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Biomedical subjects

C Galli

Publications and source records attributed to C Galli.

At least 235 records · Page 13Linked to original sources
PubMed1989

Enhancement of the pulmonary vasoconstriction reaction to alveolar hypoxia in systemic high blood pressure.

1. In systemic hypertension the pulmonary vessels show an excessive tone at rest and hyper-react to adrenoceptor stimulation. Alterations in Ca2+ handling by the vascular smooth muscle cells seem to underlie these disorders. Alveolar hypoxia also constricts pulmonary arteries, increasing the intracellular Ca2+ availability for smooth muscle contraction. This suggests the hypothesis that hypoxic pulmonary vasoconstriction depends on similar biochemical disorders, and that the response to the hypoxic stimulus may be emphasized in high blood pressure. 2. In 21 hypertensive and 10 normotensive men, pulmonary arterial pressure and arteriolar resistance have been evaluated during air respiration and after 15 min of breathing 17, 15 and 12% oxygen in nitrogen. Curves relating changes in pulmonary arterial pressure and arteriolar resistance to the oxygen content of inspired gas had a similar configuration in the two populations, but in hypertension were steeper and significantly shifted to the left of those in normotension, reflecting a lower threshold and an enhanced vasoconstrictor reactivity. 3. This pattern was not related to differences in severity of the hypoxic stimulus, degree of hypocapnia and respiratory alkalosis induced by hypoxia, and plasma catecholamines. 4. The association of high blood pressure with enhanced pulmonary vasoreactivity to alveolar hypoxia could have clinical implications in patients who are chronically hypoxic and have systemic hypertension.

Adult↗
PubMed1989

Accumulation of arachidonic acid cyclo- and lipoxygenase products in rat brain during ischemia and reperfusion: effects of treatment with GM1-lactone.

The aim of our study was to investigate the changes of various biochemical parameters (concentrations of lactate, free arachidonate, cyclo- and lipoxygenase products) in rat brain after ischemia and reperfusion and the effects of pretreatment with the ganglioside derivative GM1-lactone on the same parameters. Ischemia was induced by reversible occlusion of common carotid arteries for 20 min, which included a final 5 min of respiration of 5% oxygen in nitrogen. Reperfusion was obtained by removing the occlusion. Pre-ischemic conditions were obtained on sham-operated animals. Animals were killed by microwave irradiation of their heads. Brain levels of lactate and of free arachidonate were markedly increased after ischemia and returned to normal values at 5 min of reperfusion. Levels of the cyclooxygenase metabolites prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2 were increased after ischemia, whereas levels of the lipoxygenase metabolite leukotriene C4 (LTC4) did not change. After reperfusion, a very marked increase of the cyclooxygenase products occurred but not of LTC4. Treatment with GM1-lactone prevented the elevation of cyclo- and lipoxygenase metabolites especially during reperfusion, with limited effects on lactate and free arachidonate levels.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Enhanced hypoxic pulmonary vasoconstriction in hypertension.

In this study, we tested the hypothesis that hypoxic pulmonary vasoconstriction may be enhanced in systemic hypertension. The hypothesis took origin from the following two considerations: alveolar hypoxia constricts the pulmonary vessels by enhancing the Ca2+ penetration across sarcolemma of the smooth muscle cells and systemic high blood pressure is associated with an elevation of tone and reactivity of the lung vessels, which seems to depend on an excessive cytosol free Ca2+ concentration due to alterations in sodium handling and in the Na+-Ca2+ exchange system. These considerations suggest the possibility that the disorders in the biochemistry of smooth muscle contraction in hypertension facilitate the rise of cytosol Ca2+ concentration during alveolar hypoxia, thus resulting in a potentiation of the vasoconstrictor properties of this stimulus. In 43 hypertensive and 17 normotensive men, pulmonary arteriolar resistance has been evaluated during air respiration and after 15 minutes of breathing 17%, 15%, and 12% oxygen in nitrogen. Curves relating changes in pulmonary arteriolar resistance to oxygen breathing contents had similar configuration in the two populations but in hypertension were steeper and significantly shifted to the left, reflecting a lower threshold and an enhanced reactivity. This pattern was not related to differences in severity of the hypoxic stimulus, plasma catecholamine concentration, or hypocapnia and respiratory alkalosis induced by hypoxia and probably was not mediated through alpha-receptor activation. Calcium channel blockade with nifedipine was able to almost abolish both the normotensive and the hypertensive pulmonary vasoconstriction reaction. These findings support the hypothesis that hypoxic pulmonary vasoconstriction may be enhanced in systemic hypertension.

