates. The studies included in this analysis failed to provide data on several potential confounding variables. We conclude that studies published prior to the widespread adoption of universal precautions suggest that pediatric nurses may have been at increased risk for CMV infection due to occupational exposure, but inadequate design and sample size of the studies prevent a definitive conclusion. Well-designed, controlled studies are still needed to define the occupational risk of CMV infection.

Cytomegalovirus Infections↗
PubMed1988

Failure of heparin to prevent progression in progressing ischemic infarction.

Anticoagulation with heparin is frequently recommended for patients with progressing ischemic cerebral infarction, yet little data is available detailing the acute results of treatment with this agent. We report the results of continuous intravenous heparin treatment in 36 consecutive patients admitted with progressing ischemic infarction, all of whom had computed tomography scans to exclude the diagnosis of hemorrhage prior to treatment. Overall, 18 of 36 (50%) had continued neurologic worsening despite treatment. The incidence of further worsening was greater in carotid territory infarctions (14 of 19, 74%) than in either vertebrobasilar (2 of 8, 25%) or lacunar (2 of 9, 22%) infarctions (p less than 0.05, Fisher's exact test). These observations suggest that additional controlled studies of the efficacy of heparin in progressing ischemic infarction are warranted.

Cerebral Infarction↗
PubMed1988

Metabolic alterations in rabbit cerebral arteries caused by subarachnoid hemorrhage.

The effect of subarachnoid hemorrhage on metabolic rates in rabbit cerebral arteries was investigated by measuring adenosine triphosphate (ATP) content and L-lactate release. The mean +/- SEM ATP content was 0.38 +/- 0.02 mumol/g wet wt in control rabbit basilar arteries (n = 6). The ATP content decreased significantly to 0.17 +/- 0.02 mumol/g wet wt 2 days after experimental subarachnoid hemorrhage (n = 6), although only a slight decrease was detected in the basilar arteries 2 days after cisternal injection of the same amount of artificial cerebrospinal fluid. Hypoxia significantly decreased ATP content in the control basilar arteries to 0.26 +/- 0.04 mumol/g wet wt (n = 6). The same degree of hypoxia did not decrease ATP content in the basilar arteries after subarachnoid hemorrhage. Release of L-lactate was significantly higher from the arteries after subarachnoid hemorrhage than from the control arteries under both aerobic and hypoxic conditions. Our results indicate that subarachnoid hemorrhage induced an alteration of metabolic rates in rabbit cerebral arteries. The oxygen-requiring pathways to synthesize ATP may be important in control cerebral arteries; however, after experimental subarachnoid hemorrhage, the main pathway in the cerebral arteries may shift from oxygen-requiring pathways to an anaerobic glycolytic pathway.

Adenosine Triphosphate↗
PubMed1988

Effect of removal of the endothelium on vasocontraction in canine and rabbit basilar arteries.

The effect of endothelium removal on the contractile responses to KCl, hemoglobin, serotonin (5-HT), norepinephrine (NE), prostaglandin (PG)F2 alpha, PGD2, and PGE2 was investigated in canine and rabbit basilar arteries by an isometric tension-recording method. In canine basilar arteries, endothelium removal elevated the dose-response curves to 5-HT, PGF2 alpha, and PGD2, and PGE2, but not to KCl, hemoglobin, or NE. In rabbit basilar arteries, on the other hand, removal of the endothelium elevated the dose-response curves to 5-HT, NE, PGF2 alpha, and PGD2, but not to KCl or hemoglobin. Neither contractile nor inhibitory response was elicited by PGE2 in rabbit basilar arteries. Contraction induced by 5-HT and NE following endothelium removal had a much more pronounced effect in rabbit basilar arteries than in canine basilar arteries. These results suggest that, following endothelium removal, abolition of the spontaneous release of endothelium-derived relaxing factor is the most probable mechanism of the enhanced vasocontraction. Since endothelial damage results from subarachnoid hemorrhage, the aforementioned mechanism of vasocontraction enhancement may play a role in the pathogenesis of cerebral vasospasm.

Animals↗
PubMed1988

Pharmacological comparison of endothelium-dependent relaxation in isolated cerebral and extracerebral arteries.

