Cerebrovascular response to acute decreases in arterial PO2.

The purpose of these studies was to examine the time course of the cerebrovascular response to acute hypoxia in unanesthetized ponies. An electromagnetic flow transducer chronically placed on the internal carotid artery of the pony allowed continuous recording of internal carotid artery blood flow (ICBF) which has been shown to be representative of cerebral blood flow (CBF). The ponies were subjected to three levels of acute isocapnic hypoxia (PaO2 = 62, 44, and 39 mm Hg for hypoxia level I, II, and III, respectively), and the temporal and steady-state cerebrovascular response was examined. ICBF increased significantly at all three hypoxia levels (8, 25, and 40% at hypoxia I, II, and III, respectively). This increase was rapid in the two most severe levels of hypoxia, beginning within 45 s, and was complete within 90 s. The increase lagged behind the reduction in PaO2 by 24-28 s. During the very mild level of hypoxia (I), no such rapid increase in flow was observed; rather, the increase occurred only after 5 min of hypoxia. Microsphere (15 microns diameter) measurements from six ponies during the most severe level of hypoxia (III) demonstrated that CBF increased 38%. Noncerebral tissues known to be vascularly connected to the circle of Willis, and thus capable of receiving blood flow via the internal carotid artery, either did not change or increased so slightly during hypoxia that their effect on ICBF was minimal.(ABSTRACT TRUNCATED AT 250 WORDS)

Methylprednisolone increases absorptive capacity of rabbit ileum in vitro.

The effect of glucocorticoids on intestinal ion transport was studied in ileum in vitro from control and methylprednisolone (MP)-treated (40 mg im for 2 days) rabbits under the following conditions: a) basal rates of Na and Cl transport, b) the response to an individual absorptive stimulus (alanine, glucose, or epinephrine), and c) the response to a combination of the three absorptive stimuli. The results indicate that MP 1) increases basal absorption of Na and Cl and secretion of bicarbonate (as measured by residual ion flux), 2) does not alter the specific transport pathways stimulated by maximal doses of alanine, glucose, or epinephrine, but 3) significantly increases the absorptive capacity of ileum. After addition of combined alanine, glucose, and epinephrine, MP-treated ileum absorbed 15.8 mueq X cm-2 X h-1 Na (vs. 6.6 in controls, P less than 0.001) and 9.5 mueq X cm-2 X h-1 Cl (vs. 4.1 in controls, P less than 0.005). Additionally MP did not alter the Na dependence of either the short-circuit current or Cl absorption found in controls, although there appears to be a portion of residual ion flux insensitive to epinephrine inhibition. These data suggest that the MP-induced increase in absorptive capacity is due to an increase in a postapical transport step, most probably the Na pump.

Steroids alter ion transport and absorptive capacity in proximal and distal colon.

Steroids are potent absorbagogues, increasing Na and fluid absorption in a variety of epithelia. This study characterizes the in vitro effects of pharmacological doses of gluco- and mineralocorticoids on transport parameters of rabbit proximal and distal colon. Treatment with methylprednisolone (MP, 40 mg im for 2 days) and desoxycortone acetate (DOCA, 12.5 mg im for 3 days) resulted in a significant increase in short-circuit current (Isc) in distal colon, suggesting an increase in basal Na absorption. Amiloride (10(-4) M) caused a significantly negative Isc in MP-treated tissue, demonstrating a steroid-induced, amiloride-insensitive electrogenic ion transport in distal colon. The effect of two absorbagogues, impermeant anions (SO4-Ringer) and amphotericin, were compared in control and steroid-treated distal colon. In controls, both absorbagogues increased Isc. Impermeant anions caused a rise in Isc in both MP and DOCA tissues, suggesting that the high rate of basal Na absorption had not caused a saturation of the Na pump. The steroid-treated colons, however, did not consistently respond to amphotericin. Amiloride inhibited the entire Isc in MP-treated distal colon that had been exposed to amphotericin; this suggested that amphotericin had not exerted its characteristic effect on the apical membrane of steroid-treated colon. In proximal colon, steroids did not alter basal rates of transport; however, epinephrine-induced Na-Cl absorption was significantly greater in MP-treated vs control (P less than 0.005). Steroids increase the absorptive capacity of both proximal and distal colon for Na, while increasing basal Na absorption only in the distal colon.(ABSTRACT TRUNCATED AT 250 WORDS)

Potassium secretion in response to taurodeoxycholic acid in the newborn rabbit colon.