Adrenergic alpha-Antagonists↗
PubMed1989

Nifedipine reduces pulmonary pressure and vascular tone during short- but not long-term treatment of pulmonary hypertension in patients with chronic obstructive pulmonary disease.

We evaluated in patients suffering from COPD-related pulmonary hypertension whether nifedipine therapy lowers acutely and chronically pulmonary vascular pressure and resistance and whether pulmonary transmural pressure may be further lowered by the combined use of nifedipine and oxygen. Changes of the pulmonary vascular tone were determined on the pulmonary driving pressure/flow curve, which was generated by upright exercise. Fifteen patients with COPD and mean pulmonary pressure greater than or equal to 20 mm Hg were studied at control (Week 0) and after 1 wk of nifedipine treatment (180 mg daily, Week 1). It was possible to pursue the same nifedipine daily dosage for 2 months in 10 patients, who were re-evaluated after 8 wk of treatment and after nifedipine withdrawal the following week. At Week 1, mean pulmonary transmural pressure was reduced (32.8 +/- 4.1 versus 27.3 +/- 2.8 mm Hg, mean +/- SE, p less than 0.05) via active pulmonary vasodilation because the pulmonary driving pressure/flow curve was shifted right and downward. Both mean transmural pulmonary pressure lowering effect and active pulmonary vasodilatation regressed during long-term nifedipine treatment. Oxygen reduced pulmonary transmural pressure (32.8 +/- 4.1 versus 28.6 +/- 2.9 mm Hg, p less than 0.05, Week 0); however, this effect always disappeared during nifedipine treatment. We conclude that nifedipine should not be used as long-term treatment for COPD-related pulmonary hypertension and that nifedipine inhibits the oxygen capability to reduce pulmonary pressure.

Adult↗
PubMed1989

[The anatomo-pathologist as a necroscopy physician in the field: a balance-sheet of 4 years' experience].

The quality of the certificates of death for 2429 cases, all the residents died at home in the USL 70 during the period 1.8.83-31.12.87, was evaluated thanks to the necroscopic activity of the Legnano's Hospital pathologist. All the information, oral or written, available about each case was used to check the family doctor's certificate. Any correction to the certificate was discussed with the certifier. During the period a gradual and progressive reduction of error in the statement of the underlying cause of death was shown. The improvement comes out using different quality indicators.

Autopsy↗
PubMed1989

[Circulatory and renin response to the administration of nifedipine in renovascular hypertension].

In 12 severe (diastolic values averaging 114 mmHg) hypertensives with unilateral renal artery stenosis (angiography) and hyperreninemia, we investigated the acute effects of nifedipine (10 mg orally) on renin and systemic hemodynamics. Plasma renin activity was determined on blood samples withdrawn from the aorta and both renal veins, so that "ischemic lateralization" could be evaluated through appropriated derived indexes. Nifedipine promptly and significantly lowered the aortic pressure in all patients. At 30 min maximal circulatory responses were recorded, which consisted of 22% decrease in mean aortic pressure (from an average of 144.6 +/- 15 to an average of 113 +/- 11 mm Hg), 44% reduction of systemic vascular resistance (from 2162 +/- 540 to 1205 +/- 279 dynes.S.cm-5), 33% rise of cardiac index (from 2920 +/- 970 to 3875 +/- 986 ml/min/m2). These effects were still evident, although somewhat tempered, after 180 min continuous monitoring; they were qualitatively and quantitatively similar to those reported by some authors in primary hypertensives with similar levels of blood pressure. After nifedipine, renin activity of the systemic blood significantly rose, due to a potentiated release from the kidney with arterial stenosis. This effect, that was interfered as a due to further reduction of the renal perfusion pressure, improved the significance of "ischemic lateralization" indexes and supported the diagnosis of renovascular hypertension in all of cases. It is suggested that nifedipine may not only be regarded as an additional diagnostic tool, but also as an effective antihypertensive agent in this disorder, al least in the short term. This contrasts with the previous suggestion of nifedipine as substantially more effective in low-renin rather than high-renin hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Anomalies of diastolic filling common to both ventricular cavities in hypertension].