Endothelium-dependent relaxation was induced by acetylcholine (ACh), adenosine triphosphate (ATP), and thrombin in isolated cerebral and extracerebral arteries obtained from rabbits and dogs. Using an isometric tension-recording method, the authors then examined the difference in the extent of relaxation between the cerebral and extracerebral arteries. In rabbits, the dose-response curve of the basilar artery for ACh was significantly different (p less than 0.05) from curves of the femoral and common carotid arteries. The IC50 value (the concentration inducing a one-half inhibition of the initial contractile tone) for the basilar artery in ACh-induced relaxation was significantly higher (p less than 0.05) than for the common carotid artery, although the mean maximum relaxation of the basilar artery to ACh was not significantly different from that seen in extracerebral arteries. The relaxing effect of ACh in dogs was much less in the middle cerebral and basilar arteries than in the common carotid, vertebral, and femoral arteries. On the other hand, both ATP (in rabbits and dogs) and thrombin (in dogs) induced significantly more (p less than 0.05) relaxation in the cerebral arteries than in the extracerebral arteries. Endothelium-dependent relaxation induced by ACh or ATP has been demonstrated in a wide range of arteries from a variety of animals. The present results suggest that ATP has a more important role than ACh in the regulation of the vascular tone of the major cerebral arteries in these two species.

Acetylcholine↗
PubMed1987

Predicting cerebral ischemia after aneurysmal subarachnoid hemorrhage: influences of clinical condition, CT results, and antifibrinolytic therapy. A report of the Cooperative Aneurysm Study.

Cerebral ischemia from vasospasm is a major cause of death and disability following aneurysmal subarachnoid hemorrhage (SAH). This study examines and compares the relative utility of the initial neurologic examination and early CT in predicting cerebral ischemia after SAH. The influence of antifibrinolytic drugs (AFD) in the development of cerebral ischemia was also studied. AFD increased the risk of cerebral ischemia regardless of the admitting neurologic condition or the findings of CT. Among patients given AFD, impaired orientation or alertness was associated with a higher risk of ischemia. Other neurologic signs were not predictive of ischemia. Clinical features were not predictive of ischemia among patients not given AFD. Focal, thick collections of blood on CT were highly predictive of ischemia, whether or not patients received AFD. Admitting CT is the best prognostic indicator for the development of cerebral ischemia after SAH. It should be used to supplement the clinical examination in selecting patients best suited for therapy to prevent vasospasm.

Antifibrinolytic Agents↗
PubMed1987

Home health care: who's where?

Referrals to two home health agencies, one public and one private, were examined over a one-year period (n = 290). Clients in the public agency required greater frequency of visits, more nursing services, and care for a longer period of time than did those in the private agency. The public agency served a larger proportion of indigent and Medicaid clients. Increased service delivery with a decreased financial base may forebode an unhealthy future for traditional public home health agencies.

Health Services Needs and Demand↗
PubMed1987

Effect of subarachnoid hemorrhage on endothelium-dependent vasodilation.

The effect of subarachnoid hemorrhage (SAH) on endothelium-dependent vasodilation of the isolated rabbit basilar artery was examined using an isometric tension recording method. The SAH was induced by injecting 5 ml of fresh arterial blood into the cisterna magna. Sixty-two rabbits were separated into four groups according to the timing of sacrifice: control rabbits, and operated rabbits sacrificed on Days 2, 4, and 6 after SAH. Acetylcholine (ACh) (10(-7) M to 10(-4) M) and adenosine triphosphate (ATP) (10(-7) M to 10(-4) M) were used to evoke dose-dependent vasodilation of isolated arterial rings previously contracted by 10(-6) M serotonin (5-HT). There were no significant differences in the vasodilatory response to ACh among these four groups. Relaxation to approximately 84% of the initial contractile tone occurred with 10(-4) M ACh. On the other hand, the vasodilatory response to ATP was suppressed in the animals sacrificed 2 days after SAH; the relaxation of this group was approximately 52% at 10(-4) M ATP, compared to a relaxation of 87% observed in the other groups of animals. One of the major causes of the impairment of endothelium-dependent vasodilation seems to be an inhibition of the production of endothelium-derived relaxing factor by endothelial cells. After the relaxation studies, the dose-response curves for 5-HT were obtained. Serotonin caused significantly more contraction in the animals sacrificed 2 days after SAH than in the other groups. The present experiments suggest that impairment of the endothelium-dependent vasodilation following SAH, together with the potentiation of the contractile response to vasoactive agents in cerebral arteries, may play an important role in the pathogenesis of vasospasm.

