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P T Nowicki

Publications and source records attributed to P T Nowicki.

14 recordsLinked to original sources
PubMed1992

Effect of increased tissue oxygen uptake on autoregulation in postnatal intestine.

To determine whether the rate of tissue oxygen utilization affects pressure-flow autoregulation in an age-dependent fashion in postnatal swine intestine, in vitro gut loops from 3- and 35-day-old swine were subjected to a 35% step reduction in arterial pressure under control conditions, during intra-arterial infusion of 2,4-dinitrophenol (DNP), and 30 min after luminal instillation of predigested artificial swine milk. Autoregulation was quantitated by determining the effect of pressure reduction on vascular resistance, and also by calculating Gf, a flow-controlling gain factor that relates pressure and flow. DNP infusion increased oxygen uptake 77 and 58% in gut from 3- and 35-day-old swine, respectively, whereas feeding increased oxygen uptake approximately 50% in both groups. Under control conditions, arterial pressure reduction had no effect on vascular resistance in either group. During DNP infusion and 30 min after feeding, however, intestine from 35- but not from 3-day-old swine demonstrated significant vasodilation in response to pressure reduction. Gf averaged -0.06 +/- 0.11 vs. 0.21 +/- 0.08 (P < 0.05) before vs. DNP infusion, and 0.06 +/- 0.03 vs. 0.22 +/- 0.06 (P < 0.05) before vs. 30 min after feeding in intestine from 35-day-old swine; these increases in Gf indicate that the intensity of the pressure-flow response increased during experimental treatments. In contrast, Gf averaged -0.11 +/- 0.07 vs. -0.23 +/- 0.08 before vs. DNP infusion, and -0.23 +/- 0.06 vs. -0.23 +/- 0.09 before vs. 30 min after feeding in intestine from 3-day-old swine.(ABSTRACT TRUNCATED AT 250 WORDS)

2,4-Dinitrophenol↗
PubMed1991

Effect of sustained mesenteric nerve stimulation on intestinal oxygenation in developing swine.

The effects of sustained mesenteric nerve stimulation on intestinal oxygenation were determined in 3- and 35-day-old swine. Studies were conducted in pentobarbital-anesthetized animals during free-flow or constant-flow perfusion. Square-wave stimuli sufficient to induce maximal resistance vessel constriction were applied to postganglionic periarterial mesenteric nerves and each stimulation was sustained until measured variables reached steady state. When vascular resistance data were analyzed without data transformation, autoregulatory escape of intestinal vascular resistance was more complete in 3- than in 35-day-old animals when the escape process was complete; however, expression of these data as escape indexes revealed a similar degree of escape in both age groups. In 35-day-old animals, (a-v)O2 increased during sustained nerve stimulation under free-flow conditions; under constant-flow conditions, (a-v)O2, 86Rb extraction, and capillary permeability-surface area product were lower at completion of the escape process compared with baseline. In 3-day-old swine, these variables remained unchanged from baseline. Intestinal O2 uptake was compromised by sustained nerve stimulation, and this effect was similar in both age groups. We conclude that sustained nerve stimulation reduces intestinal oxygenation to a similar degree in 3- and 35-day-old swine. It is important to note, however, that the response of 3-day-old swine may be dissimilar from that which occurs during immediate postnatal life; indeed, the intestinal hemodynamic response of swine less than or equal to 1 day old should not be extrapolated from the response of 3-day-old animals.

Aging↗
PubMed1991

Effects of hypoxia and ischemia on autoregulation in postnatal intestine.

Pressure-flow autoregulation was quantified within in vitro intestine from 3- and 35-day-old swine before and after lowering arterial PO2 (hypoxia) or lowering baseline blood flow by means of norepinephrine infusion (ischemia). Autoregulation was elicited by reducing arterial pressure approximately 33% from an age-appropriate baseline pressure. In 3-day-old intestine, autoregulation was unaffected by hypoxia or ischemia: vascular resistance was unchanged after pressure reduction, while Gf averaged -0.33 +/- 0.15 vs. -0.26 +/- 0.05 under control vs. hypoxic conditions, and -0.48 +/- 0.15 vs. -0.46 +/- 0.11 under control vs. ischemic conditions, respectively. In 35-day-old intestine, autoregulation was enhanced by hypoxia and ischemia. Under both experimental conditions, vasodilation was noted in response to pressure reduction: Gf averaged -0.04 +/- 0.14 vs. 0.38 +/- 0.08 under control vs. hypoxic conditions, and -0.12 +/- 0.10 vs. 0.28 +/- 0.08 under control vs. ischemic conditions, respectively. Regression analysis revealed a significant inverse linear correlation between Gf and venous PO2 in older, but not younger, subjects. Significant relationships between Gf and blood flow were not demonstrated in either group under any experimental condition. We conclude that autoregulation is enhanced within in vitro intestine from 35-, but not 3-day-old, swine during hypoxia or ischemia, and that reduction of venous PO2 is the principal factor responsible for the effect noted in older subjects.

