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D W Busija

Publications and source records attributed to D W Busija.

149 records · Page 9Linked to original sources
PubMed1981

Neural effects on cerebral vessels: alteration of pressure-flow relationship.

Cerebral vessels are well innervated by adrenergic and cholinergic fibers. Effects of sympathetic stimulation on cerebral blood flow (CBF) are controversial, but we have concluded that, during normotension and hypotension, sympathetic nerves have little effect on CBF. During acute hypertension, however, sympathetic nerves may have important effects of CBF. Sympathetic stimulation attenuates the passive increase in CBF that occurs during severe steady-state hypertension and after a sudden, modest increase in pressure. Disruption of the blood-brain barrier, which occurs during severe hypertension, also is minimized by sympathetic stimulation. Thus, the concept has emerged that, in contrast to minimal effects of sympathetic nerves under most conditions, sympathetic stimulation may have important protective effects during hypertension. The role of cholinergic nerves in regulation of CBF has not yet been clarified.

Acetylcholine↗
PubMed1980

Cerebral blood flow during normocapnic hyperoxia in the unanesthetized pony.

The effect of hyperoxia on cerebral blood flow (CBF) was examined in 12 unanesthetized ponies. CBF was determined using radioactive microspheres, 15 micrometer in diam, durijng inspriation of the following gases: 1) room air (control); 2) 40% I2 in N2; and 3) approximately 100% O2 with 2.2-4.5% CO2 added to maintain isocapnia. CBF did not change from control values during either level of hyperoxia. However, cerebrospinal fluid (CSF) carbon dioxide tension (PCO2) increased during 40% O2 (delta 1.0 Torr) and approximately 100% O2 (delta 2.9 Torr). This rise in CSF PCO2, not due to a change in CBF, may have resulted from a decrease in the CO2 carrying capacity of cerebral venous blood during hyperoxia (Haldane effect). Although respiration did not change during 40% O2, expired minute volume increased 25% during approximately 100% O2 due to an increase in tidal volume. This rise in respiration was not associated with changes in any of the conventional stimuli to breathing (arterial pH, O2 tension, or PCO2 or CSF pH). One possible explanation was that cerebral extracellular fluid pH, in the vicinity of the central chemoreceptors, or cerebral intracellular fluid pH changed in a direction unlike CSF pH. An alternate explanation was that the CO2 in the inspired gas activated CO2-sensitive receptors in the lungs.

Acid-Base Equilibrium↗
PubMed1979

Isocapnic hyperpnea in awake ponies during inspiration of 4% CO2.

Unanesthetized ponies were given 4% CO2 (inspired CO2 pressure = 28 Torr) to breathe at two levels of arterial O2 pressure (PaO2): 1) near 75 Torr and 2) near 200 Torr. During 4% CO2 breathing, at either level of PaO2, the mean arterial CO2 pressure (PaCO2) was unchanged from control measurements (control measurements were made at the same PaO2, but with no CO2 in inspired air), suggesting that awake ponies can "clear" 4% CO2. The ability of individual ponies to clear 4% CO2 was quite variable: some ponies did not clear 4% CO2 and others cleared 4% CO2 on one day but not on the following day. Based on the average of 20 experiments, however, PaCO2 was unchanged from 40 Torr during inspiration of 4% CO2. Direct measurement of chemical stimuli to breathing in arterial blood and cisternal cerebrospinal fluid indicate that ventilation increased during CO2 breathing even though PaCO2, pHa, PaO2, and CSF pH were not changed in a direction that might explain the accompanying change in ventilation. The authors suggest that stimuli to receptors other than peripheral or medullary chemoreceptors may be responsible for the reported "isocapnic hyperpnea."

Acid-Base Equilibrium↗
PubMedDate not supplied

Influence of hypoxia/ischemia on cerebrovascular responses to oxytocin in piglets.

We examined the effects of hypoxic/ischemic stress on cerebral arteriolar responses to oxytocin in anesthetized piglets. Pial arteriolar diameters were measured using a cranial window and intravital microscopy. First, we evaluated arteriolar responses to topical application of oxytocin during normoxic conditions. We then determined whether 5-10 min of arterial hypoxia, ischemia, or asphyxia alters oxytocin-induced responses. Arterial hypoxia was produced by inhalation of 7.5% O2-92.5% N2 for 10 min. Ischemia was achieved by increasing intracranial pressure for 10 min. Asphyxia was achieved by turning off the ventilator for 5 min. During normoxic conditions, oxytocin dilated pial arterioles by 9 +/- 1% at 10(-8) and by 16 +/- 1% at 10(-6) mol/l (n = 47, p < 0.05). Arteriolar responses to oxytocin did not change with repeated applications (n = 10). Following hypoxia, dilator effect of oxytocin was not changed at 10(-8) (8 +/- 2%) but it was reduced at 10(-6) mol/l (7 +/- 2%; p < 0.05, n = 8). After asphyxia or ischemia, oxytocin did not dilate arterioles at 10(-8) mol/l, whereas 10(-6) mol/l resulted in a mild vasoconstriction (-4 +/- 3 to -6 +/- 4%, n = 6 and 8). Topically applied superoxide dismutase did not preserve arteriolar responses to oxytocin after asphyxia although the arterioles did not constrict to 10(-6) mol/l oxytocin (n = 5). Dilatation of cerebral arterioles in response to oxytocin was reversed to constriction by N(omega)-nitro-L-arginine methyl ester (L-NAME) (15 mg/kg, i.v.; n = 5) and by endothelial impairment by intra-arterial infusion of phorbol ester (10[-5] mol/l; n = 5). We conclude that the absence of pial arteriolar dilation to oxytocin after ischemia and asphyxia indicates endothelial dysfunction which may be involved in the pathology of perinatal brain injury.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