Acetylcholine↗
PubMed1987

Effect of hypoxia on the contractile response to KCl, prostaglandin F2 alpha, and hemoglobin.

The purpose of this experiment was to evaluate the effect of hypoxia on the in vitro contractile responses of canine basilar artery to KCl, prostaglandin (PG) F2 alpha, and hemoglobin. Hypoxia was induced by changing the bubbling gas mixture in the chamber from 95% O2/5% CO2 to 95% N2/5% CO2. Hypoxia augmented the contractile response developed at 95% O2 to 25 mM and 50 mM KCl, 3 X 10(-7) M and 10(-5) M PGF2 alpha, and 10(-6) M hemoglobin. No significant alteration of the hypoxic augmentation in any preparation exposed to 25 mM KCl, 3 X 10(-7) M PGF2 alpha, or 10(-6) M hemoglobin was observed with guanethidine (10(-5) M), prazosin (10(-5) M), methysergide (10(-5) M), or diphenhydramine (10(-5) M). Endothelial denudation did not affect hypoxic augmentation. Hypoxia did not cause any alteration of the contractile response to 10(-6) M PGF2 alpha in Ca++-free media. Pretreatment with a calcium channel blocker, nicardipine, significantly inhibited the hypoxic potentiation of the contractile response to 25 mM KCl, 3 X 10(-7) M PGF2 alpha, and 10(-6) M hemoglobin. These results suggest that hypoxia augments the contractile response to these agonists by a direct action on the smooth-muscle cells, facilitating the transmembrane influx of extracellular calcium. Hypoxia of smooth-muscle cells in the major cerebral arteries might be involved in the pathogenesis of vasospasm.

Animals↗
PubMed1986

Antifibrinolytic therapy in the treatment of aneurysmal subarachnoid hemorrhage.

At the present time, there remains considerable uncertainty regarding the safety and efficacy of antifibrinolytic therapy in the treatment of aneurysmal SAH. Furthermore, there is little to guide us on precisely how to employ the agents. Whether to continue to use antifibrinolytic therapy after considering the results of the 1984 Cooperative Aneurysm Study trial and the Glasgow-Rotterdam-Amsterdam-London trial remains very much a philosophical decision. However, rebleeding is instantly and permanently devastating and 70% fatal, while ischemic deficits from vasospasm have a gradual onset and are potentially reversible. Accordingly, our policy is to continue to use antifibrinolytic therapy in those patients in whom it is desired to delay surgery. Our feeling is that, while there is no demonstrated advantage in acute mortality in either of the previously mentioned series, hypertensive, hypervolemic therapy or calcium channel blocking agents might ameliorate the ischemic consequences of therapy. Accordingly, it is in the context of combined therapy that the reduction in rebleeding will significantly influence patient outcome.

4-Aminobenzoic Acid↗
PubMed1985

Usefulness of computed tomography in predicting outcome after aneurysmal subarachnoid hemorrhage: a preliminary report of the Cooperative Aneurysm Study.

We evaluated the ability of CT performed soon after subarachnoid hemorrhage (SAH) to predict outcome. Generally, the results of CT paralleled level of consciousness in predicting mortality or good recovery. However, CT did detect some groups of patients who were at greater or lesser risk of mortality. If an alert patient had normal CT, 6-month mortality was 2.8%; if blood was detected, mortality rose to 12.3%. Intracerebral hemorrhage or local, thick, or diffuse subarachnoid deposits of blood seen on CT among alert patients were particularly related to increased mortality. CT abnormalities could be used to detect higher mortality rates among drowsy or comatose patients. CT is useful as an adjunct to the clinical examination in predicting outcome after SAH.

Humans↗