Analysis of Variance↗
PubMed1990

Effect of O2 availability on intrinsic vascular response to venous pressure elevation in postnatal swine intestine.

The goal of these experiments was to determine whether the intrinsic vascular response of postnatal intestine to acute venous pressure elevation was dependent on the preexisting level of oxygen availability. To this end, acute venous hypertension was applied to denervated loops of small intestine from 3- and 35-day-old swine anesthetized with pentobarbital during free-flow and controlled-flow perfusion. During controlled-flow perfusion, the base-line blood flow rate was set slightly above (+5%; high flow) or significantly below (-50%; low flow) the rate noted during free-flow perfusion so as to directly alter intestinal oxygen availability. The vascular response to venous hypertension noted under controlled high-flow perfusion was similar in both age groups and generally consistent with that noted under free-flow perfusion. In contrast, the response noted during low-flow perfusion was clearly age dependent. In the older group, vascular resistance decreased (27%), while arteriovenous oxygen content difference [(a-v)O2] and tissue oxygen uptake remained unchanged. In the younger group, vascular resistance remained unchanged, whereas (a-v)O2 and oxygen uptake decreased (14%). We conclude that the intrinsic vascular response to venous pressure elevation is dependent on the preexisting level of oxygen availability in intestine from 35- but not from 3-day-old swine. We speculate that the local metabolic vascular response to venous hypertension is more effective in intestine from older than from younger swine.

Aging↗
PubMed1988

Autoregulation in the developing postnatal intestinal circulation.

The relationships among perfusion pressure, blood flow, and oxygen uptake were determined in in vitro ileal loops from 3- and 35-day-old swine. Arterial perfusion of the ileal loops was achieved using a reservoir perfusion apparatus that allowed direct manipulation of perfusion pressure. The hematocrit, partial pressure of oxygen, and partial pressure of carbon dioxide of the blood used to perfuse the gut loops were standardized. During steady-state perfusion at an arterial pressure of 100 mmHg and venous pressure of 0 mmHg, ileal loops from 3-day-old swine demonstrated a higher blood flow (55 vs. 27 ml.min-1.100 g-1, 3 vs. 35 day old) and lower arteriovenous oxygen content difference (3.5 vs. 6.6 ml O2/dl). Oxygen uptake was not statistically different between groups (1.99 vs. 1.76 ml O2.min-1.100 g-1). During perfusion pressure reduction from 150 to 25 mmHg (in successive decrements of 25 mmHg), pressure-flow autoregulation was present in ileal loops from 35-day-old swine but not in ileal loops from 3-day-old swine. Similarly, tissue oxygen uptake was more effectively maintained in ileal loops from older swine during perfusion pressure reductions. We speculate that the efficacy of intrinsic regulation of intestinal hemodynamics and oxygenation is dependent, in part, on postnatal age.

Aging↗
PubMed1988

Effects of arterial hypoxia and isoproterenol on in vitro postnatal intestinal circulation.