In a population of 43 primary hypertensive patients we investigated the mitral and tricuspid valve flow in order to test whether: a) hypertension, as compared to normotension (Group 0, 10 normotensive subjects), alters the ventricular filling; b) changes are shared by the left and the right side of the heart; c) the structural characteristics (ultrasounds) of the left ventricle (LV) correlate with these changes. Hypertensives were divided into: Group 1, 11 patients in whom thickness (th) of both the ventricular septum (VS) and LV posterior wall (PW) was within a normal range (mean +/- 1 SD of values derived from 145 normal subjects); Group 2, 8 patients whose VSth exceeded normal values by more than 1 SD; Group 3, 24 patients in whom both VSth and PWth exceeded normal values by more than 1 SD. Groups 0, 1, 2 and 3 were homogeneous regarding gender, age, heart rate, LV cavity dimensions and systolic function. Blood pressure was slightly increased from Group 1 to Group 2 to Group 3. Mitral peak flow velocity in early diastole (PFVE) was similar in the 4 groups; in late diastole peak flow velocity (PFVA) through the same valve in each of the 3 hypertensive groups was significantly higher than in Group 0; as a consequence, PFVE/PFVA and E'/A' areas in hypertensives were significantly smaller than in normotensives. The flow pattern through the tricuspid valve was quite similar to this in each group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Vitamin E influences the effects of fish oil on fatty acids and eicosanoid production in plasma and circulating cells in the rat.

An EPA enriched oil (MaxEPA, Seven Seas, U.K. containing 18% EPA and 12% DHA) alone or supplemented with 10 mg/ml/alpha tocopherol, was administered by gastric intubation at the dose of 3.2 ml/kg/day for a period of eight weeks to male rats fed a standard diet. An additional group of animals was treated with the same amount of olive oil. The administration of MaxEPA alone resulted, as expected, in accumulation of EPA and reduction of AA levels in plasma, platelet, red blood cell and PMNL phospholipids, when compared to values in the olive oil group. In addition, levels of linoleic acid were elevated, suggesting inhibition of the conversion of linoleic to arachidonic acid. Formation of i.r. TxB2 by stimulated PRP, of i.r. 6-keto-PGF1 alpha by perfused aortas, and of IR LTB4 and C4 by stimulated PMNL were reduced, but production of superoxide anion by PMNL was enhanced by MaxEPA treatment vs the olive oil treatment. Supplementation of MaxEPA with vitamin E caused a smaller reduction of 20:4 levels and a smaller increase of 20:5 levels in plasma and cell phospholipids and modified the effects of MaxEPA on eicosanoid and superoxide anion production, suggesting that lipid peroxidation may mediate some of the biological effects of omega 3 fatty acids.

Animals↗
PubMed1988

Combined hemodynamic overload of the left and right ventricles as a possible cause of interventricular septum preponderance in high blood pressure.

We tested whether overload of the two ventricles may be associated with a preponderance of interventricular septum in patients with high blood pressure. The rationale is that the septum is shared by the greater and lesser circulation and that in hypertension the latter shows the same qualitative hemodynamic alterations as the former. Among 65 hypertensive patients, 40 (group 1) showed (echo) posterior wall thickness within the mean +/- 1 SD of 62 normal subjects, and 25 (group 2) had a posterior wall thickness exceeding the mean + 1 SD of the normal population. Both groups were subdivided into subgroups A and B, which included patients whose ventricular septum was similar to (within the mean + 1 SD) and thicker than (exceeding the mean + 1 SD) the posterior wall thickness in the corresponding group, respectively. Resting differences in systemic and pulmonary pressure and vascular resistance among subgroups 1A, 1B, and 2A were not significant; however, in subgroup 2B these variables exceeded those in the other subgroups to a significant extent. During cold pressor testing (CPT) the levels reached and the changes in pressure and resistance from baseline values in both circuits were much greater in subgroups B than in subgroups A. The baseline plasma norepinephrine value showed a trend toward an increase from subgroup 1A to 1B and from subgroup 2A and 2B; during CPT norepinephrine invariably changed and in subgroups B it rose significantly more than in subgroups A. It was not determined whether this caused the hemodynamic overload in subgroups B.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Phosphatidylinositol (PI) and PI-associated arachidonate are elevated in platelet total membranes of type IIa hypercholesterolemic subjects.

