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Biomedical subjects

M J Breslow

Publications and source records attributed to M J Breslow.

60 records · Page 4Linked to original sources
PubMed1987

Role of hypotension in decreasing cerebral blood flow in porcine endotoxemia.

The role of reduced arterial blood pressure (MAP) in decreasing cerebral blood flow (CBF) during endotoxemia was studied in pentobarbital-anesthetized pigs. Microspheres (15 microns diam) were used to measure regional CBF changes during MAP manipulations in animals with and without endotoxin. Endotoxin (0.2 mg/kg iv) decreased MAP to 50 mmHg and decreased blood flow to the cortex and cerebellum without affecting cerebral cortical oxygen consumption (CMRO2). Elevating MAP from 50 to 70 mmHg during endotoxemia with norepinephrine (1.82 +/- 0.58 micrograms . kg-1 . min-1, iv) did not change cortical blood flow or CMRO2 but increased cerebellar blood flow. Brain stem blood flow was not affected by endotoxin or norepinephrine. When MAP was decreased to 50 mmHg by hemorrhage without endotoxin, no change in blood flow to cortex, cerebellum, or brain stem was observed from base-line levels. These results suggest that decreased MAP below a lower limit for cerebral autoregulation does not account for the decreased CBF observed after endotoxin.

Animals↗
PubMed1986

Adrenal medullary and cortical blood flow during hemorrhage.

We used a radiolabeled microsphere technique to measure adrenal medullary and cortical blood flow during hemorrhagic hypotension. Twenty pentobarbital-anesthetized, ventilated, adult mongrel dogs were bled into a pressurized bottle system to reduce and maintain mean arterial blood pressure at 100, 80, 60, or 40 mmHg (n = 5/group). Blood flow was measured prior to and 2, 5, 10, 15, and 25 min posthemorrhage. Adrenal medullary blood flow increased markedly (100-400%) at all levels of hemorrhage. In contrast, decreases in cortical blood flow were observed (approximately 50%) with hemorrhage to 80, 60, and 40 mmHg. Cortical blood flow returned to control levels at 25 min, except in the 40-mmHg group. Whole adrenal gland blood flow showed early, transient decreases, consistent with the fact that the adrenal cortex comprises the bulk of the gland, but it did not precisely reflect either cortical or medullary blood flow changes. Since this method for measuring adrenal medullary and cortical blood flow was developed for the current experiment, extensive evaluation of the technique was performed (n = 31 animals). These studies included demonstration that injection of 4 X 10(6) microspheres results in sufficient numbers of microspheres in the adrenal medulla and cortex to permit estimation of blood flow (greater than or equal to 400 spheres/sample), that 15-micron spheres are almost completely entrapped in the adrenal gland (greater than 98%), that multiple injections of microspheres (n = 5) do not alter blood flow, and that streaming of microspheres does not appear to occur to any significant extent in this vascular bed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMedDate not supplied

Adrenal insufficiency--an unusual cause of shock in postoperative patients.

OBJECTIVE: To remind physicians that adrenal insufficiency can cause postoperative shock and that the manifestations are difficult to distinguish from those of sepsis. METHODS: We present detailed case reports of three patients who had hyperdynamic shock in the surgical intensive-care unit and describe their response to the cosyntropin stimulation test. RESULTS: All three patients were diagnosed as having adrenal insufficiency with use of the cosyntropin stimulation test. Two of the three patients rapidly recovered; however, because of delay in the diagnosis of adrenal insufficiency, the third patient succumbed to multisystem organ failure. CONCLUSION: The cases presented highlight the need to exclude adrenal insufficiency as a possible cause of hyperdynamic circulatory shock, particularly when no clear-cut diagnosis exists. Early recognition of adrenal insufficiency is important and can result in reversal of shock and prevention of death. Adrenal insufficiency can be diagnosed through screening random cortisol levels and by use of the cosyntropin stimulation test. Patients in addisonian crisis often respond to the first dose of glucocorticoid with dramatic improvement in blood pressure and systemic vascular resistance. Administration of glucocorticoid can thus lead to improved organ perfusion and recovery of organ function. Delays in diagnosis and treatment of acute hypoadrenalism can have a fatal outcome.

Journal Article↗
PubMedDate not supplied

Epidural morphine decreases postoperative hypertension by attenuating sympathetic nervous system hyperactivity.

Twenty-four adults who were undergoing operations on the abdominal aorta were enrolled in a randomized, double-blind, placebo-controlled study in which epidural morphine sulfate (6 mg) was employed to attenuate the sympathoadrenal response to surgery to evaluate the possible contribution of sympathetic nervous system hyperactivity to postoperative hypertension. Patients who received epidural morphine required less parenteral morphine in the 24 hours following surgery, had lower analogue pain scores, and had markedly lower plasma norepinephrine levels when compared with patients in the control group who received an identical volume of saline in the epidural space. Epidural morphine had no effect on plasma epinephrine or arginine vasopressin levels. Fewer patients in the morphine group (4 of 12 vs 9 of 12 patients in the saline group) required treatment for hypertension (mean arterial blood pressure, greater than or equal to 110 mm Hg) in the 24 hours following surgery. In addition, patients in the morphine group had lower blood pressures in the 24 hours following surgery. These data suggest that sympathetic nervous system activity and not adrenal epinephrine or pituitary secretion of arginine vasopressin is responsible for the development of hypertension following aortic surgery. Furthermore, epidural narcotics appear to provide a means of attenuating this response.

Adult↗