We have previously speculated that intestinal vasodilation and hyperemia that occur in response to moderate arterial hypoxia in newborn swine in vivo are mediated by factors intrinsic to the intestinal circulation. To test this speculation, we vascularly perfused in vitro loops of jejunum from postnatal swine with control (PO2 98 +/- 4 mmHg) and hypoxic (PO2 38 +/- 2 mmHg) blood obtained from donor swine. In response to hypoxic perfusion, jejunal vascular resistance decreased 12 +/- 2, 13 +/- 3, 33 +/- 5, and 42 +/- 3% in in vitro loops from 1-, 7-, 14-, and 30-day-old swine, respectively, whereas jejunal oxygen uptake decreased 53 +/- 6, 29 +/- 6, 31 +/- 4, and 13 +/- 6% in these age groups. To clarify whether this age-dependent vasodilation was unique to the stimulus of arterial hypoxia or a response characteristic of the postnatal swine intestine to other vasodilator stimuli, we also determined the effect of intra-arterial isoproterenol infusion at rates of 0.01, 0.1, and 1.0 micrograms/min on jejunal hemodynamics and oxygenation in vitro. In jejunal loops taken from 7- and 30-day-old swine, isoproterenol caused a similar degree of vasodilation at each drug-infusion rate. We conclude that vasodilation of the postnatal swine intestine in response to moderate arterial hypoxia is mediated, at least in part, by intrinsic vascular regulation. We speculate that the age dependency of hypoxic vasodilation may reflect a relative inability of the intestine from very young swine to respond to the stimulus of arterial hypoxia.

Aging↗
PubMed1987

Intestinal blood flow and oxygen uptake in the neonatal piglet during reduced perfusion pressure.

The effect of reduced perfusion pressure on neonatal intestinal blood flow, vascular resistance, arterio-venous oxygen content (a-v O2), and oxygen uptake was studied in nine fasted newborn piglets, aged 5-6 days. Successive reductions of intestinal perfusion pressure were achieved by a clamp on the thoracic aorta. Intestinal blood flow decreased after each reduction of perfusion pressure. Intestinal vascular resistance increased and Gf, a measure of flow control, was negative after all but the final, most severe reduction of perfusion pressure. However, intestinal a-v O2 increased after each pressure reduction and intestinal oxygen uptake was thus maintained at greater than or equal to 95% of its baseline value until perfusion pressure was reduced to less than or equal to 70% of its base-line value. The neonatal intestine maintains tissue oxygen uptake during moderate hypotension, and this is accomplished by regulation of a-v O2, rather than by regulation of blood flow.

Animals↗
PubMed1987

Effect of intestinal denervation on intestinal vascular response to severe arterial hypoxia in newborn swine.

We examined the effects of alpha-adrenergic blockade (phentolamine) and intestinal denervation on the circulatory response of the newborn swine intestine to severe arterial hypoxia. Intestinal vascular resistance significantly increased during severe arterial hypoxia in the control group, whereas no change in intestinal vascular resistance was observed in the phentolamine or denervation groups at this time. Intestinal perfusion pressure increased in the control group but decreased in the phentolamine and denervation groups during severe arterial hypoxia. Despite the difference in intestinal vascular resistance, intestinal blood flow decreased in a similar manner in all groups during severe arterial hypoxia. Intestinal arteriovenous O2 content difference [(a-v)O2] and O2 uptake were greater during severe arterial hypoxia in the phentolamine and denervation groups than in the control group. We speculate that the sympathetic stimulation mediates the increase in intestinal vascular resistance in newborn swine during severe arterial hypoxia; and sympathetic stimulation limits the increase in intestinal (a-v)O2, which occurs during severe arterial hypoxia in the newborn swine intestine.

Animals↗
PubMed1986

Intestinal blood flow and O2 uptake during hypoxemia in the newborn piglet.

Previous work has indicated that the neonatal intestinal circulation responds to hypoxemia with vasoconstriction and subsequent intestinal ischemia. This work was carried out in newborn lambs, a ruminant species, and may not be representative of all newborns. Therefore, we measured intestinal blood flow, vascular resistance, tissue O2 uptake, and cardiac output during normoxemia and varying degrees of hypoxemia in newborn piglets, a nonruminant species. Hypoxemia was induced by adding N2 gas to the inspired gas mixture, and measurements were obtained over a wide range of arterial O2 contents (2.2-15.6 ml O2 X dl-1). Intestinal blood flow increased in response to moderate hypoxemia and decreased in response to severe hypoxemia. The changes in intestinal blood flow were primarily due to change in intestinal vascular resistance, not cardiac output. Intestinal O2 was independent of arterial O2 content until the latter decreased below approximately 6.5 ml O2 X dl-1. These data indicate that the response of the neonatal intestinal circulation to hypoxemia is species specific and that the nonruminant neonatal intestine is capable of vasodilation in response to moderate hypoxemia.

Animals↗
PubMed1986

Alterations in cerebral blood flow and oxygen consumption during prolonged hypocarbia.