The lipid composition (phospholipid distribution and fatty acid patterns of individual glycerophospholipids) and levels of lipid components (cholesterol, total and individual phospholipid classes, arachidonic acid) have been determined in total membranes of platelets from type IIa hypercholesterolemic (HC) and control (C) subjects. Levels of cholesterol and total phospholipid, relative to the protein content, were about 80% and 60% higher respectively in platelet total membranes from HC subjects. Small differences between the two groups of samples were observed for the phospholipid distribution and the fatty acid patterns. Concentrations of individual phospholipid classes, were on the average 60% higher in HC than in C platelet membranes, with an even greater difference for phosphatidylinositol (PI) and sphingomyelin. Levels of arachidonic acid, relative to the protein content, were also 60-80% higher in membranes from HC platelet with a more than 100% increase in PI. The higher levels of the eicosanoid precursor fatty acid in phospholipids and especially in PI, which is considered a donor pool for eicosanoid synthesis, may be a contributing factor for the greater thromboxane formation and enhanced aggregation, upon stimulation, of platelets from HC patients in comparison to platelets from control subjects.

Adult↗
PubMed1988

The carbochromene derivative AD6 reduces the TxB2/6-keto-PGF1 alpha ratio in cerebral cortex during hypoxia and recovery and leukotriene synthesis in brain tissue, in the rat.

Pretreatments of rats with the Carbochromene derivative AD6 (4 mg/kg i.p., 2 h before sacrifice) resulted in elevation of brain levels of 6-keto-PGF1 alpha in cerebral cortex under physiological conditions, had no effect on levels of TxB2 and 6-Keto-PGF1 alpha at 30 min of hypoxia (respiration of 5% O2 in N2) and prevented the accumulation of TxB2 occurring in brain at 5 min of recovery after hypoxia. In addition, the accumulation of LTC4 and B4 in brain slices incubated in the presence of the Ca++ ionophore A23187 and arachidonic acid, was reduced in samples obtained from pretreated rats. The drug, thus, had favourable effects on the 6-keto-PGF1 alpha/TxB2 ratio in normal conditions, as well as in conditions of altered oxygen supply. In addition it reduced the formation of compounds, the leukotrienes, which may exert pro-inflammatory activities on the cerebral microcirculation.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

A study of the interaction between the Na+, K+ pump and Na+:Ca2+ exchange in macrophages and vascular smooth muscle cells.

Blaustein (Am J Physiol 1977;232:C165-C173) postulated that Na+:Ca2+ exchange in vascular smooth muscle plays a key role in the link between sodium and hypertension. Investigation of this hypothesis was facilitated by the use of: a) Sr2+, a slowly transported Ca2+ analogue, and b) new quasispecific inhibitors of Na+:Ca2+ exchange such as 2',4'-dimethylbenzamil. Preliminary experiments in mouse macrophages showed that the initial rate of Sr2+ uptake lasted for at least 15 minutes and was therefore easier to measure than the initial rate of unidirectional isotopic Ca2+ influx (which lasted less than 30 seconds). In cells with normal Na+ content, basal Sr2+ influx (432 +/- 77 mumol [L cells X h]-1; mean +/- SEM of seven experiments) exhibited properties compatible with a ground membrane leak for divalent cations (quasilinear dependence on the external Sr2+ concentration, partial or full resistance to external Ca2+, Ba2+, verapamil, and 2',4'-dimethylbenzamil). Membrane depolarization by external K+ was unable to modify basal Sr2+ uptake. Conversely, a 100% increase in cell Na+ content by preincubation with ouabain increased the rate of Sr2+ uptake by 233 +/- 48 mumol (L cells X h)-1 (mean +/- SEM of seven experiments). 2',4'-Dimethylbenzamil, but not the Ca2+ antagonists diltiazem or methoxyverapamil, inhibited ouabain-stimulated Sr2+ influx (IC50 of about 3 X 10(-5) M). 2',4'-Dimethylbenzamil was also able to inhibit Na+ efflux (by 3.05 +/- 0.98 mmol (L cells X h)-1; mean +/- SEM of three experiments) suggesting the existence of Na+:Sr2+ exchange.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