The newborn colon fails to secrete Cl in response to concentrations of dihydroxy bile acid that cause Cl secretion in adult colonic tissue in vitro. Bile acids also cause secretion of potassium in adult tissues, but there is no information concerning bile acid effects on potassium transport in newborn colon. We mounted newborn rabbit distal colon in Ussing chambers specially designed for newborn colon and measured potassium transport. Basal potassium transport was secretory. Taurodeoxycholic acid, 100 microM, (TDC) decreased JKnet from -0.76 +/- 0.07 to -0.94 +/- 0.11 microEq cm-2 h-1, p less than 0.05, without increasing Isc. Serosal ouabain, 0.1 mM, abolished the secretory response to TDC. Mucosal Ba2+, a potassium channel blocker in many epithelia, did not inhibit K secretion. Similar serosal exposure to TDC in adult colon tissues decreased JKnet from -0.09 +/- 0.29 to -1.63 microEq cm-2 h-1, p less than 0.01, and increased Isc. We conclude that, although the chloride secretory response to dihydroxy bile acids is absent in the newborn, K secretion is elicited in the newborn, similar to the adult colon.

Regional cerebral blood flow during hypercapnia in the anesthetized rabbit.

These experiments were designed to test the hypothesis that increases in blood flow to the lower brainstem would be greater than forebrain regions during arterial hypercapnia. Total and regional cerebral blood flow (CBF) was measured via the tracer microsphere technique in seven anesthetized New Zealand white rabbits during normocapnia (arterial PCO2 congruent to 40 torr) and hypercapnia (arterial PCO2 congruent to 80 torr). During normocapnia average CBF was 0.77 ml/min/g, and regional measurements of blood flow indicated significantly greater flow to the cerebrum (0.86 ml/min/g) than either the medulla (0.52 ml/min/g) or the pons (0.49 ml/min/g). When arterial PCO2 was increased average CBF increased 113%, and a significant linear regression was calculated for arterial PCO2 vs CBF [CBF (ml/min/g) = 0.028 PCO2 (torr) - 0.502]. The distribution of blood flow within the brain was similar to normocapnia except that blood flow to the cerebellum was now greater than any other brain region (1.97 ml/min/g for the cerebellum compared to 1.66 ml/min/g for the cerebrum). Absolute increases in blood flow to the lower brainstem were equal to or less than other areas of the brain. We conclude that ponto-medullary blood flow does not increase disproportionate to other areas of the brain during hypercapnia, but some redistribution of CBF does occur in that cerebellar blood flow increased significantly more than the cerebrum, medulla, or pons.

Effect of upper airway carbon dioxide on ventilation and blood gases in the awake pony.

Carbon dioxide concentrations were increased during expiration in the upper one-half of the trachea, pharynx, and nasal sinuses to determine if elevation of upper airway CO2 would alter breathing or arterial blood gases in the awake pony. Carbon dioxide (100%) was injected into the midcervical trachea via a chronically implanted transcutaneous cannula during the first part of the animal's expiration. This maneuver elevated upper airway expiratory CO2 concentrations but prevented any exogenous CO2 from entering the lung and being absorbed into the arterial blood. Twelve experiments were performed on six ponies in which upper airway CO2 was elevated 2, 4, and 6% above the normal expired CO2 concentrations. Tidal volume increased in a dose dependent manner during upper airway CO2 exposure, but total ventilation was unchanged from base-line measurements made while the animal breathed room air. Arterial Po2 also increased during upper airway CO2 administration, reaching a mean value 6 Torr (1 Torr = 133.322 Pa) greater than the base-line values at the +6% CO2 exposure. We conclude that upper airway CO2 exposure alters breathing pattern slightly (increases tidal volume) and increases arterial PO2 in the awake pony.

Migrating motility complexes persist after severe traumatic shock in patients who tolerate enteral nutrition.

BACKGROUND: Postinjury small bowel ileus is poorly characterized and may be an important factor in intolerance to enteral nutrition (EN). We, therefore, placed jejunal manometry catheters in high-risk trauma patients. Our hypothesis was that the presence of "fasting migrating motility complex (MMC)" activity and conversion to a "fed pattern" at goal rate of EN would be present in those patients who tolerate jejunal feeding. METHODS: After obtaining baseline fasting manometry pressure tracings, jejunal feeding was advanced stepwise to a set goal while tolerance was monitored and intolerance was treated by a standard approach. RESULTS: Of the 10 study patients, 7 were able to be maintained on EN. Five (50%) had "fasting MMCs" and had good tolerance to early advancement of EN. The remaining five patients did not exhibit "fasting MMCs" and four had poor tolerance to early advancement of EN. Overall, nine patients reached goal rate of EN of which four converted to a "fed pattern." This, however, was not associated with later tolerance to EN. CONCLUSION: EN is feasible following severe traumatic shock. Surprisingly, half of the patients had fasting MMCs. This requires intact neural and motor function and was associated with good tolerance of early EN.