The effect of prolonged (2 h) hypocarbia on cerebral blood flow, oxygen delivery, extraction, and consumption was studied in eight, 1- to 4-day-old piglets. Hyperventilation to PaCO2 less than 20 mm Hg acutely (30 min) decreased cerebral blood flow and oxygen consumption. Cerebral oxygen consumption was subsequently restored via increases in cerebral blood flow and thus, cerebral oxygen delivery. Cerebral oxygen extraction rose from a normocarbic baseline of 50 to 75% with acute hypocarbia and was maintained at this level. The percent decrease in blood flow to the cerebrum was greater than that to other brain regions during hypocarbia.

Animals↗
PubMed1986

The effect of naloxone on the hemodynamics of the newborn piglet with septic shock.

Naloxone has been shown to reverse the hemodynamic sequelae of experimental septic shock in adult animal models. Its effectiveness in the newborn has not been studied. To further investigate the efficacy of naloxone, we instrumented 18 piglets for continuous measurement of mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, heart rate, left ventricular pressure, contractility, cardiac output, and O2. Oxygen consumption, systemic vascular resistance, and pulmonary vascular resistance were calculated. Following a stabilization period, group B beta-hemolytic Streptococci were infused over 30 min. Following the infusion, naloxone (1 mg/kg) was given followed by a continuous infusion of 1 mg/kg/h in nine treatment animals. Nine control animals were given an equal volume of saline. Both groups developed significant increases in mean pulmonary arterial pressure followed by a return to baseline. Oxygen consumption, cardiac output, contractility and mean arterial pressure decreased in both groups. Treatment with naloxone was associated with a cessation in the fall in the mean arterial pressure and the contractility. The difference in mean arterial pressure and contractility between groups was significant. The naloxone group had significantly improved 5-h survival. We speculate that naloxone may reverse some of the hemodynamic sequelae and improve survival in newborns with septic shock.

Animals↗
PubMed1985

The effect of blood volume expansion on gastrointestinal oxygenation in piglets.

Regional and total gastrointestinal (GI) blood flow, O2 delivery, O2 extraction, and O2 consumption were measured before and after acute blood volume expansion in 2-day-old piglets. Blood flow was measured with radionuclide-labeled microspheres. Sixty minutes after a rapid transfusion of age- and hematocrit-matched piglet donor blood, 51Cr-measured blood volume increased 19% while an increase in hematocrit suggested plasma transudation to the extravascular space had occurred in response to blood volume loading. Following transfusion, total GI blood flow and O2 delivery did not change, although O2 extraction decreased by 31 +/- 4%. O2 consumption by the GI tract decreased from 2.0 +/- 0.19 ml O2 X min-1 X 100 g-1 to 1.46 +/- 0.24 ml O2 X min-1 X 100 g-1 1 h after transfusion. Feeding was then accomplished via orogastric tube to determine if animals stressed by blood volume loading would increase GI O2 consumption in response to feeding. The postprandial increase in GI O2 consumption was similar to that previously reported in newborn piglets. Therefore, in the fasting state, acute blood volume loading disrupts GI O2 transport at the capillary level and decreases GI O2 consumption. However, animals subjected to blood volume loading appear capable of increasing GI O2 consumption after feeding.

Animals↗
PubMed1985

Gastrointestinal blood flow and O2 uptake in piglets: recovery from hypoxemia.

Gastrointestinal (GI) blood flow, O2 transport, and O2 uptake were measured during recovery from severe hypoxemia in newborn piglets. Hypoxemia was induced by lowering the inspired O2 concentration to 0.05 for 15 min. This resulted in an 82% decrease in GI O2 uptake. Recovery measurements were obtained 5 and 65 min after restoration of normoxia. During early recovery (5 min), GI O2 uptake increased above prehypoxemia baseline, presumably to "repay" the O2 deficit incurred during hypoxemia. This was mediated by an increase in the arteriovenous O2 content difference, as GI blood flow did not increase above prehypoxemia baseline. During late recovery (65 min), GI blood flow, O2 delivery, and arteriovenous O2 content difference decreased below prehypoxemia baseline. This resulted in a 52% decrease in GI O2 uptake below prehypoxemia baseline. Therefore, early recovery was characterized by an appropriate increase in GI O2 uptake; however, late recovery was characterized by a significant reduction in GI O2 transport and uptake. Circulatory homeostasis was not reestablished during the late recovery period.

Animals↗