Хуудас 1 -аас 698 үр дүн
BACKGROUND
This study investigated the relationship between recent morphine use and risk of subdural haemorrhage (SDH) in patients with cancer.
METHODS
This study identified a malignancy cohort of 25,322 patients who had never received morphine treatment. In this malignancy cohort, 200 patients who
The endogenous opioid system has been reported to depress the cardiovascular system during shock states, since naloxone, a potent opiate antagonist, enhances recovery of hemodynamic variables in various shock states. However, the effect of naloxone on long-term survival of experimental animals
Awake rats were bled 2.5 per cent of their body weight during 15 min. This caused a 50-fold increase of plasma adrenaline and a 15-fold increase of plasma noradrenaline after 90 min. Treatment with naloxone or morphine did not significantly affect blood pressure or plasma catecholamine levels. The
The effects of acute, progressive haemorrhage, 1 ml/s were examined in the same mongrel dogs on separate days, unanaesthetized and anaesthetized with morphine (2 mg/kg i.v.) and with administration of nasal oxygen to maintain arterial blood gases at physiological levels. In normal, unanaesthetized
In haemorrhage-shocked rats, the recovery of mean arterial pressure (MAP), pulse pressure (PP) and respiratory rate (RR), as well as the improvement of survival rate, induced by the i.v. administration of centrally acting cholinergic drugs (physostigmine, oxotremorine) are not affected by morphine
Paroxysmal sympathetic storm (PSS) is a rare complication of severe traumatic brain injury or cerebrovascular disease. Various medications have been tried in patients with PSS, but the clinical responses of the patients were variable. We report a classic case of PSS after spontaneous pontine
Primary thoracic blast injury causes a triad of bradycardia, hypotension and apnoea mediated in part via a vagal reflex. Blast casualties may also suffer blood loss, and the response to progressive simple haemorrhage is biphasic: an initial tachycardia followed by a vagally mediated reflex
OBJECTIVE
Naloxone is reported to improve the clinical condition of patients with subarachnoid hemorrhage (SAH). If this effect is vascular determined is unknown, wherefore the influence of morphine and naloxone on cerebral blood flow (CBF) and metabolic rate of oxygen (CMRO2) after SAH was
BACKGROUND
This retrospective cohort study was designed to assess the impact of intrathecal morphine compared with no intrathecal morphine on blood loss and on hemodynamic stability during surgery for pediatric idiopathic scoliosis correction.
METHODS
A retrospective review was done of 256
During extensive blood loss, a plasma volume refill will take place by transfer of extravascular fluid into the circulation. Drugs present in this fluid may follow and cause a rise or a drop in blood drug concentration, depending on their levels and accessibility in the restoration fluid. This study
BACKGROUND
Severe simple hemorrhage (blood loss in the absence of tissue damage and nociception) leads to a reflex bradycardia and hypotension. Earlier studies showed that this reflex can be attenuated by prior administration of morphine. However, some patients may receive morphine, e.g., for
The influence of hemorrhagic shock (removal of 30% of the blood volume) on the pharmacokinetics and the analgesic effect of morphine was investigated in conscious rats. Plasma concentrations of morphine after a bolus injection (5 mg/kg) are higher in the shock animals, which is attributed to a small
Previous reports show that naloxone improves ischemic deficits and clinical conditions in patients after subarachnoid hemorrhage (SAH). These observations have raised concern about the routine use of morphine in the treatment of severe headache after SAH. The present study was carried out to
The effects of naloxone hydrochloride and morphine sulfate on survival were examined in LD40 hemorrhagic shock in rats. Bolus IV injection of naloxone (1.6 mg/kg) following hemorrhage significantly (p less than 0.025) increased the 24 hour survival rate (14/15, 93%), compared to that in
We have previously reported that analgesic doses of morphine accelerate mortality of rats exposed to hemorrhage (Feuerstein and Sirén: Circ Shock 19:293-300, 1986). To study the potential mechanisms involved in this phenomenon, rats were chronically implanted with catheters in the femoral vessels